Endonotes 2

LOM Endocrine System Notes
CHAPTER 16 -ENDOCRINE SYSTEM

INTRODUCTION
The endocrine system is an information signaling system much like the nervous system.
However, the nervous system uses nerves to conduct information, whereas the endocrine
system uses blood vessels as information channels. Glands located in many regions of the
body release into the bloodstream specific chemical messengers called hormones (from
the Greek word hormōn, meaning urging on) that regulate the many and varied functions of
an organism. For example, one hormone stimulates the growth of bones, another causes the
maturation of sex organs and reproductive cells, and another controls the metabolic rate
(metabolism) within all the individual cells of the body. In addition, one powerful endocrine
gland below the brain secretes a wide variety of different hormones that travel through
the bloodstream and regulate the activities of other endocrine glands.
Hormones produce their effects by binding to receptors, which are recognition sites in the
various target tissues on which the hormones act. The receptors initiate specific biologic
effects when the hormones bind to them. Each hormone has its own receptor, and binding
of a receptor by a hormone is much like the interaction of a key and a lock.
Endocrine glands, no matter which hormones they produce, secrete their hormones
directly into the bloodstream. Exocrine glands send chemical substances (tears, sweat,
milk, saliva) via ducts to the outside of the body. Examples of exocrine glands are sweat,
mammary, mucous, salivary, and lacrimal (tear) glands.
The ductless, internally secreting endocrine glands are listed as follows.

[1] thyroid gland
[2] parathyroid glands (four glands)
[3] adrenal glands (one pair)
[4] pancreas (islets of Langerhans)
[5] pituitary gland
[6] ovaries in female (one pair)
[7] testes in male (one pair)
[8] pineal gland
[9} Thymus gland
The last two glands on this list, the pineal and the thymus glands, are included as endocrine
glands because they are ductless, although little is known about their endocrine function in
the human body. The pineal gland, located in the central portion of the brain, secretes
melatonin. Melatonin functions to support the body’s “biological clock” and is thought to
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induce sleep. The pineal gland has been linked to a mental condition, seasonal affective
disorder (SAD), in which the person suffers depression in winter months. Melatonin
secretion increases with deprivation of light and is inhibited by sunlight. Calcification of
the pineal gland can occur and can be an important radiologic landmark when x-rays of the
brain are examined.
Hormones are also secreted by endocrine tissue in other organs apart from the major
endocrine glands. Examples are erythropoietin (kidney), human chorionic gonadotropin
(placenta), and cholecystokinin (gallbladder). Prostaglandins are hormone-like substances
that affect the body in many ways. First found in semen (produced by the prostate gland)
but now recognized in cells throughout the body, prostaglandins (1) stimulate the
contraction of the uterus; (2) regulate body temperature, platelet aggregation, and acid
secretion in the stomach; and (3) have the ability to lower blood pressure.
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ENDOCRINE TISSUE (APART FROM MAJOR GLANDS): LOCATION,

SECRETION, AND ACTION
Location Secretion Action
Body cells Prostaglandins Aggregation of platelets
Contract uterus
Lower acid secretion in stomach
Lower blood pressure
Gastrointestinal tract Cholecystokinin Contracts gallbladder
Gastrin Stimulates gastric secretion
Secretin Stimulates pancreatic enzymes
Kidney Erythropoietin Stimulates erythrocyte production
Pineal gland Melatonin Induces sleep and affects mood
Placenta Human chorionic gonadotropin Sustains pregnancy
Skin Vitamin D Affects absorption of calcium
THYROID GLAND
LOCATION AND STRUCTURE
The thyroid gland is composed of a right and a left lobe on either side of the trachea, just
below a large piece of cartilage called the thyroid cartilage. The thyroid cartilage covers
the larynx and produces the prominence on the neck known in men as the “Adam’s apple.”
The isthmus of the thyroid gland is a narrow strip of glandular tissue that connects the
two lobes on the ventral (anterior) surface of the trachea.
FUNCTION
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Two of the hormones secreted by the thyroid gland are thyroxine or tetraiodothyronine
(T4) and triiodothyronine (T3). These hormones are synthesized in the thyroid gland from
iodine, which is picked up from the blood circulating through the gland, and from an amino
acid called tyrosine. T4 (containing four atoms of iodine) is much more concentrated in the
blood, whereas T3 (containing three atoms of iodine) is far more potent in affecting the
metabolism of cells. Most thyroid hormone is bound to protein molecules as it travels in
the bloodstream.
T4 and T3 are necessary in the body to maintain a normal level of metabolism in all body
cells. Cells need oxygen to carry on metabolic processes, one aspect of which is burning
food to release the energy stored within it. Thyroid hormone aids cells in their uptake of
oxygen and thus supports the metabolic rate in the body. Injections of thyroid hormone
raise the metabolic rate, whereas removal of the thyroid gland, diminishing thyroid
hormone content in the body, results in a lower metabolic rate, heat loss, and poor physical
and mental development.
A more recently discovered hormone produced by the thyroid gland is calcitonin.
Calcitonin is secreted when calcium levels in the blood are high. It stimulates calcium to
leave the blood and enter the bones, thus lowering blood calcium back to normal. Calcitonin
contained in a nasal spray may be used for treatment of osteoporosis (loss of bone
density). By increasing calcium storage in bone, calcitonin strengthens weakened bone
tissue and prevents spontaneous bone fractures.
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PARATHYROID GLANDS
The parathyroid glands are four small oval bodies located on the dorsal aspect of the
thyroid gland.
FUNCTION
Parathyroid hormone (PTH) is secreted by the parathyroid glands. This hormone (also
known as parathormone) mobilizes calcium (a mineral substance) from bones into the
bloodstream, where calcium is necessary for proper functioning of body tissues, especially
muscles. Normally, calcium in the food we eat is absorbed from the intestine and carried
by the blood to the bones, where it is stored. The adjustment of the level of calcium in the
blood is a good example of the way hormones in general control the homeostasis
(equilibrium or constancy in the internal environment) of the body. If blood calcium
decreases (as in pregnancy or in vitamin D deficiency), parathyroid hormone secretion
increases, causing calcium to leave bones and enter the bloodstream. In this way, blood
calcium levels are brought back to normal.
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ADRENAL GLANDS
The adrenal glands are two small glands, one on top of each kidney. Each gland consists of
two parts: an outer portion, the adrenal cortex, and an inner portion, the adrenal medulla.
The adrenal cortex and adrenal medulla are two glands in one, secreting different
hormones. The adrenal cortex secretes steroids or corticosteroids (complex chemicals
derived from cholesterol); the adrenal medulla secretes catecholamines (chemicals derived
from amino acids).
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FUNCTION
The adrenal cortex secretes three types of corticosteroids.
1. Glucocorticoids—These steroid hormones have an important influence on the metabolism

of sugars, fats, and proteins within all body cells and have a powerful anti-inflammatory
effect. Cortisol helps regulate glucose, fat, and protein metabolism. It raises blood glucose
as part of a response to stress. Cortisone is a hormone very similar to cortisol and can be
prepared synthetically. Cortisone is useful in treating inflammatory conditions such as
rheumatoid arthritis.
2. Mineralocorticoids—The major mineralocorticoid is aldosterone. It regulates the

concentration of mineral salts (electrolytes) in the body. Aldosterone acts on the kidney
to reabsorb sodium (an important electrolyte) and water and to excrete potassium
(another major electrolyte). Thus, it regulates blood volume and blood pressure and
electrolyte concentration.
3. Sex hormones—Androgens (testosterone) and estrogens are secreted in small amounts

and influence secondary sex characteristics, such as pubic and axillary hair in boys and
girls. In females, the masculinizing effects of adrenal androgens (increased body hair),
may appear when levels of ovarian estrogen decrease after menopause.
Think of the “three S’s” to recall the main adrenal cortex hormones that influence sugar
(cortisol), salt (aldosterone), and sex (androgens and estrogens).
The adrenal medulla secretes two types of catecholamine hormones:

1. Epinephrine (adrenaline)—Increases heart rate and blood pressure, dilates bronchial
tubes, and releases glucose (sugars) from glycogen (storage substance) when the body
needs it for more energy.
2. Norepinephrine (noradrenaline)—Constricts blood vessels to raise blood pressure. Both

epinephrine and norepinephrine are sympathomimetic agents because they mimic, or copy,
the actions of the sympathetic nervous system. They are released to help the body meet
the challenges of stress in response to stimulation by the sympathetic nervous system.
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PANCREAS
LOCATION AND STRUCTURES
The pancreas is located near and partly behind the stomach in the region of the first and
second lumbar vertebrae. The endocrine tissue of the pancreas consists of specialized
hormone-producing cells called the islets of Langerhans or islet cells. More than 98% of
the pancreas consists of exocrine cells (glands and ducts). These cells secrete digestive
enzymes into the gastrointestinal tract.
FUNCTION
The islets of Langerhans produce insulin (produced by beta cells) and glucagon (produced
by alpha cells). Both play a role regulating blood glucose (sugar) levels. When blood glucose
rises, insulin lowers blood sugar by helping it enter body cells. Insulin also lowers blood
sugar by causing conversion of glucose to glycogen (a starch storage form of sugar) in the
liver. If blood glucose levels fall too low, glucagon raises blood sugar by acting on liver cells
to promote conversion of glycogen back to glucose. Thus, the endocrine function of the
pancreas is another example of homeostasis, the body’s ability to regulate its inner
environment to maintain stability.
PITUITARY GLAND
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The pituitary gland, also called the hypophysis, is a small pea-sized gland located at the
base of the brain in a small pocket-like depression of the skull called the sella turcica. It is
a well-protected gland, with the entire mass of the brain above it and the nasal cavity
below. The ancient Greeks incorrectly imagined that its function was to produce pituita, or
nasal secretion.
The pituitary consists of two distinct parts: an anterior lobe or adenohypophysis,
composed of glandular epithelial tissue, and a posterior lobe or neurohypophysis, composed
of nervous tissue. The hypothalamus [3] is a region of the brain under the thalamus and
above the pituitary gland. Signals transmitted from the hypothalamus control secretions
by the pituitary gland. Special secretory neurons in the hypothalamus send releasing and
inhibiting factors (hormones) via capillaries to the anterior pituitary gland. These factors
stimulate or inhibit secretion of hormones from the anterior pituitary. The hypothalamus
also produces and secretes hormones directly to the posterior pituitary gland, where the
hormones are stored and then released.
FUNCTION
Although no bigger than a pea, the pituitary gland is often called the “master gland”
because it makes hormones that control several other endocrine glands.
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The major hormones of the anterior pituitary gland are:
1. Growth hormone (GH), or somatotropin (STH)—Promotes protein synthesis that

results in the growth of bones, muscles, and other tissues. GH also stimulates the liver to
make insulin-like growth factor, which stimulates the growth of bones. It increases blood
glucose levels and is secreted during exercise, sleep, and hypoglycemia.
2. Thyroid-stimulating hormone (TSH), or thyrotropin—Stimulates the growth of the

thyroid gland and secretion of thyroxine (T4) and triiodothyronine (T3).
3. Adrenocorticotropic hormone (ACTH), or adrenocorticotropin—Stimulates the growth

of the adrenal cortex and increases its secretion of steroid hormones (primarily cortisol).
4. Gonadotropic hormones—Several gonadotropic hormones influence the growth and

hormone secretion of the ovaries in females and the testes in males.
In the female, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) stimulate
the growth of eggs in the ovaries, the production of hormones, and ovulation. In the male,
FSH influences the production of sperm, and LH (an interstitial cell–stimulating hormone)
stimulates the testes to produce testosterone.
5. Prolactin (PRL)—Stimulates breast development during pregnancy and sustains milk

production after birth.
The posterior pituitary gland stores and releases two important hormones that are
synthesized in the hypothalamus:
1. Antidiuretic hormone (ADH), also called vasopressin—Stimulates the reabsorption of

water by the kidney tubules. In addition, ADH also increases blood pressure by
constricting arterioles.
2. Oxytocin (OT)—Stimulates the uterus to contract during childbirth and maintains labor
during childbirth. Oxytocin is also secreted during suckling and causes the production of
milk from the mammary glands.
OVARIES
The ovaries are two small glands located in the lower abdominal region of the female. The
ovaries produce the female gamete, the ovum, as well as hormones that are responsible for
female sex characteristics and regulation of the menstrual cycle.
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FUNCTION
The ovarian hormones are estrogens (estradiol and estrone) and progesterone. Estrogens
stimulate development of ova (eggs) and development of female secondary sex
characteristics. Progesterone is responsible for the preparation and maintenance of the
uterus in pregnancy.
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TESTES

The testes are two small ovoid glands suspended from the inguinal region of the male by
the spermatic cord and surrounded by the scrotal sac. The testes produce the male
gametes, spermatozoa, as well as the male hormone called testosterone.
FUNCTION
Testosterone is an androgen (male steroid hormone) that stimulates development of sperm

and secondary sex characteristics in the male (development of beard and pubic hair,
deepening of voice, and distribution of fat).
ENDOCRINE GLANDS: HORMONES AND ACTIONS

Endocrine gland Hormones Actions
Thyroid Thyroxin, triiodothyronine Increases metabolism in body
cells
Calcitonin Lowers blood calcium

