Introduction

Hyperthyroidism is the term for

overactive tissue within the thyroid gland causing
an overproduction of thyroid hormones (thyroxine
or "T4" and/or triiodothyronine or "T3").
Hyperthyroidism is thus a cause of thyrotoxicosis,
the clinical condition of increased thyroid
hormones in the blood. It is important to note that
hyperthyroidism and thyrotoxicosis are not
synonymous. Hyperthyroidism is a hypersecretion
of thyroid hormones from the thyroid gland.
Elevated levels of thyroid hormones increase
basal metabolic rate while, thyrotoxicosis is a
hypermetabolic syndrome caused by excess thyroid hormones which may come
from endogenous or exogenous sources. The endogenous source of hormone may
be thyroid hyperplasia; thyroid neoplasm; or hormone-producing extrathyroidal
tissue. Thyrotoxicosis is characterized by nervousness; tachycardia; fatigue; weight
loss; heat intolerance; and excessive sweating.
Thyroid hormone functions as a controller of the pace of all of the processes
in the body. This pace is called metabolism. If there is too much thyroid hormone,
every function of the body tends to speed up. Hyperthyroidism is suggested by
several signs and symptoms; however, patients with mild disease usually
experience no symptoms. In patients older than 70 years, the typical signs and
symptoms also may be absent. In general, the symptoms become more obvious as
the degree of hyperthyroidism increases. The symptoms usually are related to an
increase in the metabolic rate of the body.
Common symptoms include:
• Excessive sweating
• Heat intolerance
• Increased bowel movements
• Tremor (usually fine shaking)
• Nervousness; agitation
• Rapid heart rate
• Weight loss
• Fatigue
• Decreased concentration
• Irregular and scant menstrual flow
In older patients, irregular heart rhythms and heart failure can occur. In its
most severe form, untreated hyperthyroidism may result in "thyroid storm," a
condition involving high blood pressure, fever, and heart failure. Mental changes,
such as confusion and delirium, also may occur.

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Calcitonin: A hormone produced by the thyroid gland that lowers the levels of
calcium and phosphate in the blood and promotes the formation of bone.
Bone is in a constant state of remodeling whereby old bone is removed by cells
called osteoclast and new bone is laid down by cells called osteoblasts. Calcitonin
inhibits bone removal by the osteoclasts and at the same time promotes bone
formation by the osteoblasts.
Calcitonin is given in hypercalcemia (high blood calcium) to lower the calcium level;
inosteoporosis to increases bone density and decrease the risk of a fracture; and in
Paget disease to decrease bone turnover and bone pain.
Calcitonin is also called thyrocalcitonin.
Some common causes of hyperthyroidism include:
• Graves' Disease
• Functioning adenoma ("hot nodule") and toxic multinodular goiter (TMNG)
• Excessive intake of thyroid hormones
• Abnormal secretion of TSH
• Thyroiditis (inflammation of the thyroid gland)
• Excessive iodine intake

Graves‘ Disease
Graves' disease, which is caused by a generalized overactivity of the thyroid
gland, is the most common cause of hyperthyroidism. In this condition, the thyroid
gland usually is renegade, which means it has lost the ability to respond to the
normal control by the pituitary gland via TSH. Graves' disease is hereditary and is
up to five times more common among women than men. Graves' disease is thought
to be an autoimmune disease, and antibodies that are characteristic of the illness
may be found in the blood. These antibodies include thyroid stimulating
immunoglobulin (TSI antibodies), thyroid peroxidase antibodies (TPO), and TSH
receptor antibodies. The triggers for Grave's disease include:
• stress,
• smoking,
• radiation to the neck,
• medications, and
• infectious organisms such as viruses.
Graves' disease can be diagnosed by a standard, nuclear medicine thyroid
scan which shows diffusely increased uptake of a radioactively-labeled iodine. In
addition, a blood test may reveal elevated TSI levels.
Grave's disease may be
associated with eye disease (Graves'
ophthalmopathy) and skin lesions
(dermopathy). Ophthalmopathy can occur
before, after, or at the same time as the
hyperthyroidism. Early on, it may cause

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sensitivity to light and a feeling of "sand in the eyes." The eyes may protrude and
double vision can occur. The degree of ophthalmopathy is worsened in those who
smoke. The course of the eye disease is often independent of the thyroid disease,
and steroid therapy may be necessary to control the inflammation that causes the
ophthalmopathy. In addition, surgical intervention may be required. The skin lesions
rare and causes a painless, red, lumpy skin rash that appears on the front of the
legs.
Functioning adenoma ("hot nodule") and toxic
multinodular goiter (TMNG)
The thyroid gland becomes lumpier as we
get older. In the majority of cases, these lumps do
not produce thyroid hormones and require no
treatment. Occasionally, a nodule may become
"autonomous," which means that it does not
respond to pituitary regulation via TSH and
produces thyroid hormones independently. This
becomes more likely if the nodule is larger that 3 cm. When there is a single nodule
that is independently producing thyroid hormones, it is called a functioning nodule.
If there is more than one functioning nodule, the term toxic, multinodular goiter is
used. Functioning nodules may be readily detected with a thyroid scan.

Excessive intake of thyroid hormones

Taking too much thyroid hormone medication is actually quite common.
Excessive doses of thyroid hormones frequently go undetected due to the lack of
follow-up of patients taking their thyroid medicine. Other persons may be abusing
the drug in an attempt to achieve other goals such as weight loss. These patients
can be identified by having a low uptake of radioactively-labelled iodine
(radioiodine) on a thyroid scan.
Abnormal secretion of TSH
A tumor in the pituitary gland may produce an abnormally high secretion of
TSH (the thyroid stimulating hormone). This leads to excessive signaling to the
thyroid gland to produce thyroid hormones. This condition is very rare and can be
associated with other abnormalities of the pituitary gland. To identify this disorder,
an endocrinologist performs elaborate tests to assess the release of TSH.
Thyroiditis (inflammation of the thyroid)
Inflammation of the thyroid gland may occur after a viral illness (subacute
thyroiditis). This condition is association with a fever and a sore throat that is often
painful on swallowing. The thyroid gland is also tender to touch. There may be
generalized neck aches and pains. Inflammation of the gland with an accumulation
of white blood cells known as lymphocytes (lymphocytic thyroiditis) may also occur.
In both of these conditions, the inflammation leaves the thyroid gland "leaky," so

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that the amount of thyroid hormone entering the blood is increased. Lymphocytic
thyroiditis is most common after a pregnancy and can actually occur in up to 8% of
women after delivery. In these cases, the hyperthyroid phase can last from 4 to 12
weeks and is often followed by a hypothyroid (low thyroid output) phase that can
last for up to 6 months. The majority of affected women return to a state of normal
thyroid function. Thyroiditis can be diagnosed by a thyroid scan.
Excessive iodine intake
The thyroid gland uses iodine to make thyroid hormones. An excess of iodine
may cause hyperthyroidism. Iodine-induced hyperthyroidism is usually seen in
patients who already have an underlying abnormal thyroid gland. Certain
medications, such as amiodarone (Cordarone), which is used in the treatment of
heart problems, contain a large amount of iodine and may be associated with
thyroid function abnormalities.
On the other hand, a lack of functioning thyroid tissue results in a symptomatic lack
of thyroid hormone, termed hypothyroidism. Hyperthyroidism often eventually leads
to hypothyroidism.
Hypothyroidism is a condition
characterized by abnormally low thyroid
hormone production. There are many disorders
that result in hypothyroidism. These disorders
may directly or indirectly involve the thyroid
gland. Because thyroid hormone affects growth,
development, and many cellular processes, inadequate thyroid hormone has
widespread consequences for the body.
There can be many reasons why the cells in the thyroid gland can’t make
enough thyroid hormone. Here are the major causes, from the most to the least
common.

■ Autoimmune disease. In some people’s

bodies, the immune system that protects
the body from invading infections can
mistake thyroid gland cells and their
enzymes for invaders and can attack them.
Then there aren’t enough thyroid cells and
enzymes left to make enough thyroid
hormone. This is more common in women than men. Autoimmune thyroiditis
can begin suddenly or it can develop slowly over years. The most common
forms are Hashimoto’s thyroiditis and atrophic thyroiditis.

■ Surgical removal of part or all of the thyroid gland. Some people with thyroid
nodules, thyroid cancer, or Graves’ disease need to have part or all of their thyroid

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removed. If the whole thyroid is removed, people will definitely become
hypothyroid. If part of the gland is left, it may be able to make enough thyroid
hormone to keep blood levels normal.

■ Radiation treatment. Some people with Graves’ disease, nodular goiter, or thyroid
cancer are treated with radioactive iodine (I-131) for the purpose of destroying their
thyroid gland. Patients with Hodgkin’s disease, lymphoma, or cancers of the head or
neck are treated with radiation. All these patients can lose part or all of their thyroid
function.