Parathyroids Parathyroid hormone Increases blood calcium
Adrenals - cortex Aldosterone Increases reabsorption of
(mineralocorticoid) sodium
Cortisol (glucocorticoid) Increases blood sugar
Androgens, estrogens and Maintain secondary sex

progestins characteristics
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Adrenals - medulla Epinephrine (adrenaline) Sympathomimetic
Norepinephrine Sympathomimetic
Pancreas – islet cells Insulin Decreases blood sugar (glucose

to glycogen)
Glucagon Increases blood sugar

(glycogen to glucose)
Pituitary – anterior lobe Growth hormone (GH, Increases bone and tissue
somatotropin) growth
Thyroid-stimulating hormone Stimulates production of

(TSH) thyroxine and growth of the
thyroid gland
Adrenocorticotropic hormone Stimulates secretion of

hormones from the adrenal
cortex, especially cortisol
Gonadotropins; follicle- Oogenesis and spermatogenesis

stimulating hormone
Promotes ovulation; testosterone
Gonadotropins; secretion
luteinizing hormone
Promotes growth of breast tissue
Prolactin and milk secretion
Increases pigmentation of the

Melanocyte-stimulating skin
hormone
Pituitary – posterior Antidiuretic hormone Stimulates reabsorption of water
lobe Oxytocin by kidney tubules
Stimulates contraction of the
uterus during labor and childbirth
Ovaries Estradiol Develops and maintains
Progesterone secondary sex characteristics in
female
Prepares and maintains the
uterus in pregnancy
Testes Testosterone Promotes growth and
maintenance of secondary sex
characteristics in the male
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VOCABULARY
Adrenal cortex The outer section of each adrenal gland

Adrenaline Produced by the adrenal medulla; also called
epinephrine. Adrenaline increases heart rate and
blood pressure.
Adrenal medulla The inner section of each adrenal gland
Adrenocorticotropic hormone Produced by the anterior lobe of the pituitary gland
(adenohypophysis); also called adrenocorticotropin.
ACTH stimulates the adrenal cortex.
Aldosterone Produced by the adrenal cortex; increases sat
(sodium) reabsorption.
Androgen Male hormone produced by the testes and to a
lesser extent by the adrenal cortex; testosterone
is an example.
Antidiuretic hormone Secreted by the posterior lobe of the pituitary
gland (neurohypophysis). ADH increases
reabsorption of water by the kidney and is also
known as vasopressin
Calcitonin Produced by the thyroid gland. Calcitonin lowers
blood calcium. Also called thyrocalcitonin.
Catecholamines Hormones derived from an amino acid and secreted
by the adrenal medulla. Epinephrine is a
catecholamine.
Corticosteroids Hormones (steroid) produced by the adrenal cortex.
Glucocorticoids and mineralocorticoids are
examples.
Cortisol Produced by the adrenal cortex; increases blood
sugar.
Electrolyte A mineral salt found in the blood and tissues and
necessary for proper functioning of cells;
potassium, sodium and calcium are examples.
Epinephrine Produced by the adrenal medulla; also called
adrenaline. Epinephrine (a sympathomimetic)
increases heart rate and blood pressure and dilates
airways.
Estradiol: An estrogen (female hormone) produced
by the ovaries.
Estrogen Female hormone produced by the ovaries and to a
lesser extent by the adrenal cortex
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Follicle-stimulating hormone Hormone produced by the anterior lobe of the

pituitary gland (adenohypophysis). FSH stimulates
hormone secretion and egg production by the
ovaries and sperm production by the testes.
Glucagon Hormone produced by the islet cells of the
pancreas; increases blood sugar by conversion of
glycogen (starch) to glucose.
Glucocorticoid Hormone secreted by the adrenal cortex; necessary
for use of sugars, fats and proteins by the body and
for the body’s normal response to stress. Cortisol is
an example.
Growth hormone Produced by the anterior lobe of the pituitary gland
(adenohypophysis); also called somatotropin. GH
stimulates the growth of bones and tissues.
Homeostasis The tendency in an organism to maintain a constant
internal environment.
Hormone A substance that is produced by an endocrine gland
and that travels through the blood to a distant
organ or gland where it acts to modify the
structure or function of that organ or gland.
Hypothalamus A region of the brain that lies below the thalamus
and above the pituitary gland. It produces releasing
factors that stimulate the pituitary gland to release
hormones.
Insulin Produced by the islet cells of the pancreas. Insulin
lowers blood sugar by transport and conversion of
glucose to glycogen (starch).
Luteinizing hormone Produced by the anterior lobe of the pituitary gland
(adenohypophysis). LH stimulates ovulation in
females and (as ICSH) stimulates testosterone
secretion in males.
Melanocyte-stimulating hormone Produced by the anterior lobe of the pituitary gland
(adenohypophysis). High levels of MSH increase
pigmentation of the skin.
Mineralocorticoid Steroid hormone produced by the adrenal cortex to
regulate the mineral salts (electrolytes) and water
balance in the body. Aldosterone is an example.
Norepinephrine Produced by the adrenal medulla; also called
noradrenaline. Norepinephrine(a sympathomimetic)
increases heart rate and blood pressure.
Ovaries Two endocrine glands in a female’s lower
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abdomen; responsible for egg production and

estrogen and progesterone secretion.
Oxytocin Secreted by the posterior lobe of the pituitary
(neurohypophysis). Oxytocin stimulates contraction
of the uterus during labor and childbirth.
Pancreas Endocrine gland behind the stomach. Islet cells
(islets of Langerhans) secrete hormones from the
pancreas.
Parathormone Produced by the parathyroid gland; also called
parathyroid hormone. PTH increases blood calcium.
Parathyroid glands Four small endocrine glands on the posterior side of
the thyroid gland.
Pituitary gland (hypophysis) Endocrine gland at the base of the brain; composed
of an anterior (adenohypophysis) and a posterior
(neurohypophysis) lobes.
Progesterone Produced by the ovaries. Progesterone prepares the
uterus for pregnancy.
Prolactin Produced by the anterior lobe of the pituitary gland
(adenohypophysis). PRL promotes milk secretion.
Sella turcica The cavity in the skull that contains the pituitary
gland.
Somatotropin Produced by the anterior lobe of the pituitary gland
(adenohypophysis); also called the growth hormone.
Steroid A complex substance related to fats and of which
many hormones are made. Examples of steroids are
estrogens, androgens, glucocorticoids and
mineralocorticoids.
Sympathomimetic Pertaining to mimicking or copying the effect of the
sympathetic nervous system. Adrenaline is a
sympathomimetic hormone (raises blood pressure
and heart rate and dilates airways).
Testes Two endocrine glands enclosed in the scrotal sac of
a male; responsible for sperm production and
testosterone secretion.
Testosterone Male hormone produced by the testes.
Thyroid gland Endocrine gland in the neck.
Thyroid-stimulating hormone Produced by the anterior lobe of the pituitary gland
(adenohypophysis). TSH acts on the thyroid gland to
promote its functioning; also called thyrotropin.
Thyroxine Produced by the thyroid gland; also called
tetraiodothyronine. T4 increases metabolism in
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cells.
Triiodothyronine Produced by the thyroid gland. T3 increases
metabolism in cells.
Vasopressin Secreted by the posterior lobe of the pituitary
gland (neurohypophysis); also called antidiuretic
hormone.
SYMPTOMS
Exophthalmia
Weight loss
Weight gain
Fatigue
Darkening of skin
Shaking of hands
Rapid heartbeat
Difficulty sleeping
Flank pain
Goiter: hyperthyroidism
Tremors
Nervousness
Excessive sweating
Palpitations
Heat intolerance
Light or absent periods
Insomnia
Hair loss
Dry, rough, pale skin
Coarse And dry hair
Cold intolerance
Irritability
Depression
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PATHOLOGY
THYROID GLAND
Topic Description
Disease Goiter
Definition Enlargement of the thyroid gland is goiter.
Cause  Endemic (en- = in; dem/o = people) goiter occurs in
certain regions where there is a lack of iodine in the
diet.
 low iodine levels lead to low T3 and T4 levels
Risk Factors  Have a family history of thyroid cancer, nodules, and
other problems that affect the thyroid.
 Don’t get enough iodine in your diet.
 Have a condition that decreases the iodine in your
body.
 Are female. Women have a higher risk for goiter than
men.
 Are over the age of 40. Aging may affect the health
of your thyroid.
 Are pregnant or experiencing menopause. These risk
factors aren’t easily understood, but pregnancy and
menopause may trigger problems in the thyroid.
 Have radiation therapy in the neck or chest area.
Radiation may change the way your thyroid functions.
Types  Colloid goiter (endemic) - A colloid goiter develops
from the lack of iodine, a mineral essential to the
production of thyroid hormones. People who get this
type of goiter usually live in areas where iodine is
scarce.
 Nontoxic goiter (sporadic) - The cause of a nontoxic
goiter is usually unknown, though it may be caused by
medications like lithium. Lithium is used to treat mood
disorders such as bipolar disorder.Nontoxic goiters
don’t affect the production of thyroid hormone, and
thyroid function is healthy. They’re also benign.
 Toxic nodular or multinodular goiter- This type of
goiter forms one or more small nodules as it enlarges.
The nodules produce their own thyroid hormone,
causing hyperthyroidism. It generally forms as an
extension of a simple goiter.
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Signs and symptoms  Swelling in your neck - If nodules on thyroid, they may
range in size from very small to very large. The
presence of nodules may increase the appearance of
swelling.
 difficulty swallowing or breathing
 coughing
 hoarseness in your voice
 dizziness when you raise your arm above your head
Diagnosis/ Investigation  Blood tests - Blood tests can detect changes in
hormone levels and an increased production of
antibodies, which are produced in response to an
infection or injury or overactivity of immune system.
 Thyroid scan - This is usually done when your thyroid
level is elevated. These scans show the size and
condition of your goiter, overactivity of some parts or
whole thyroid.
 Ultrasound - An ultrasound produces images of your
neck, the size of your goiter, and whether there are
nodules. Over time, an ultrasound can track changes in
those nodules and the goiter.
 Biopsy - A biopsy is a procedure that involves taking
small samples of your thyroid nodules if present. The
samples are sent to a laboratory for examination.
Treatment  Prevention includes increasing the supply of iodine (as
iodized salt) in the diet.
 Medications - If hypothyroidism or hyperthyroidism,
medications to treat these conditions may be enough
to shrink a goiter. Medications (corticosteroids) to
reduce inflammation may be used if thyroiditis.
 Surgeries - Surgical removal of thyroid, known as
thyroidectomy, is an option if grows too large or
doesn’t respond to medication therapy.
 Radioactive iodine - In people with toxic multinodular
goiters, radioactive iodine (RAI) may be necessary.
The RAI is ingested orally, and then travels to your
thyroid through blood, where it destroys the
overactive thyroid tissue.
Complication  Large goiters may cause compression of the trachea,
with tracheomalacia and asphyxiation.
 Hyperthyroidism occurs in some patients exposed to
iodine (ie, Jodbasedow phenomenon).
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 A patient with autoimmune goiters may develop

lymphoma. ...
 Nodular goiters may cause pain, intranodular necrosis,
or hemorrhage.
Hypersecretion
Topic Description
Disease Hyperthyroidism
Definition Having an excessive amount of thyroid hormone resulting
from an overactive thyroid gland or from taking too much
thyroid hormone.
Cause Several conditions can cause hyperthyroidism.
 Graves’ disease. This immune system disorder is the
most common cause of hyperthyroidism. It’s more
likely to affect women under the age of 40.
 Thyroid nodules. These lumps of tissue in your thyroid
can become overactive, creating too much thyroid
hormone.
 Thyroiditis. An infection or an immune system problem
can cause your thyroid to swell and leak hormones.
This is often followed by hypothyroidism, in which
your thyroid doesn’t make enough hormones. These
conditions are usually temporary.
Risk Factors  A family history, particularly of Graves' disease
 Female sex
 A personal history of certain chronic illnesses, such as
type 1 diabetes, pernicious anemia and primary adrenal
insufficiency
Signs and symptoms  Nervousness, anxiety, or crankiness
 Mood swings
 Fatigue or weakness
 Sensitivity to heat
 A swollen thyroid (called a goiter). You might see
swelling at the base of your neck.
 Losing weight suddenly, without trying
 Fast or uneven heartbeat or palpitations (pounding in
your heart)
 Having more bowel movements
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 Shaking in your hands and fingers (tremor)

 Sleep problems
 Thinning skin
 Fine, brittle hair
 Changes in your menstrual cycle
Diagnosis/ Investigation  Medical history
 Physical exam
 Blood tests - Blood tests that measure thyroxine and
thyroid-stimulating hormone (TSH) can confirm the
diagnosis. High levels of thyroxine and low or
nonexistent amounts of TSH indicate an overactive
thyroid. The amount of TSH is important because it's
the hormone that signals your thyroid gland to
produce more thyroxine.
 Radioiodine uptake test - For this test, you take a
small, oral dose of radioactive iodine (radioiodine) to
see how much will collect in your thyroid gland. You'll
be checked after four, six or 24 hours — and
sometimes after all three time periods — to see how
much iodine your thyroid has absorbed.A high uptake
of radioiodine indicates your thyroid gland is producing
too much thyroxine. The most likely cause is either
Graves' disease or hyperfunctioning thyroid nodules.
If you have hyperthyroidism and your radioiodine
uptake is low, this indicates that the thyroxine stored
in the gland is leaking into the bloodstream, which may
mean you have t -yroiditis.
 Thyroid scan - During this test, you'll have a
radioactive isotope injected into the vein on the inside
of your elbow or sometimes into a vein in your hand.
You then lie on a table with your head stretched
backward while a special camera produces an image of
your thyroid gland on a computer screen. This test
shows how iodine collects in your thyroid.
 Thyroid ultrasound. This test uses high-frequency
sound waves to produce images of the thyroid.
Ultrasound may be better at detecting thyroid nodules
than other tests, and there's no exposure to any
radiation.
Treatment  Radioactive iodine - Taken by mouth, radioactive iodine
is absorbed by thyroid gland, where it causes the
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gland to shrink. Symptoms usually subside within

several months. Excess radioactive iodine disappears
from the body in weeks to months.This treatment may
cause thyroid activity to slow enough to be considered
underactive (hypothyroidism), and you may eventually
need to take medication every day to replace
thyroxine.
 Anti-thyroid medications - These medications
gradually reduce symptoms of hyperthyroidism by
preventing your thyroid gland from producing excess
amounts of hormones. They include methimazole
(Tapazole) and propylithiouracil. Symptoms usually
begin to improve within several weeks to months, but
treatment with anti-thyroid medications typically
continues at least a year and often longer. For some
people, this clears up the problem permanently, but
other people may experience a relapse. Both drugs can
cause serious liver damage, sometimes leading to
death. Because propylthiouracil has caused far more
cases of liver damage, it generally should be used only
when you can't tolerate methimazole. A small number
of people who are allergic to these drugs may develop
skin rashes, hives, fever or joint pain. They also can
make you more susceptible to infection.
 Beta blockers - Although these drugs are usually used
to treat high blood pressure and don't affect thyroid
levels, they can ease symptoms of hyperthyroidism,
such as a tremor, rapid heart rate and palpitations.
For that reason, your doctor may prescribe them to
help you feel better until your thyroid levels are
closer to normal. These medications generally aren't
recommended for people who have asthma, and side
effects may include fatigue and sexual dysfunction.
 Surgery (thyroidectomy) - In a thyroidectomy,
removes most of your thyroid gland. Risks of this
surgery include damage to your vocal cords and
parathyroid glands — four tiny glands situated on the
back of your thyroid gland that help control the level
of calcium in your blood.
Complication  Heart problems. Some of the most serious
complications of hyperthyroidism involve the heart.
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These include a rapid heart rate, a heart rhythm

disorder called atrial fibrillation that increases your
risk of stroke, and congestive heart failure — a
condition in which your heart can't circulate enough
blood to meet your body's needs.
 Brittle bones. Untreated hyperthyroidism can also lead
to weak, brittle bones (osteoporosis). The strength of
your bones depends, in part, on the amount of calcium
and other minerals they contain. Too much thyroid
hormone interferes with your body's ability to
incorporate calcium into your bones.
 Eye problems. People with Graves' ophthalmopathy
develop eye problems, including bulging, red or swollen
eyes, sensitivity to light, and blurring or double vision.
Untreated, severe eye problems can lead to vision loss.
 Red, swollen skin. In rare cases, people with Graves'
disease develop Graves' dermopathy. This affects the
skin, causing redness and swelling, often on the shins
and feet.
 Thyrotoxic crisis. Hyperthyroidism also places you at
risk of thyrotoxic crisis — a sudden intensification of
your symptoms, leading to a fever, a rapid pulse and
even delirium. If this occurs, seek immediate medical
care.
Topic Description
Disease Graves disease
Definition Graves’ disease is an autoimmune disease that leads to a
generalized overactivity of the entire thyroid gland
(hyperthyroidism).
Cause  Graves' disease is caused by a malfunction in the
body's disease-fighting immune system, although the
exact reason why this happens is still unknown.
Risk Factors Although anyone can develop Graves' disease, a number of
factors can increase the risk of disease. These risk factors
include the following:
 Family history - Because a family history of Graves'
disease is a known risk factor, there is likely a gene or
genes that can make a person more susceptible to the
disorder.
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 Gender - Women are much more likely to develop

Graves' disease than are men.
 Age - Graves' disease usually develops in people
younger than 40.
 Other autoimmune disorders - People with other
disorders of the immune system, such as type 1
diabetes or rheumatoid arthritis, have an increased
risk.
 Emotional or physical stress - Stressful life events or
illness may act as a trigger for the onset of Graves'
disease among people who are genetically susceptible.
 Pregnancy - Pregnancy or recent childbirth may
increase the risk of the disorder, particularly among
women who are genetically susceptible.
 Smoking - Cigarette smoking, which can affect the
immune system, increases the risk of Graves' disease.
Smokers who have Graves' disease are also at
increased risk of developing Graves' ophthalmopathy.
Signs and symptoms  Anxiety and irritability
 A fine tremor of your hands or fingers
 Heat sensitivity and an increase in perspiration or
warm, moist skin
 Weight loss, despite normal eating habits
 Enlargement of your thyroid gland (goiter)
 Change in menstrual cycles
 Erectile dysfunction or reduced libido
 Frequent bowel movements
 Bulging eyes (Graves' ophthalmopathy)
 Fatigue
 Thick, red skin usually on the shins or tops of the feet
(Graves' dermopathy)
 Rapid or irregular heartbeat (palpitations)
Diagnosis/ Investigation  History collection
 Physical exam
 blood tests
 thyroid scan
 radioactive iodine uptake test
 thyroid stimulating hormone (TSH) test
 thyroid stimulating immunoglobulin (TSI) test
Treatment  anti-thyroid drugs
 radioactive iodine (RAI) therapy
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 thyroid surgery
Complication  Pregnancy issues - Possible complications of Graves'
disease during pregnancy include miscarriage, preterm
birth, fetal thyroid dysfunction, poor fetal growth,
maternal heart failure and preeclampsia. Preeclampsia
is a maternal condition that results in high blood
pressure and other serious signs and symptoms.
 Heart disorders - If left untreated, Graves' disease
can lead to heart rhythm disorders, changes in the
structure and function of the heart muscles, and the
inability of the heart to pump enough blood to the
body (congestive heart failure).
 Thyroid storm - A rare, but life-threatening
complication of Graves' disease is thyroid storm, also
known as accelerated hyperthyroidism or thyrotoxic
crisis. It's more likely when severe hyperthyroidism is
untreated or treated inadequately.
 The sudden and drastic increase in thyroid hormones
can produce a number of effects, including fever,
profuse sweating, vomiting, diarrhea, delirium, severe
weakness, seizures, markedly irregular heartbeat,
yellow skin and eyes (jaundice), severe low blood
pressure, and coma. Thyroid storm requires immediate
emergency care.
 Brittle bones - Untreated hyperthyroidism also can
lead to weak, brittle bones (osteoporosis). The
strength of your bones depends, in part, on the amount
of calcium and other minerals they contain. Too much
thyroid hormone interferes with your body's ability to
incorporate calcium into your bones.
Hyposecretion
Topic Description
Disease Hypothyroidism
Definition Hypothyroidism, also called underactive thyroid or low
thyroid, is a disorder of the endocrine system in which the
thyroid gland does not produce enough thyroid hormone.
Cause  Autoimmune disease. The most common cause of
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hypothyroidism is an autoimmune disorder known as

Hashimoto's thyroiditis.
 Over-response to hyperthyroidism treatment.
 Thyroid surgery.
 Radiation therapy.
 Medications.
Risk Factors  Being female.
 Being older than age 60.
 Exposure to radiation in the neck.
 Prior thyroid surgery.
 Having a family history of thyroid disease.
 Having a family history of autoimmune disease.
 Having an autoimmune disease.
 Being of Caucasian or Asian ethnicity.
Signs and symptoms  fatigue
 depression
 constipation
 feeling cold
 dry skin
 weight gain
 muscle weakness
 decreased sweating
 slowed heart rate
 elevated blood cholesterol
 pain and stiffness in your joints
 dry, thinning hair
 impaired memory
 fertility difficulties or menstrual changes
 muscle stiffness, aches, and tenderness
 hoarseness
 puffy, sensitive face
 Physical exam
 Diagnosis of hypothyroidism is based on your
symptoms and the results of blood tests that measure
the level of TSH and sometimes the level of the
thyroid hormone thyroxine. A low level of thyroxine
and high level of TSH indicate an underactive thyroid.
Treatment  daily use of the synthetic thyroid hormone
levothyroxine (Levo-T, Synthroid, others)
Complication  An enlarged thyroid, or goitre, which may cause
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problems with swallowing and breathing.

 High cholesterol and associated heart disease.
 Nerve damage causing tingling, numbness and pain in
the legs, arms or other affected areas.
 Infertility.
Topic Description
Disease Myxedema
Definition severe hypothyroidism characterized by firm inelastic edema,
dry skin and hair, and loss of mental and physical vigor
Cause Hypothyroidism occurs when the thyroid stops functioning
properly. This may be caused by:
 an autoimmune condition, including Hashimoto’s disease
 surgical removal of your thyroid
 radiation therapy for cancer
 certain medications, such as lithium or amiodarone
(Pacerone)
 iodine deficiency or an excess of iodine
 pregnancy
 immune system medications, like those used in cancer
treatment
Myxedema is a result of undiagnosed or untreated severe
hypothyroidism. It can also develop when someone stops
taking their thyroid medication. It’s more common in the
elderly and in women.
Risk Factors  Age over 50 years.
 Autoimmune disorders (diseases in which the immune
system attacks the body's own tissues as foreign
substances)
 Current or previous hypothyroidism.
 Female gender.
 Surgical removal of the thyroid gland.
 Therapeutic suppression of thyroid gland activity.
Signs and symptoms  Myxedema can occur in the lower leg (pretibial
myxedema) and behind the eyes (exophthalmos).
 Severe cases, requiring hospitalization can exhibit
signs of hypothermia, hypoglycemia, hypotension,
respiratory depression, and coma.
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 Physical exam
 Results of the total serum thyroxine and free
thyroxine index tests usually will confirm the diagnosis
Treatment  Administration of adequate doses of either the
thyroid hormone L-thyroxine given intravenously or by
giving liothyronine via a nasogastric tube.
 Antibiotics
 steroid treatment
 breathing support
Complication  depression.
 heart attack.
 heart failure.
 kidney problems.
 cardiac arrhythmias.
 hypothermia.
 decreased drug metabolism, leading to overdosing of
medications.
 pregnancy complications, such as preeclampsia,
miscarriage, and stillbirth.
Topic Description
Disease Cretinism
Definition Congenital hypothyroidism (underactivity of the thyroid gland
at birth), which results in growth retardation, developmental
delay, and other abnormal features.
Cause  a missing, poorly formed, or abnormally small thyroid
gland
 a genetic defect that affects thyroid hormone
production
 too little iodine in the mother’s diet during pregnancy
 radioactive iodine or antithyroid treatment for
thyroid cancer during pregnancy
 use of medicines that disrupt thyroid hormone
production — such as antithyroid drugs, sulfonamides,
or lithium — during pregnancy
Risk Factors  Numerous genetic syndromes.
 Underactive pituitary gland (secondary) eg due to a
pituitary tumour or the absence of the pituitary gland.
 Trauma.
 In most cases no underlying cause of the deficiency is
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found. ...
 Early diagnosis is imperative.
Signs and symptoms  lack of weight gain
 stunted growth
 fatigue, lethargy
 poor feeding
 thickened facial features
 abnormal bone growth
 mental retardation
 very little crying
 excessive sleep
 constipation
 yellowing of the skin and whites of the eyes (jaundice)
 floppiness, low muscle tone
 hoarse voice
 unusually large tongue
 swelling near the navel (umbilical hernia)
 cool, dry skin
 pale skin
 swelling of the skin (myxedema)
 swelling in the neck from an enlarged thyroid gland
(goiter)
Diagnosis/ Investigation  Physical examination
 Routine screening of the newborn using a blood-spot,
as in the Guthrie test, to detect a high TSH level as
an indicator of primary hypothyroidism is efficient and
cost-effective, usually done at 5-7 days
Treatment  early diagnosis and thyroid hormone replacement
 Only levothyroxine is recommended for treatment.
Complication  Children who are born with a severely underactive
thyroid gland can develop intellectual disability if the
condition isn’t treated quickly. A child’s IQ can drop
several points for every few months that treatment is
delayed. Growth and bone strength can also be
affected.
Other complications of congenital hypothyroidism include:
 an abnormal walk
 muscle spasticity
 an inability to speak (mutism)
 autistic behavior
 vision and hearing problems
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 problems with memory and attention
Topic Description
Disease Thyroiditis
Definition Thyroiditis is an inflammation (not an infection) of the
thyroid gland.
Cause  The thyroid can be attacked by different agents. The
attacks cause inflammation and injury to the thyroid
cells, leading to thyroiditis.
Some of the agents known to cause thyroiditis are
 antibodies (the most common cause)
 drugs
 radiation
 organisms (viruses and bacteria)
 Autoimmune diseases
Risk Factors  Sex
 Age
 Heredity.
 Other autoimmune disease.
 Radiation exposure.
Phases There are three phases to thyroiditis:
 Thyrotoxic phase. Thyrotoxicosis means that the
thyroid is inflamed and releases too many hormones.
 Hypothyroid phase. Following the excessive release of
thyroid hormones for a few weeks or months, the
thyroid will not have enough thyroid hormones to
release. This leads to a lack of thyroid hormones or
hypothyroidism.
 Euthyroid phase. During the third euthyroid phase, the
thyroid hormone levels are normal. This phase may
come temporarily after the thyrotoxic phase before
going to the hypothyroid phase, or it may come at the
end after the thyroid gland has recovered from the
inflammation and is able to maintain a normal hormone
level.
Types  Hashimoto’s thyroiditis: an autoimmune condition
caused by anti-thyroid antibodies. This is the most
common form of thyroiditis and is around five times
more common in women than in men. Hashimoto’s
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thyroiditis usually results in hypothyroidism, and

thyroid hormone replacement treatment is needed.
 Silent thyroiditis or painless thyroiditis: another
autoimmune disease caused by anti-thyroid antibodies.
It is also common in women and the next common cause
after Hashimoto’s thyroiditis.
 Post-partum thyroiditis: an autoimmune condition
caused by anti-thyroid antibodies that sometimes
occurs shortly after a woman gives birth
 Radiation-induced thyroiditis: a condition caused by
external radiation used as a medical treatment for
certain cancers, or by radioactive iodine used to treat
hyperthyroidism
 Subacute thyroiditis or de Quervain’s thyroiditis: an
often painful condition thought to be caused by a virus
 Acute thyroiditis or suppurative thyroiditis: a
relatively rare condition caused by an infectious
organism or bacterium
 Drug-induced thyroiditis: a condition is caused by the
use of drugs such as amiodarone, interferons, lithium,
and cytokines. It only occurs in a small fraction of
patients using the offending drugs, so it is not common
in the normal population.
Signs and symptoms The symptoms of thyroiditis depend on the type of
thyroiditis and phase of thyroiditis.
Hyperthyroid phase: Usually short lasting (1-3 months.) If

cells are damaged quickly and there is a leak of excess
thyroid hormone, you might show symptoms of
hyperthyroidism, such as:
 Being worried
 Feeling irritable
 Trouble sleeping
 Fast heart rate
 Fatigue
 Unplanned weight loss
 Increased sweating and heat intolerance
 Anxiety and nervousness
 Increased appetite
 Tremors
Hypothyroid phase (more common): Can be long-lasting and
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may become permanent. If cells are damaged and thyroid

hormone levels fall, you might show symptoms of
hypothyroidism, such as:
 Fatigue
 Unexpected weight gain
 Constipation
 Depression
 Dry skin
 Difficulty performing physical exercise
 Decreased mental ability to concentrate and focus
Diagnosis/ Investigation  Thyroid function tests measure the amounts of
hormones (thyroid-stimulating hormone or TSH, T3,
and T4) in the blood. TSH comes from the pituitary
gland and stimulates the thyroid gland to produce T4
and T3. The thyroid gland produces the hormones T4
and T3 that exert the action of thyroid hormone in
the body. T3 and T4 are called thyroid hormones.
 Thyroid antibody tests measure thyroid antibodies
that include antithyroid (microsomal) antibodies (TPO)
or thyroid receptor stimulating antibodies (TRAb).
 Erythrocyte sedimentation rate (ESR or sed rate)
indicates inflammation by measuring how fast red
blood cells fall. The ESR is high in sub-acute
thyroiditis.
 Ultrasound (US), sonogram of the thyroid, is used very
frequently to evaluate the anatomy of the thyroid
gland. It can show a nodule (a growth) in the thyroid
gland, a change in blood flow (Doppler mode) and echo
texture (intensity/density) of the gland.
 Radioactive iodine uptake (RAIU) measures how much
radioactive iodine is absorbed by the thyroid gland.
The amount is always low in the thyrotoxic phase of
thyroiditis.
Treatment  Thyrotoxic phase: Usually temporary, it will eventually
either recover and go to the euthyroid phase, or go to
the hypothyroid phase. This hypothyroid phase could
be temporary or permanent. It may not be necessary
to treat symptoms in subacute, painless, or post-
partum thyroiditis. During the thyrotoxic phase,
treatment is symptomatic. Antithyroid medications are
rarely needed.
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 Palpitations/anxiety/tremors/heat
intolerance/increased sweating: These symptoms are
treated with beta blockers.
 Thyroidal pain: The pain can usually be managed with
anti-inflammatory medications such as aspirin or
ibuprofen. If the pain is severe enough, steroid
therapy may be required (not very often).
 In other forms, treating the infection will be
necessary to eliminate acute (suppurative) thyroiditis.
Drug-induced thyroiditis generally lasts as long as the
drugs are taken.
 Hypothyroid phase: If necessary, thyroid hormone
replacement therapy is used to treat hypothyroidism.
This type of therapy usually continues for 6 to 12
months. Hashimoto's thyroiditis usually causes
permanent hypothyroidism and requires continued
treatment.
Complication  enlarged heart, heart failure, or other forms of heart
disease
Neoplasms
Topic Description
Disease Thyroid carcinoma
Definition Cancer of the thyroid gland
Cause  unknown
Risk Factors  Female sex. Thyroid cancer occurs more often in
women than in men.
 Exposure to high levels of radiation. Radiation therapy
treatments to the head and neck increase the risk of
thyroid cancer.
 Certain inherited genetic syndromes
Types  Papillary thyroid cancer: Papillary thyroid cancer
develops from follicular cells and usually grow slowly.
It is the most common type of thyroid cancer. It is
usually found in 1 lobe. Only 10% to 20% of papillary
thyroid cancer appears in both lobes. It is a
differentiated thyroid cancer, meaning that the tumor
looks similar to normal thyroid tissue under a
microscope. Papillary thyroid cancer can often spread
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to lymph nodes.
 Follicular thyroid cancer: Follicular thyroid cancer also
develops from follicular cells and usually grows slowly.
Follicular thyroid cancer is also a differentiated
thyroid cancer, but it is far less common than papillary
thyroid cancer. Follicular thyroid cancer rarely
spreads to lymph nodes.
 Follicular thyroid cancer and papillary thyroid cancer
are the most common differentiated thyroid cancers.
They are very often curable, especially when found
early and in people younger than 50. Together,
follicular and papillary thyroid cancers make up about
95% of all thyroid cancer.
 Hurthle cell cancer: Hurthle cell cancer, also called
Hurthle cell carcinoma, is cancer that is arises from a
certain type of follicular cell. Hurthle cell cancers are
much more likely to spread to lymph nodes than other
follicular thyroid cancers.
 Medullary thyroid cancer (MTC): MTC develops in the
C cells and is sometimes the result of a genetic
syndrome called multiple endocrine neoplasia type 2
(MEN2). This tumor has very little, if any, similarity to
normal thyroid tissue. MTC can often be controlled if
it is diagnosed and treated before it spreads to other
parts of the body. MTC accounts for about 3% of all
thyroid cancers. About 25% of all MTC is familial. This
means that family members of the patient will have a
possibility of a similar diagnosis. The RET proto-
oncogene test (see Risk Factors) can confirm if family
members also have familial MTC (FMTC).
 Anaplastic thyroid cancer: This type is rare,
accounting for about 1% of thyroid cancer. It is a
fast-growing, poorly differentiated thyroid cancer
that may start from differentiated thyroid cancer or
a benign thyroid tumor. Anaplastic thyroid cancer can
be subtyped into giant cell classifications. Because
this type of thyroid cancer grows so quickly, it is more
difficult to treat successfully.
Signs and symptoms Thyroid cancer typically doesn't cause any signs or symptoms
early in the disease. As thyroid cancer grows, it may cause:
 A lump (nodule) that can be felt through the skin on
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your neck
 Changes to your voice, including increasing hoarseness
 Difficulty swallowing
 Pain in your neck and throat
 Swollen lymph nodes in your neck
Diagnosis/ Investigation  Physical exam
 Blood tests
 Ultrasound imaging
 Removing a sample of thyroid tissue. During a fine-
needle aspiration biopsy, inserts a long, thin needle
through skin and into the thyroid nodule. Ultrasound
imaging is typically used to precisely guide the needle
into the nodule. uses the needle to remove samples of
suspicious thyroid tissue. The sample is analyzed in the
laboratory to look for cancer cells.
 Other imaging tests: Imaging tests may include CT,
MRI and nuclear imaging tests that use a radioactive
form of iodine.
 Genetic testing: Some people with medullary thyroid
cancer may have genetic changes that can be
associated with other endocrine cancers.
Treatment  Treatment may not be needed right away
 Surgery
 Thyroid hormone therapy
 Radioactive iodine
 External radiation therapy.
 Chemotherapy
 Targeted drug therapy
 Injecting alcohol into cancers.
Complication  Injury to the voice box and hoarseness after thyroid
surgery.
 Low calcium level from accidental removal of the
parathyroid glands during surgery.
 Spread of the cancer to the lungs, bones, or other
parts of the body.
.
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PARATHYROID GLANDS
Hypersecretion
Topic Description
Disease Hyperparathyroidism
Definition It is the presence of excess parathyroid hormone in the body
resulting in disturbance of calcium metabolism with increase
in serum calcium and decrease in inorganic phosphorus, loss of
calcium from bone, and renal damage with frequent kidney-
stone formation
Cause Common causes of parathyroid problems include
 benign growths on the gland and enlargement of at
least two glands. In rare cases, a cancerous tumor
causes this condition.
Risk Factors  Are a woman who has gone through menopause
 Have had prolonged, severe calcium or vitamin D
deficiency
 Have a rare, inherited disorder, such as multiple
endocrine neoplasia, type 1, which usually affects
multiple glands
 Have had radiation treatment for cancer that has
exposed your neck to radiation
 Have taken lithium, a drug most often used to treat
bipolar disorder
Types  Primary Hyperparathyroidism - This type occurs when
there is a problem with at least one of your
parathyroid glands.An increased risk of developing
primary hyperparathyroidism also occurs in people
who:
 have certain inherited disorders that affect several
glands throughout the body, such as multiple endocrine
neoplasia
 have a long history of calcium and vitamin D
deficiencies
 have been exposed to radiation from cancer treatment
 have taken a drug called lithium, which mainly treats
bipolar disorder
 Secondary Hyperparathyroidism - This type occurs
when there is an underlying condition that causes
calcium levels to be abnormally low. Most cases of
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secondary hyperparathyroidism are due to chronic

kidney failure that results in low vitamin D and calcium
levels.
 Tertiary Hyperparathyroidism - This type occurs when
your parathyroid glands keep making too much PTH
after your calcium levels return to normal. This type
usually occurs in people with kidney problems.
Signs and symptoms Hyperparathyroidism is often diagnosed before signs or
symptoms of the disorder are apparent. Symptoms may be so
mild and nonspecific that they don't seem at all related to
parathyroid function, or they may be severe.
The range of signs and symptoms include:
 Fragile bones that easily fracture (osteoporosis)
 Kidney stones
 Excessive urination
 Abdominal pain
 Tiring easily or weakness
 Depression or forgetfulness
 Bone and joint pain
 Frequent complaints of illness with no apparent cause
 Nausea, vomiting or loss of appetite
Diagnosis/ Investigation  Blood Tests - Additional blood tests can help to make
a more accurate diagnosis.check your blood for high
PTH levels, high alkaline phosphatase levels, and low
levels of phosphorus.
 Urine Tests - A urine test can help to determine how
severe the condition is and whether kidney problems
are the cause. check your urine to see how much
calcium it contains.
 Kidney Tests - Take X-rays of abdomen to check for
kidney abnormalities.
Treatment Primary Hyperparathyroidism
 Patient might not need treatment if kidneys are
working fine, if calcium levels are only slightly high, or
if bone density is normal. In this case, monitor
condition once a year and check blood-calcium levels
twice a year.
 drink plenty of water to reduce your risk of kidney
stones
 Should get regular exercise to strengthen your bones.
 Surgical procedures involve removing enlarged
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parathyroid glands or tumors on the glands.

Complications are rare and include damaged vocal cord
nerves and long-term, low levels of calcium.
 Calcimimetics, which act like calcium in the blood, are
another treatment. These drugs can trick your glands
into making less PTH. Prescribe these in some cases if
surgery is unsuccessful or not an option.
 Bisphophonates, which keep your bones from losing
calcium, can help reduce the risk of osteoporosis.
 Hormone replacement therapy can help bones hold on
to calcium. This therapy can treat postmenopausal
women with osteoporosis, although there are risks
involved with prolonged use. These include an
increased risk of some cancers and cardiovascular
disease.
Secondary Hyperparathyroidism
 Treatment involves bringing PTH level back to normal
by treating the underlying cause.
Methods of treatment include
 Taking prescription vitamin D for severe deficiencies
and calcium and vitamin D for chronic kidney failure.
 Medication and dialysis, if Chronic kidney failure.
Complication  Osteoporosis. The loss of calcium often results in
weak, brittle bones that fracture easily
(osteoporosis).
 Kidney stones. The excess of calcium in your blood may
lead to excess calcium in your urine, which can cause
small, hard deposits of calcium and other substances
to form in your kidneys. A kidney stone usually causes
significant pain as it passes through the urinary tract.
 Cardiovascular disease. Although the exact cause-and-
effect link is unclear, high calcium levels are
associated with cardiovascular conditions, such as high
blood pressure (hypertension) and certain types of
heart disease.
 Neonatal hypoparathyroidism. Severe, untreated
hyperparathyroidism in pregnant women may cause
dangerously low levels of calcium in newborns.
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ADRENAL CORTEX
Hypersecretion
Topic Description
Disease Adrenal virilism
Definition Adrenal virilism is the development or premature
development of male secondary sexual characteristics caused
by male sex hormones (androgens) excessively produced by
the adrenal gland. This disorder can occur before birth and
can lead to sexual abnormalities in newborns. It can also
occur in girls and women later in life.
Cause  In infants and children, adrenal virilism is usually the
result of adrenal gland enlargement that is present at
birth. This is called congenital adrenal hyperplasia.
The cause is usually a genetic problem that leads to
severe enzyme deficiencies.
 In rare cases, adrenal virilism is caused by an adrenal
gland tumor. The tumor can be benign (adrenal
adenoma) or cancerous (adrenal carcinoma). Sometimes
virilism is caused by a type of tumor on a woman's
ovary (arrhenoblastoma).
Signs and symptoms  Newborn girls with adrenal virilism have external sex
organs that seem to be a mixture of male and female
organs (called female pseudohermaphrodism).
 Newborn boys with the disorder have enlarged
external sex organs, and these organs develop at an
abnormally rapid pace.
 Children with congenital adrenal hyperplasia

 begin growing abnormally fast, but they stop growing
earlier than normal.
 Later in childhood, they are typically shorter than
normal but have well-developed trunks.

 Women with adrenal virilization
 may develop facial hair
 Typically, their menstrual cycles are infrequent or
absent
 They may also develop a deeper voice, a more
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prominent Adam's apple, and other masculine signs.

 Physical examination
 This blood sample will be tested for testosterone,
estrogen, progesterone, and other hormones. An
increased level of androgens, such as testosterone,
often accompanies virilization.
 CT Scan
Treatment  Recommended treatment plan for virilization will
depend on the cause of the condition.
 If a tumor on adrenal gland, surgically removed.
 If the tumor is located in an area that’s dangerous or
hard to reach, they may recommend chemotherapy or
radiation treatments. These treatments can help
shrink the tumor before it’s removed.
 If a tumor isn’t to blame, prescribe birth control pills.
These may help regulate your hormone levels.
 Also prescribe medications that block androgen
receptors. These medications are also known as anti-
androgens.
Complication 
Topic Description
Disease Cushing syndrome
Definition Cushing’s syndrome or hypercortisolism, occurs due to
abnormally high levels of the hormone cortisol.
Cause  Cushing's syndrome is caused by either excessive
cortisol-like medication such as prednisone or a tumor
that either produces or results in the production of
excessive cortisol by the adrenal glands.
Risk Factors  adrenal or pituitary tumors
 long-term therapy with corticosteroids
 being female.
Signs and symptoms  high blood pressure
 abdominal obesity but with thin arms and legs
 reddish stretch marks
 a round red face, a fat lump between the shoulders
 weak muscles
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 weak bones
 acne
 fragile skin that heals poorly
 Women may have more hair and irregular menstruation
Occasionally there may be changes in mood,
headaches, and a chronic feeling of tiredness.
 physical Exam
 24-hour urinary free cortisol test: For this test, you’ll
be asked to collect your urine over a 24-hour period.
The levels of cortisol will then be tested.
 Salivary cortisol measurement: In people without
Cushing’s syndrome, cortisol levels drop in the evening.
This test measures the level of cortisol in a saliva
sample that’s been collected late at night to see if
cortisol levels are too high.
 Low-dose dexamethasone suppression test: For this
test, you’ll be given a dose of dexamethasone late in
the evening. Blood will be tested for cortisol levels in
the morning. Normally, dexamethasone causes cortisol
levels to drop. If you have Cushing’s syndrome, this
won’t occur.
 Imaging tests- Computerized tomography (CT) scans
or magnetic resonance imaging (MRI) scans can provide
images of your pituitary and adrenal glands to detect
abnormalities, such as tumors.
Treatment  Reducing corticosteroid use - If the cause of Cushing
syndrome is long-term use of corticosteroid
medications, may be able to keep your Cushing
syndrome signs and symptoms under control by
reducing the dosage of the drug over a period of time,
while still adequately managing your asthma, arthritis
or other condition.
 Surgery - If the cause of Cushing syndrome is a
tumor, may recommend complete surgical removal.
 Radiation therapy - If the surgeon can't totally
remove a pituitary tumor, he or she will usually
prescribe radiation therapy to be used in conjunction
with the operation. Additionally, radiation may be used
for people who aren't suitable candidates for surgery.
 Medications - Medications can be used to control
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cortisol production when surgery and radiation don't

work. Medications may also be used before surgery in
people who have become very sick with Cushing
syndrome.
 ketoconazole, mitotane (Lysodren) and metyrapone
(Metopirone).
Complication Without treatment, complications of Cushing syndrome may
include:
 Bone loss (osteoporosis), which can result in unusual
bone fractures, such as rib fractures and fractures of
the bones in the feet
 High blood pressure (hypertension)
 Type 2 diabetes
 Frequent or unusual infections
 Loss of muscle mass and strength
Hyposecretion
Topic Description
Disease Addison disease
Definition Addison disease is a disorder that occurs when the adrenal
glands do not produce enough hormones.
Cause Addison disease results from damage to the adrenal cortex.
The damage causes the cortex to produce hormone levels
that are too low. This damage may be caused by the following:
 The immune system mistakenly attacking the adrenal
glands (autoimmune disease)
 Infections such as tuberculosis, HIV, or fungal
infections
 Hemorrhage into the adrenal glands
 Tumors
Risk Factors  Swelling (inflammation) of the thyroid gland that
often results in reduced thyroid function (chronic
thyroiditis)
 Thyroid gland produces too much thyroid hormone
(overactive thyroid, Graves disease)
 Itchy rash with bumps and blisters (dermatitis
herpetiformis)
 Parathyroid glands in the neck do not produce enough
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parathyroid hormone (hypoparathyroidism)

 Pituitary gland does not produce normal amounts of
some or all of its hormones (hypopituitarism)
 Autoimmune disorder that affects the nerves and the
muscles they control (myasthenia gravis)
 Body does not have enough healthy red blood cells
(pernicious anemia)
 Testicles cannot produce sperm or male hormones
(testicular failure)
 Type I diabetes
 Loss of brown color (pigment) from areas of the skin
(vitiligo)
Signs and symptoms  Abdominal pain
 Chronic diarrhea, nausea, and vomiting
 Darkening of the skin
 Dehydration
 Dizziness when standing up
 Low-grade fever
 Low blood sugar
 Low blood pressure
 Extreme weakness, fatigue, and slow, sluggish
movement
 Darker skin on the inside of the cheeks and lips
(buccal mucosa)
 Salt craving (eating food with a lot of added salt)
 Weight loss with reduced appetite
 Symptoms may not be present all the time. Many
people have some or all of these symptoms when they
have an infection or other stress on the body. Other
times, they have no symptoms.
Diagnosis/ Investigation  Blood tests will likely be ordered and may show:
o Increased potassium
o Low blood pressure, especially with a change in
body position
o Low cortisol level
o Low sodium level
o Low pH
o Normal testosterone and estrogen levels, but
low DHEA level
o High eosinophil count
 Abdominal x-ray
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 Abdominal CT scan
 Cosyntropin (ACTH) stimulation test
Treatment All treatment for Addison's disease involves medication.
Hormone replacement therapy to correct the levels of
steroid hormones,If body isn't producing. Some options for
treatment include oral corticosteroids such as:
 Hydrocortisone (Cortef), prednisone or
methylprednisolone to replace cortisol. These
hormones are given on a schedule to mimic the normal
24-hour fluctuation of cortisol levels.
 Fludrocortisone acetate to replace aldosterone.
Other treatment recommendations include:
 Carry a medical alert card and bracelet at all times. A
steroid emergency card and medical alert
identification will let emergency medical personnel
know what kind of care you need. Also have a written
action plan.
 Keep extra medication handy. Missing even one day of
medication may be dangerous, so keep a small supply of
medication at work and with you whenever you travel.
 Carry a glucocorticoid injection kit. The kit contains a
needle, syringe and injectable form of corticosteroids
to use in case of emergency.
 Stay in contact with your doctor. Keep an ongoing
relationship with your doctor to make sure that the
doses of replacement hormones are adequate, but not
excessive. If you're having ongoing problems with your
medications, you may need adjustments in the doses or
timing of the medications.
 Have annual checkups. See your doctor or an
endocrinology specialist at least once a year. Your
doctor may recommend annual screening for a number
of autoimmune diseases.
Treatment for an addisonian crisis, which is a medical
emergency, typically includes intravenous injections of:
 Corticosteroids
 Saline solution
 Sugar (dextrose)
Complication  If untreated Addison's disease, may develop an
addisonian crisis as a result of physical stress, such as
an injury, infection or illness. Normally, the adrenal
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glands produce two to three times the usual amount of

cortisol in response to physical stress. With adrenal
insufficiency, the inability to increase cortisol
production with stress can lead to an addisonian crisis.
 An addisonian crisis is a life-threatening situation that
results in low blood pressure, low blood levels of sugar
and high blood levels of potassium. You will need
immediate medical care.
ADRENAL MEDULLA
Hypersecretion
Topic Description
Disease Pheochromocytoma
Definition Pheochromocytoma is a rare tumor of adrenal gland tissue. It
results in the release of too much epinephrine and
norepinephrine, hormones that control heart rate,
metabolism, and blood pressure.
Cause  Pheochromocytoma may occur as a single tumor or as
more than one growth. It usually develops in the
center (medulla) of one or both adrenal glands. The
adrenal glands are two triangle-shaped glands. One
gland is located on top of each kidney. In rare cases, a
pheochromocytoma occurs outside the adrenal gland.
When it does, it is usually somewhere else in the
abdomen.
 In few instances, the condition may also be seen among
family members (hereditary).
Risk Factors People who have certain rare inherited disorders have an
increased risk of pheochromocytoma or paraganglioma.
Tumors associated with these disorders are more likely to be
cancerous. These genetic conditions include:
 Multiple endocrine neoplasia, type 2 (MEN 2) is a
disorder that results in tumors in more than one part
of the body's hormone-producing (endocrine) system.
Other tumors associated with this condition can
appear on the thyroid, parathyroid, lips, tongue and
gastrointestinal tract.
 Von Hippel-Lindau disease can result in tumors at
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multiple sites, including the central nervous system,

endocrine system, pancreas and kidneys.
 Neurofibromatosis 1 (NF1) results in multiple tumors
in the skin (neurofibromas), pigmented skin spots and
tumors of the optic nerve.
 Hereditary paraganglioma syndromes are inherited
disorders that result in either pheochromocytomas or
paragangliomas.
Signs and symptoms Most people with this tumor have attacks of a set of
symptoms, which happen when the tumor releases hormones.
The attacks usually last from a few minutes to hours. The set
of symptoms include:
 Headaches
 Heart palpitations
 Sweating
 High blood pressure
 As the tumor grows, the attacks often increase in
frequency, length, and severity.
Other symptoms that may occur include:
 Abdominal or chest pain
 Irritability, nervousness
 Pallor
 Weight loss
 Nausea and vomiting
 Shortness of breath
 Seizures
 Problems sleeping
Diagnosis/ Investigation  History Collecttion
 Physical Examination
 Abdominal CT scan
 Adrenal biopsy
 Catecholamines blood test (serum catecholamines)
 Glucose test
 Metanephrine blood test (serum metanephrine)
 An imaging test called an MIBG scintiscan
 MRI of abdomen
 Urine catecholamines
 Urine metanephrines
 PET scan of abdomen
Treatment  The primary treatment for a pheochromocytoma is
surgery to remove the tumor. Before the surgery,
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prescribe specific blood pressure medications that

block the actions of the high-adrenaline hormones to
lower the risk of developing dangerously high blood
pressure during surgery.
 Preoperative preparations- Take two drugs for seven
to 10 days that help lower blood pressure before
surgery. These drugs will either replace or be added
to other blood pressure drugs.
 Alpha blockers - These drugs keep smaller arteries
and veins open and relaxed, improving blood flow and
decreasing blood pressure. Alpha blockers include
phenoxybenzamine, doxazosin (Cardura) and prazosin
(Minipress). Side effects might include irregular
heartbeat, dizziness, fatigue, vision problems, sexual
dysfunction in men and swelling in the limbs.
 Beta blockers - These drugs cause heart to beat more
slowly and with less force. They also help keep blood
vessels open and relaxed. In your surgery preparation,
your doctor will likely prescribe a beta blocker several
days after starting the alpha blocker.Beta blockers
include atenolol (Tenormin), metoprolol (Lopressor,
Toprol-XL) and propranolol (Inderal, Innopran XL).
Possible side effects include fatigue, upset stomach,
headache, dizziness, constipation, diarrhea, irregular
heartbeat, difficulty breathing and swelling in the
limbs.
 High-salt diet- Alpha and beta blockers widen the
blood vessels, causing the amount of fluid within the
blood vessels to be low. This can cause dangerous
drops in blood pressure with standing. A high-salt diet
will draw more fluid inside the blood vessels,
preventing the development of low blood pressure
during and after surgery.
 Surgery - In most cases, your surgeon removes the
entire adrenal gland with a pheochromocytoma with
minimally invasive surgery. Your surgeon will make a
few small openings through which he or she inserts
wandlike devices equipped with video cameras and
small tools.
 The remaining healthy adrenal gland carries out the
functions normally performed by two. Blood pressure
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usually returns to normal.

 In some cases, such as when the other adrenal gland
has been removed, your doctor might remove only the
tumor, sparing some healthy tissue.
 If a tumor is cancerous, the tumor and other
cancerous tissue will be removed. However, even if all
of the cancerous tissue isn't removed, surgery might
limit hormone production and provide some blood
pressure control.
Cancer treatments - Very few pheochromocytomas are
cancerous. As such, research about the best treatments is
limited. Treatments for cancerous tumors and cancer that
has spread in the body, related to a pheochromocytoma,
include:
 MIBG. This radiation therapy combines MIBG, a
compound that attaches to adrenal tumors, with a type
of radioactive iodine. The treatment goal is to deliver
radiation therapy to a specific site and kill cancerous
cells.
 Peptide receptor radionuclide therapy (PRRT). PRRT
combines a drug that targets cancer cells with a small
amount of a radioactive substance. It allows radiation
to be delivered directly to the cancer cells. One PRRT
drug, lutetium Lu 177 dotatate (Lutathera), is used to
treat advanced neuroendocrine tumors.
 Chemotherapy. Chemotherapy is the use of powerful
drugs that kill fast-growing cancer cells.
 Radiation therapy. This may be used for symptomatic
treatment of tumors that have spread to the bone, for
example, that are causing pain.
 Targeted cancer therapies. These medications hinder
the function of naturally occurring molecules that
promote the growth and spread of cancerous cells.
Complication  High blood pressure can damage multiple organs,
particularly tissues of the cardiovascular system,
brain and kidneys. This damage can cause a number of
critical conditions, including:
 Heart disease
 Stroke
 Kidney failure
 Problems with the nerves of the eye
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PANCREAS
Hypersecretion
Topic Description
Disease Hyperinsulinism
Definition It is the presence of excess insulin in the body resulting in
hypoglycemia.
Cause  tumor of the pancreas (benign adenoma or carcinoma)
 an overdose of insulin
Risk Factors  Maternal diabetes
 Poor fetal growth
 Birth asphyxia
Signs and symptoms  Weight gain
 Cravings for sugar
 Intense hunger
 Feeling frequently hungry
 Difficulty concentrating
 Feeling anxious or panicky
 Lacking focus or motivation
 Fatigue
 Blood test
 CT Scan
Treatment  Medication
o Diazoxide (Proglycem)- First-line treatment. PO
diazoxide (Proglycem) opens KATP channels and
inhibits insulin secretion. The IV preparation
(Hyperstat) is not used in hyperinsulinism.
o Octreotide (Sandostatin)- Somatostatin
analogue, activates G-protein K channel.
Hyperpolarization of beta cell results in
inhibition of calcium influx and insulin release.
Octreotide also used for acromegaly, carcinoid
tumors, and VIPomas.
o Nifedipine (Adalat, Procardia) - Blocks calcium
channels and insulin release. Also used to treat
hypertension and angina.
o Dextrose (D-glucose) - IV glucose is used to
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elevate serum glucose levels promptly. PO

glucose is rapidly absorbed from intestine and
stored or used by the tissues. Parenterally
injected dextrose is used in patients unable to
sustain adequate PO intake. Direct PO
absorption results in a rapid increase in blood
glucose concentrations. Dextrose is effective in
small doses, and no evidence exists that it may
cause toxicity.
 Surgery - In general, maintenance of normoglycemia
should be attempted before pancreatectomy is
considered. At the same time, because hypoglycemia
can result in irreversible brain damage, surgical
excision should not be delayed in patients with severe
hypoglycemia.
Complication  seizures.
 coma.
 cognitive function issues (especially in young children)
Hyposecretion
Topic Description
Disease Diabetes mellitus (DM)
Definition More commonly referred to as "diabetes" -- a chronic disease
associated with abnormally high levels of the sugar glucose in
the blood.
Cause Diabetes is due to one of two mechanisms:
 Inadequate production of insulin (which is made by the
pancreas and lowers blood glucose), or
 Inadequate sensitivity of cells to the action of insulin.
Risk Factors  Family history of diabetes
 African-American, Hispanic, Native American, or
Asian-American race, Pacific Islander or ethnic
background
 Being overweight
 Physical stress (such as surgery or illness)
 Use of certain medications, including steroids
 Injury to the pancreas (such as infection, tumor,
surgery or accident)
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 Autoimmune disease
 High blood pressure
 Abnormal blood cholesterol or triglyceride levels
 Age (risk increases with age)
 Smoking
 History of gestational diabetes
Pregnant women who have a greater risk of developing
gestational diabetes include those who:
 Are over 35 years old
 Are overweight
 Have a family history of diabetes
Types  Type 1 diabetes occurs because the insulin-producing
cells of the pancreas (beta cells) are damaged. In type
1 diabetes, the pancreas makes little or no insulin, so
sugar cannot get into the body's cells for use as
energy. People with type 1 diabetes must use insulin
injections to control their blood glucose. Type 1 is the
most common form of diabetes in people who are
under age 30, but it can occur at any age. Ten percent
of people with diabetes are diagnosed with type 1.
 In type 2 diabetes (adult onset diabetes), the
pancreas makes insulin, but it either doesn't produce
enough, or the insulin does not work properly. Nine out
of 10 people with diabetes have type 2. This type
occurs most often in people who are over 40 years old
but can occur even in childhood if there are risk
factors present. Type 2 diabetes may sometimes be
controlled with a combination of diet, weight
management and exercise. However, treatment also
may include oral glucose-lowering medications (taken
by mouth) or insulin injections (shots).
 Gestational diabetes occurs when there is a high blood
glucose level during pregnancy. As pregnancy
progresses, the developing baby has a greater need
for glucose. Hormone changes during pregnancy also
affect the action of insulin, which brings about high
blood glucose levels.
Signs and symptoms  Increased thirst
 Increased hunger (especially after eating)
 Dry mouth
 Frequent urination
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 Unexplained weight loss (even though you are eating

and feel hungry)
 Weak, tired feeling
 Blurred vision
 Numbness or tingling in the hands or feet
 Slow-healing sores or cuts
 Dry and itchy skin
 Frequent yeast infections or urinary tract infections
Common early symptoms of low blood sugar include the
following:
 Feeling weak
 Feeling dizzy
 Feeling hungry
 Trembling and feeling shaky
 Sweating
 Pounding heart
 Pale skin
 Feeling frightened or anxious
Late symptoms of low blood sugar include:
 Feeling confused
 Headache
 Feeling cranky
 Poor coordination
 Bad dreams or nightmares
 Being unable keep your mind on one subject
 Numbness in your mouth and tongue
 Passing out
Diagnosis/ Investigation  Fasting Glucose Test
 Random (anytime) Glucose Test
 .A1c Test
Treatment Type 1 diabetes
 Insulin is the main treatment for type 1 diabetes. It
replaces the hormone your body isn’t able to produce.
There are four types of insulin that are most commonly used.
They’re differentiated by how quickly they start to work, and
how long their effects last:
 Rapid-acting insulin starts to work within 15 minutes
and its effects last for 3 to 4 hours.
 Short-acting insulin starts to work within 30 minutes
and lasts 6 to 8 hours.
 Intermediate-acting insulin starts to work within 1 to
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2 hours and lasts 12 to 18 hours.

 Long-acting insulin starts to work a few hours after
injection and lasts 24 hours or longer.
Type 2 diabetes
 Diet and exercise can help some people manage type 2
diabetes. If lifestyle changes aren’t enough to lower
blood sugar, need to take medication.
Types of drug How they work Example(s)
Alpha-glucosidase Slow your Acarbose (Precose) and
inhibitors body’s miglitol (Glyset)
breakdown of
sugars and
starchy foods
Biguanides Reduce the Metformin (Glucophage)
amount
of glucose your
liver makes
DPP-4 inhibitors Improve your Linagliptin (Tradjenta),
blood sugar saxagliptin (Onglyza),
without making and sitagliptin (Januvia)
it drop too low
Glucagon-like Change the Dulaglutide (Trulicity),
peptides way your body exenatide (Byetta), and
produces liraglutide (Victoza)
insulin
Meglitinides Stimulate your Nateglinide (Starlix) and
pancreas to repaglinide (Prandin)
release more
insulin
SGLT2 inhibitors Release more Canagliflozin (Invokana)
glucose into and dapagliflozin
the urine (Farxiga)
Sulfonylureas Stimulate your Glyburide (DiaBeta,
pancreas to Glynase), glipizide (Gluco
release more trol),
insulin and glimepiride (Amaryl)
Thiazolidinediones Help insulin Pioglitazone (Actos) and
work better rosiglitazone (Avandia)
Complication Complications associated with diabetes include:
 heart disease, heart attack, and stroke
 neuropathy
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 nephropathy
 retinopathy and vision loss
 hearing loss
 foot damage such as infections and sores that don’t
heal
 skin conditions such as bacterial and fungal infections
 depression
 dementia
PITUITARY GLAND: ANTERIOR LOBE
Hypersecretion
Topic Description
Disease Acromegaly
Definition It is a disorder caused by excessive production of growth
hormone by the pituitary gland and marked especially by
progressive enlargement of hands, feet, and face
Cause  benign tumor affecting their pituitary
Risk Factors  Age
Signs and symptoms Common symptoms of acromegaly are:
 enlarged bones in the face, feet, and hands
 excessive hair growth in women
 an enlarged jaw or tongue
 a prominent brow
 excessive growth spurts, which are more common in
people who’ve had abnormal growth before adolescence
 weight gain
 swollen and painful joints that limit movement
 spaces between the teeth
 splayed fingers and toes
 a hoarse, deep voice
 fatigue
 headaches
 an inability to sleep
 muscle weakness
 profuse sweating
 body odor
 enlarged sebaceous glands, which are glands that
produce oils in the skin
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 thickened skin
 skin tags, which are noncancerous growths
Diagnosis/ Investigation  GH and IGF-I measurement. After fasted
overnight,will take a blood sample to measure levels of
GH and IGF-I. Elevated levels of these hormones
suggest acromegaly.
 Growth hormone suppression test - This is the
definitive method for verifying acromegaly. In this
test, blood levels of GH are measured before and
after you drink a preparation of sugar (glucose).
Normally, glucose ingestion depresses levels of GH. If
acromegaly, GH level will tend to stay high.
 Magnetic resonance imaging (MRI)- to help pinpoint
the location and size of a tumor of pituitary gland. If
no pituitary tumors are seen,look for nonpituitary
tumors as the cause of your high GH levels.
Treatment Treatment focuses on lowering your production of GH, as well
as reducing the negative effects of the tumor on the
pituitary gland and surrounding tissues.
 Surgery - transsphenoidal surgery. In this procedure,
extract the pituitary tumor.Removing the tumor can
normalize GH production and eliminate the pressure on
the tissues surrounding your pituitary gland to relieve
associated signs and symptoms. In some cases,surgeon
may not be able to remove the entire tumor. This may
result in persistently elevated GH levels after
surgery, requiring further medical or radiation
treatments.
 Medications - Drugs used to lower the production or
block the action of GH include:
o Drugs that reduce excess growth hormone
secretion (somatostatin analogues): The drugs
octreotide (Sandostatin) and lanreotide
(Somatuline Depot) are synthetic versions of
the brain hormone somatostatin. They can
interfere with the excessive secretion of GH
by the pituitary gland, causing rapid declines in
GH levels.
o Drugs to lower hormone levels (dopamine
agonists): The oral medications cabergoline and
bromocriptine (Parlodel) lower levels of GH and
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IGF-I in some people. The tumor may decrease

in size in some people taking a dopamine agonist.
Some people may develop compulsive behaviors,
such as gambling, while taking these
medications.
o Drug to block the action of GH (growth
hormone antagonist): The medication
pegvisomant (Somavert) blocks the effect of
GH on body tissues. Pegvisomant may be
particularly helpful for people who haven't had
good success with other forms of treatment.
 Radiation - recommend radiation treatment when
tumor cells remain after surgery. Radiation therapy
destroys any lingering tumor cells and slowly reduces
GH levels.
Types of radiation therapy include:
o Conventional radiation therapy: This type of
radiation therapy is usually given every weekday
over a period of four to six weeks. You may not
realize the full effect of conventional radiation
therapy for 10 or more years after treatment.
o Proton beam therapy: Proton beam therapy
delivers a targeted, high dose of radiation to
the tumor, sparing radiation exposure to normal
tissues. Proton beam therapy is provided in
fractions over time, but treatment times are
generally less than conventional radiation.
o Stereotactic radiosurgery: Stereotactic
radiosurgery delivers a high dose of radiation
to tumor cells in a single dose while limiting the
amount of radiation to normal surrounding
tissues. This type of radiation may bring GH
levels back to normal within five years.
Complication Progression of acromegaly can result in major health
problems. Complications may include:
 High blood pressure (hypertension)
 Cardiovascular disease, particularly enlargement of
the heart (cardiomyopathy)
 Osteoarthritis
 Diabetes mellitus
 Goiter
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 Precancerous growths (polyps) on the lining of your

colon
 Sleep apnea, a condition in which breathing repeatedly
stops and starts during sleep
 Carpal tunnel syndrome
 Spinal cord compression
 Vision loss
Topic Description
Disease Gigantism
Definition Gigantism is abnormal growth due to an excess of growth
hormone (GH) during childhood.
Cause  Pituitary tumor
There are other less common causes of gigantism:
 McCune-Albright syndrome causes abnormal growth in
bone tissue, patches of light-brown skin, and gland
abnormalities.
 Carney complex is an inherited condition that causes
noncancerous tumors on connective tissue, cancerous
or noncancerous endocrine tumors, and spots of darker
skin.
 Multiple endocrine neoplasia type 1 (MEN1) is an
inherited disorder that causes tumors in the pituitary
gland, pancreas, or parathyroid glands.
 Neurofibromatosis is an inherited disorder that
causes tumors in the nervous system.
Signs and symptoms The child will grow in height, as well as in the muscles and
organs. This excessive growth makes the child extremely
large for his or her age.
Other symptoms include:
 Delayed puberty
 Double vision or difficulty with side (peripheral) vision
 Very prominent forehead (frontal bossing) and a
prominent jaw
 Gaps between the teeth
 Headache
 Increased sweating
 Irregular periods (menstruation)
 Joint pain
 Large hands and feet with thick fingers and toes
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 Release of breast milk

 Sleep problems
 Thickening of the facial features
 Weakness
 Voice changes
 Laboratory tests that may be ordered include:
o Cortisol
o Estradiol (girls)
o GH suppression test
o Prolactin
o Insulin-like growth factor-I
o Testosterone (boys)
o Thyroid hormone
 CT or MRI scan of the head, also may be ordered to
check for a pituitary tumor.
Treatment  Surgery
 Medication
 Radation
Complication  Adrenal insufficiency (adrenal glands do not produce
enough of their hormones)
 Diabetes insipidus (extreme thirst and excessive
urination; in rare cases)
 Hypogonadism (body's sex glands produce little or no
hormones)
 Hypothyroidism (thyroid gland does not make enough
thyroid hormone)
Hyposecretion
Topic Description
Disease Dwarfism
Definition Dwarfism is short stature that results from a genetic or
medical condition. Dwarfism is generally defined as an adult
height of 4 feet 10 inches (147 centimeters) or less. The
average adult height among people with dwarfism is 4 feet
(122 cm).
Cause Most dwarfism-related conditions are genetic disorders, but
the causes of some disorders are unknown. Most occurrences
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of dwarfism result from a random genetic mutation in either

the father's sperm or the mother's egg rather than from
either parent's complete genetic makeup.
 Achondroplasia - About 80 percent of people with
achondroplasia are born to parents of average height.
A person with achondroplasia and with two average-
size parents received one mutated copy of the gene
associated with the disorder and one normal copy of
the gene. A person with the disorder may pass along
either a mutated or normal copy to his or her own
children.
 Turner syndrome - Turner syndrome, a condition that
affects only girls and women, results when a sex
chromosome (the X chromosome) is missing or partially
missing. A female inherits an X chromosome from each
parent. A girl with Turner syndrome has only one fully
functioning copy of the female sex chromosome rather
than two.
 Growth hormone deficiency - The cause of growth
hormone deficiency can sometimes be traced to a
genetic mutation or injury, but for most people with
the disorder, no cause can be identified.
 Other causes
o other genetic disorders
o deficiencies in other hormones
o poor nutrition
o Sometimes the cause is unknown.
Risk Factors  hormone deficiency
 malnutrition
Types  Disproportionate dwarfism. If body size is
disproportionate, some parts of the body are small,
and others are of average size or above-average size.
Disorders causing disproportionate dwarfism inhibit
the development of bones.
 Proportionate dwarfism. A body is proportionately
small if all parts of the body are small to the same
degree and appear to be proportioned like a body of
average stature. Medical conditions present at birth
or appearing in early childhood limit overall growth and
development.
Signs and symptoms  Disproportionate dwarfism - Most people with
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dwarfism have disorders that cause disproportionately

short stature. Usually, this means that a person has an
average-size trunk and very short limbs, but some
people may have a very short trunk and shortened (but
disproportionately large) limbs. In these disorders,
the head is disproportionately large compared with the
body.Almost all people with disproportionate dwarfism
have normal intellectual capacities. Rare exceptions
are usually the result of a secondary factor, such as
excess fluid around the brain (hydrocephalus).
 The most common cause of dwarfism is a disorder
called achondroplasia, which causes disproportionately
short stature. This disorder usually results in the
following:
o An average-size trunk
o Short arms and legs, with particularly short
upper arms and upper legs
o Short fingers, often with a wide separation
between the middle and ring fingers
o Limited mobility at the elbows
o A disproportionately large head, with a
prominent forehead and a flattened bridge of
the nose
o Progressive development of bowed legs
o Progressive development of swayed lower back
o An adult height around 4 feet (122 cm)
 Another cause of disproportionate dwarfism is a rare
disorder called spondyloepiphyseal dysplasia congenita
(SEDC). Signs may include:
o A very short trunk
o A short neck
o Shortened arms and legs
o Average-size hands and feet
o Broad, rounded chest
o Slightly flattened cheekbones
o Opening in the roof of the mouth (cleft palate)
o Hip deformities that result in thighbones
turning inward
o A foot that's twisted or out of shape
o Instability of the neck bones
o Progressive hunching curvature of the upper
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spine
o Progressive development of swayed lower back
o Vision and hearing problems
o Arthritis and problems with joint movement
o Adult height ranging from 3 feet (91 cm) to
just over 4 feet (122 cm)
 Proportionate dwarfism - Proportionate dwarfism
results from medical conditions present at birth or
appearing in early childhood that limit overall growth
and development. So the head, trunk and limbs are all
small, but they're proportionate to each other.
Because these disorders affect overall growth, many
of them result in poor development of one or more
body systems. Growth hormone deficiency is a
relatively common cause of proportionate dwarfism. It
occurs when the pituitary gland fails to produce an
adequate supply of growth hormone, which is essential
for normal childhood growth. Signs include:
o Height below the third percentile on standard
pediatric growth charts
o Growth rate slower than expected for age
o Delayed or no sexual development during the
teen years
Diagnosis/ Investigation  Measurements - A regular part of a well-baby medical
exam is the measurement of height, weight and head
circumference. At each visit, will plot these
measurements on a chart to show child's current
percentile ranking for each one. This is important for
identifying abnormal growth, such as delayed growth
or a disproportionately large head. If any trends in
these charts are a concern, may make more-frequent
measurements.
 Appearance - Many distinct facial and skeletal
features are associated with each of several dwarfism
disorders.Child's appearance also may help to make a
diagnosis.
 Imaging technology - Imaging studies, such as X-rays,
because certain abnormalities of the skull and skeleton
can indicate which disorder child may have. Various
imaging devices may also reveal delayed maturation of
bones, as is the case in growth hormone deficiency. A
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magnetic resonance imaging (MRI) scan may reveal

abnormalities of the pituitary gland or hypothalamus,
both of which play a role in hormone function.
 Genetic tests - Genetic tests are available for many of
the known causal genes of dwarfism-related disorders,
but these tests often aren't necessary to make an
accurate diagnosis. It is likely to suggest a test only to
distinguish among possible diagnoses when other
evidence is unclear or as a part of further family
planning.
 Family history - may take a history of stature in
siblings, parents, grandparents or other relatives to
help determine whether the average range of height in
your family includes short stature.
 Hormone tests - may order tests that assess levels of
growth hormone or other hormones that are critical
for childhood growth and development.
Treatment  The goal of treatment is to maximize functioning and
independence. Most dwarfism treatments don't
increase stature but may correct or relieve problems
caused by complications.
 Surgical treatments - Surgical procedures that may
correct problems in people with disproportionate
dwarfism include:
o Correcting the direction in which bones are
growing
o Stabilizing and correcting the shape of the
spine
o Increasing the size of the opening in bones of
the spine (vertebrae) to alleviate pressure on
the spinal cord. Placing a shunt to remove
excess fluid around the brain (hydrocephalus),
if it occurs
 Hormone therapy - For individuals with dwarfism due
to growth hormone deficiency, treatment with
injections of a synthetic version of the hormone may
increase final height. In most cases, children receive
daily injections for several years until they reach a
maximum adult height — often within the average
adult range for their family.
o Treatment may continue throughout the teen
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years and early adulthood to ensure adult

maturation, such as appropriate gain in muscle
or fat. Some individuals may need lifelong
therapy. The treatment may be supplemented
with other related hormones if they are also
deficient.
o Treatment for girls with Turner syndrome also
requires estrogen and related hormone therapy
in order for them to begin puberty and achieve
adult sexual development. Estrogen
replacement therapy usually continues
throughout life until women with Turner
syndrome reach the average age of menopause.
o Growth hormone supplementation for children
with achondroplasia does not increase final
adult height.
o Ongoing health care - Regular checkups and
ongoing care by a doctor familiar with dwarfism
can improve quality of life. Because of the
range of symptoms and complications,
treatments are tailored to address problems as
they occur, such as assessment and treatment
for ear infections, spinal stenosis or sleep
apnea.
o Adults with dwarfism should continue to be
monitored and treated for problems that occur
throughout life.
 Limb lengthening - Some people with dwarfism choose
to undergo surgery called extended limb lengthening.
This procedure is controversial for many people with
dwarfism because, as with all surgeries, there are
risks. Waiting to decide about limb lengthening until
the person with dwarfism is old enough to participate
in the decision is recommended because of the
emotional and physical stress involved with multiple
procedures.
Complication  Disproportionate dwarfism - The characteristic
features of the skull, spine and limbs shared by most
forms of disproportionate dwarfism result in some
common problems:
o Delays in motor skills development, such as
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sitting up, crawling and walking

o Frequent ear infections and risk of hearing loss
o Bowing of the legs
o Difficulty breathing during sleep (sleep apnea)
o Pressure on the spinal cord at the base of the
skull
o Excess fluid around the brain (hydrocephalus)
o Crowded teeth
o Progressive severe hunching or swaying of the
back with back pain or problems breathing
o Narrowing of the channel in the lower spine
(spinal stenosis), resulting in pressure on the
spinal cord and subsequent pain or numbness in
the legs
o Arthritis
o Weight gain that can further complicate
problems with joints and the spine and place
pressure on nerves
 Proportionate dwarfism - With proportionate
dwarfism, problems in growth and development often
result in complications with poorly developed organs.
For example, heart problems that often occur with
Turner syndrome can have a significant effect on
health. An absence of sexual maturation associated
with growth hormone deficiency or Turner syndrome
affects both physical development and social
functioning.
 Pregnancy - Women with disproportionate dwarfism
may develop respiratory problems during pregnancy. A
C-section (cesarean delivery) is almost always
necessary because the size and shape of the pelvis
doesn't allow for successful vaginal delivery.
Topic Description
Disease Panhypopituitarism
Definition Panhypopituitarism is a condition of inadequate or absent
production of the anterior pituitary hormones.
Cause  A tumor, or cyst, on or near the pituitary gland or
hypothalamus.
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 Underdeveloped or poorly formed pituitary gland.

 Birth trauma or other injury.
 Infection.
 Autoimmune reaction.
 Pressure from hydrocephalus.
 Surgery.
 Radiation treatment.
Risk Factors  Damage to the pituitary gland, which may occur from
trauma , radiation therapy , cancer spread, bleeding
after childbirth (postpartum hemorrhage)
Signs and symptoms  Abnormal slowing of growth.
 Delayed puberty.
 Excessive thirst and excessive urination.
 Less frequent menstrual periods.
 Low blood sugar (hypoglycemia)
 Prolonged jaundice in infants.
 Sensitivity to cold.
 Poor appetite.
Diagnosis/ Investigation  Blood tests - These tests measure your hormone
levels. For example, blood tests can identify low levels
of thyroid, adrenal or sex hormones. The tests can
determine if these low levels are associated with
pituitary hormone production.
 Stimulation or dynamic testing - These tests also
measure hormone levels.These tests check hormone
levels after taken certain medications to stimulate
hormone production.
 Brain imaging - Magnetic resonance imaging (MRI) or
high-resolution computerized tomography (CT) of your
brain can detect a pituitary tumor or other pituitary
gland problems.
 Vision tests - These tests can determine if growth of
a pituitary tumor has impaired your sight or visual
fields
Treatment  Medications - Hormone replacement medications may
include:
o Corticosteroids - These drugs, such as
hydrocortisone (Cortef) or prednisone (Rayos),
replace the adrenal hormones that aren't being
produced because of an adrenocorticotropic
hormone (ACTH) deficiency.
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o Levothyroxine (Levoxyl, Synthroid, others) -

This medication treats the low thyroid hormone
levels (hypothyroidism) that a thyroid-
stimulating hormone (TSH) deficiency can
cause.
o Sex hormones - These include testosterone in
men and estrogen or a combination of estrogen
and progesterone in women. Testosterone is
administered either by injection or through the
skin with a patch or a gel. Female hormone
replacement can be administered with pills, gels
or patches.
o Growth hormone - Also called somatropin
(Genotropin, Humatrope, others), growth
hormone is administered through an injection
beneath your skin. It promotes growth, which
helps produce a more normal height in children.
Adults with symptoms of growth hormone
deficiency also may benefit from growth
hormone replacement, but they won't grow
taller.
o Fertility hormones- If infertile, gonadotropins
can be administered by injection to stimulate
ovulation in women and sperm production in men.
 Surgery - Treatment for pituitary tumors may involve
surgery to remove the growth. In some cases,
radiation treatment or medications are recommended
to control the underlying cause.
PITUITARY GLAND: POSTERIOR LOBE
Hypersecretion
Topic Description
Disease Syndrome of inappropriate ADH (SIADH)
Definition Syndrome of inappropriate antidiuretic hormone secretion
(SIADH) is characterized by excessive unsuppressible
release of antidiuretic hormone (ADH) either from the
posterior pituitary gland, or an abnormal non-pituitary source.
Cause A variety of conditions can trigger abnormal ADH production,
including:
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 brain infections
 bleeding in or around the brain
 head trauma
 hydrocephalus
 Guillian-Barre syndrome
 multiple sclerosis
 infections including HIV and Rocky Mountain spotted
fever
 cancers of the lung or gastrointestinal or
genitourinary tract, lymphoma, sarcoma
 lung infections
 asthma
 cystic fibrosis
 medications
 anesthesia
 hereditary factors
 sarcoidosis
Signs and symptoms Symptoms may be mild and vague at first, but tend to build.
Severe cases may involve these symptoms:
 irritability and restlessness
 loss of appetite
 cramps
 nausea and vomiting
 muscle weakness
 confusion
 hallucinations
 personality changes
 seizures
 stupor
 coma
 Urinalysis
 Blood test – Specially ADH Test
Treatment  The first line of treatment is to limit fluid intake to
avoid further buildup.
 Medications may include those that can reduce fluid
retention, such as furosemide (Lasix), and those that
can inhibit ADH, like demeclocycline.
Complication  Hyponatremia
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Hyposecretion
Topic Description
Disease Diabetes insipidus (DI)
Definition Excessive urination and extreme thirst as a result of
inadequate output of the pituitary hormone ADH (antidiuretic
hormone, also called vasopressin) or the lack of the normal
response by the kidney to ADH.
Cause Central diabetes insipidus often the result of:
 head trauma
 diseases that cause brain swelling
 surgery
 tumors
 loss of blood supply to the pituitary gland
 rare genetic conditions
Nephrogenic diabetes insipidus can also be caused by:
 medications, such as lithium or tetracycline
 high levels of calcium in the body
 low potassium levels in the body
 chronic kidney disease
 urinary tract blockage
Risk Factors  Genetics.
 Polycystic kidney disease.
 Pituitary disorders.
 Hypothalamic injury.
 Hypercalcemia.
 Head tumors.
 Pregnancy.
 Sickle cell disease.
Types  Central diabetes insipidus - This is the most common
form of DI and is caused by damage to the pituitary
gland or hypothalamus. This damage means ADH cannot
be produced, stored, or released normally. Without
ADH, large amounts of fluid are released into the
urine.
 Nephrogenic diabetes insipidus - Certain genetic
defects can damage the kidneys, making them unable
to respond to the ADH.
 Dipsogenic diabetes insipidus - This form of the
disease is caused by dysfunction of the thirst
mechanism in the hypothalamus. That can cause you to
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feel excessively thirsty and drink too much liquid. The

same things that lead to central DI can lead to
dipsogenic diabetes insipidus, and it has also been
associated with certain mental illness and other
medications.
 Gestational diabetes insipidus - This type of DI occurs
only during pregnancy when an enzyme made by the
placenta destroys a mother’s ADH. It may also be
caused by an increased level of a hormone-like
chemical that makes the kidneys less sensitive to
ADH. The placenta plays an important role in the
exchange of nutrients and waste products between
the fetus and the mother. The condition should
resolve after pregnancy.
Signs and symptoms  Excessive thirst that may be intense or uncontrollable,
usually with the need to drink large amounts of water
or craving for ice water
 Excessive urine volume
 Excessive urination, often needing to urinate every
hour throughout the day and night
 Very dilute, pale urine
Diagnosis/ Investigation  Blood sodium and osmolality
 Desmopressin (DDAVP) challenge
 MRI of the head
 Urinalysis
 Urine concentration and osmolality
 Urine output
Treatment  Central diabetes insipidus - If you have mild diabetes
insipidus, you may only need to increase your water
intake. If the condition is caused by an abnormality in
the pituitary gland or hypothalamus (such as a tumor),
will first treat the abnormality.
 Typically, this form is treated with a man-made
hormone called desmopressin (DDAVP, Minirin, others).
This medication replaces the missing anti-diuretic
hormone (ADH) and decreases urination. You can take
desmopressin as a nasal spray, as oral tablets or by
injection.
 Most people still make some ADH, though the amount
can vary day to day. So, the amount of desmopressin
you need also may vary. Taking more desmopressin
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than you need can cause water retention and

potentially serious low-sodium levels in the blood.
 Other medications may also be prescribed, such as
indomethacin (Indocin, Tivorbex) and chlorpropamide.
These drugs can make ADH more available in the body.
 Nephrogenic diabetes insipidus - Since the kidneys
don't properly respond to ADH in this form of
diabetes insipidus, desmopressin won't help. Instead,
your doctor may prescribe a low-salt diet to help
reduce the amount of urine your kidneys make. You'll
also need to drink enough water to avoid dehydration.
 Treatment with the drug hydrochlorothiazide
(Microzide) may improve your symptoms. Although
hydrochlorothiazide is a type of drug that usually
increases urine output (diuretic), in some people it can
reduce urine output for people with nephrogenic
diabetes insipidus.
 If your symptoms are due to medications you're
taking, stopping these medicines may help. However,
don't stop taking any medication without first talking
to your doctor.
 Gestational diabetes insipidus. Treatment for most
people with gestational diabetes insipidus is with the
synthetic hormone desmopressin.
Complication  Dehydration - Diabetes insipidus may lead to
dehydration. Dehydration can cause:
o Dry mouth
o Changes in skin elasticity
o Thirst
o Fatigue
 Electrolyte imbalance - Diabetes insipidus can cause an
imbalance in electrolytes — minerals in your blood,
such as sodium and potassium, that maintain the fluid
balance in your body. Symptoms of an electrolyte
imbalance may include:
o Weakness
o Nausea
o Vomiting
 Loss of appetite
 Muscle cramps
 Confusion
Page 70 of 75
ABNORMAL CONDITIONS OF ENDOCRINE GLANDS

Endocrine gland Hypersecretion Hyposecretion
Adrenal cortex Adrenal virilism Addison’s disease
Cushing’s disease
Adrenal medulla Pheochromocytoma
Pancreas Hyperinsulinism Diabetes mellitus
Parathyroid glands Hyperparathyroidism Hypoparathyroidism
Pituitary (anterior lobe) Acromegaly Dwarfism
Gigantism Panhypopituitarism
Pituitary (posterior lobe) Syndrome of inappropriate antidiuretic Diabetes insipidus
hormone
Thyroid gland Goiter, Graves disease, thyrotoxicosis Cretinism
Myxedema
LABORATORY TESTS
Fasting plasma glucose(FPG)

Also known as fasting blood sugar test. Measures circulating glucose level in a patient who
has fasted at least 8 hours.
The glycosylated hemoglobin (HbA1c) test (A1c for short), by measuring the percentage of
red blood cells with glucose attached, monitors long-term glucose control. A high level
indicates poor glucose control in diabetic patients.
Serum and urine tests

Measurement of hormones, electrolytes, glucose, and other substances in serum (blood)
and urine as indicators of endocrine function.
Urine studies include dipstick testing for glucose (Clinistix, Labstix) and
ketones (Acetest, Ketostix), and measurement of 17-ketosteroids (to check adrenaland
gonadal function).
A urinary microalbumin assay may detect small quantities of albumin in urine as a marker or
harbinger of diabetic nephropathy.
Thyroid function tests Measurement of T3, T4, and TSH in the bloodstream.
Page 71 of 75
CLINICAL PROCEDURES
Exophthalmometry
Measurement of eyeball protrusion (as in Graves disease) with an exophthalmometer.
Computed tomography (CT) scan
X-ray imaging of endocrine glands in cross section and other views, to assess size and
infiltration by tumor.
Magnetic resonance imaging (MRI)
Magnetic waves produce images of the hypothalamus and pituitary gland to locate
abnormalities.
Thyroid scan
Scanner detects radioactivity and visualizes the thyroid gland.
Administration of radioactivity is either intravenous (with radioactive technetium) or oral
(with radioactive iodine). The latter is called RAIU (radioactive iodine uptake scan).
Thyroid function is assessed; nodules and tumors can be evaluated. Ultrasound
examination
Sound waves show images of endocrine organs.
Thyroid ultrasound is the best method to evaluate thyroid structures and abnormalities
(nodules).
Page 72 of 75
ABBREVIATIONS
ACTH: Adrenocorticotropic hormone

ADH: Antidiuretic hormone
BMR: Basal metabolic rate
DI: Diabetes insipidus
DM: Diabetes mellitus
FBS: Fasting blood sugar
FSH: Follicle-stimulating hormone
GH: Growth hormone
GTT: Glucose tolerance test
HGH: Human growth hormone
ICSH: Interstitial cell-stimulating hormone
IDDM: Insulin-dependent diabetes mellitus
K: Potassium
LH: Luteinizing hormone
MSH: Melanocyte-stimulating hormone
Na: Sodium
NIDDM: Non-insulin-dependent diabetes mellitus
PRL: Prolactin
PTH: Parathyroid hormone
RIA: Radioimmunoassay
SIADH: Syndrome of inappropriate ADH
T3: Triiodothyronine
T4: Thyroxine
TFT: Thyroid function tests
TSH: Thyroid-stimulating hormone
Page 73 of 75
DRUGS USED IN ENDOCRINE DISORDERS
Drugs used to treat thyroid problems

Thyroid supplements
 Eltroxin (levothyroxine)
 Levothroid (levothyroxine)
 Thyrox (levothyroxine)
 Synthroid (levothyroxine)
 Levoxyl (levothyroxine)
Drugs for pituitary gland

 Genotropin (human growth hormone)
 Humatrope (human growth hormone)
 Norditropin (human growth hormone)
 Protropin (human growth hormone)
 Saizen (human growth hormone)
Drugs used to treat diabetes insipidus

 DDAVP (desmopressin acetate)
 Stimate (desmopressin acetate)
 Pitressin (vasopressin)
Drugs used to treat diabetes mellitus (IDDM)

 Humalog (insulin preparations)
 Humulin (insulin preparations)
 Lantus (insulin preparations)
 Lente (insulin preparations)
 Novolin (insulin preparations)
 NovoLog (insulin preparations)
 NPH (insulin preparations)
 Regular insulin (insulin preparations)
Drugs used to treat diabetes mellitus (NIDDM)

 Actos (pioglitazone)
 Amaryl (glimepiride)
 Avandia (rosiglitazone)
 Diabinese (chlorpropamide)
 DiaBeta (glyburide)
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 Glucophage (metformin)
 Glucotrol (glipizide)
 Glucovance (potassium gluconate)
 Micronase (glyburide)
 Prandin (repaglinide) 
 Starlix (nateglinide)
Corticosteroids
 Celestone (betamethasone)
 Decadron (dexamethasone)
 Cortef (hydrocortisone)
 Medrol (methylprednisolone)
 Pediapred (prednisolone)
 Kenacort (triamcinolone)
Anabolic steroids
 Oxandrin (oxandrolone)
Page 75 of 75

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LOM Endocrine System Notes

CHAPTER 16 -ENDOCRINE SYSTEM

The ductless, internally secreting endocrine glands are listed as follows.

ENDOCRINE TISSUE (APART FROM MAJOR GLANDS): LOCATION,

LOCATION AND STRUCTURE

LOCATION AND STRUCTURE

LOCATION AND STRUCTURE

The adrenal cortex secretes three types of corticosteroids.

1. Glucocorticoids—These steroid hormones have an important influence on the metabolism

2. Mineralocorticoids—The major mineralocorticoid is aldosterone. It regulates the

3. Sex hormones—Androgens (testosterone) and estrogens are secreted in small amounts

The adrenal medulla secretes two types of catecholamine hormones:

2. Norepinephrine (noradrenaline)—Constricts blood vessels to raise blood pressure. Both

LOCATION AND STRUCTURES

LOCATION AND STRUCTURE

The major hormones of the anterior pituitary gland are:

1. Growth hormone (GH), or somatotropin (STH)—Promotes protein synthesis that

2. Thyroid-stimulating hormone (TSH), or thyrotropin—Stimulates the growth of the

3. Adrenocorticotropic hormone (ACTH), or adrenocorticotropin—Stimulates the growth

4. Gonadotropic hormones—Several gonadotropic hormones influence the growth and

5. Prolactin (PRL)—Stimulates breast development during pregnancy and sustains milk

1. Antidiuretic hormone (ADH), also called vasopressin—Stimulates the reabsorption of

LOCATION AND STRUCTURE

LOCATION AND STRUCTURE

Testosterone is an androgen (male steroid hormone) that stimulates development of sperm

ENDOCRINE GLANDS: HORMONES AND ACTIONS

Calcitonin Lowers blood calcium

Cortisol (glucocorticoid) Increases blood sugar

Androgens, estrogens and Maintain secondary sex

Adrenals - medulla Epinephrine (adrenaline) Sympathomimetic

Pancreas – islet cells Insulin Decreases blood sugar (glucose

Glucagon Increases blood sugar

Thyroid-stimulating hormone Stimulates production of

Adrenocorticotropic hormone Stimulates secretion of

Gonadotropins; follicle- Oogenesis and spermatogenesis

Increases pigmentation of the

Adrenal cortex The outer section of each adrenal gland

Follicle-stimulating hormone Hormone produced by the anterior lobe of the

abdomen; responsible for egg production and

 A patient with autoimmune goiters may develop

 Shaking in your hands and fingers (tremor)

gland to shrink. Symptoms usually subside within

These include a rapid heart rate, a heart rhythm

 Gender - Women are much more likely to develop

hypothyroidism is an autoimmune disorder known as

problems with swallowing and breathing.

 problems with memory and attention

thyroiditis usually results in hypothyroidism, and

Hyperthyroid phase: Usually short lasting (1-3 months.) If

may become permanent. If cells are damaged and thyroid

secondary hyperparathyroidism are due to chronic

parathyroid glands or tumors on the glands.

prominent Adam's apple, and other masculine signs.

cortisol production when surgery and radiation don't

parathyroid hormone (hypoparathyroidism)

glands produce two to three times the usual amount of

multiple sites, including the central nervous system,

prescribe specific blood pressure medications that