■ Congenital hypothyroidism (hypothyroidism that a baby is born with). A few

babies are born without a thyroid or with only a partly formed one. A few have part
or all of their thyroid in the wrong place (ectopic thyroid). In some babies, the
thyroid cells or their enzymes don’t work right.

■ Thyroiditis. Thyroiditis is an inflammation of the thyroid gland, usually caused by

an autoimmune attack or by a viral infection. Thyroiditis can make the thyroid dump
its whole supply of stored thyroid hormone into the blood at once, causing brief
hyperthyroidism (too much thyroid activity); then the thyroid becomes underactive.

■ Medicines. Medicines such as amiodarone, lithium, interferon alpha, and

interleukin-2 can prevent the thyroid gland from being able to make hormone
normally. These drugs are most likely to trigger hypothyroidism in patients who
have a genetic tendency to autoimmune thyroid disease.

■ Too much or too little iodine. The thyroid gland must have iodine to make thyroid
hormone. Iodine comes into the body in food and travels through the blood to the
thyroid. Keeping thyroid hormone production in balance requires the right amount
of iodine. Taking in too much iodine can cause or worsen hypothyroidism.

■ Damage to the pituitary gland. The pituitary, the “master gland,” tells the thyroid
how much hormone to make. When the pituitary is damaged by a tumor, radiation,
or surgery, it may no longer be able to give the thyroid instructions, and the thyroid
may stop making enough hormone.

■ Rare disorders that infiltrate the thyroid. In a few people, diseases deposit
abnormal substances in the thyroid and impair its ability to function. For example,
amyloidosis can deposit amyloid protein, sarcoidosis can deposit granulomas, and
hemochromatosis can deposit iron.
Common symptoms are listed below:
• Abnormal menstrual cycles

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 • Coarse, dry hair
• Cold intolerance (you can't tolerate cold temperatures like those around you)
• Constipation
• Decreased libido
• Depression
• Dry, rough pale skin
• Excessive sleepiness
• Fatigue
• Hair loss
• Increased cholesterol levels
• Irritability
• Memory loss
• Modest Weight gain or increased difficulty losing weight
• Muscle cramps and frequent muscle aches
• Weakness

Each individual patient may have any number of

these symptoms, and they will vary with the
severity of the thyroid hormone deficiency and the
length of time the body has been deprived of the
proper amount of hormone.
You may have one of these symptoms as your main
complaint, while another will not have that problem
at all and will be suffering from an entirely different symptom. Most people will have
a combination of these symptoms. Occasionally, some patients with hypothyroidism
have no symptoms at all, or they are just so subtle that they go unnoticed.
As the disease becomes more severe, there may be puffiness around the
eyes, a slowing of the heart rate, a drop in body temperature, and heart failure. In
its most profound form, severe hypothyroidism may lead to a life-threatening coma
(myxedema coma). In a severely hypothyroid individual, a myxedema coma tends
to be triggered by severe illness, surgery, stress, or traumatic injury. This condition
requires hospitalization and immediate treatment with thyroid hormones given by
injection.
Properly diagnosed, hypothyroidism can be easily and completely treated
with thyroid hormone replacement. On the other hand, untreated hypothyroidism
can lead to an enlarged heart (cardiomyopathy), worsening heart failure, and an
accumulation of fluid around the lungs (pleural effusion).
Cretinism refers to congenital hypothyroidism, which affects 1 per 4000 newborns.

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 Hypoparathyroidism is a condition in
which your body secretes abnormally low levels
of parathyroid hormone (parathormone). This
hormone plays a key role in regulating and
maintaining a balance of your body's levels of
two minerals — calcium and phosphorus. The
low production of parathyroid hormone in
hypoparathyroidism leads to abnormally low
calcium levels in your blood and bones and to an
increased amount of phosphorus.
The parathyroid glands help control calcium use and removal by the body. They do
this by producing parathyroid hormone, or PTH. PTH helps control calcium,
phosphorus, and vitamin D levels within the blood and bone.
There are a number of causes of hypoparathyroidism:
• Underdeveloped or missing parathyroid glands at birth
• Medical treatment (radiation to thyroid gland, drug treatment, thyroid or
parathyroid surgery)
• An underlying medical condition such as cancer, neck trauma, Wilson's
disease, too much iron in tissues, low levels of magnesium
The most common cause of hypoparathyroidism is iatrogenic
hypoparathyroidism which is caused by the removal of all parathyroid tissue
during total parathyroidectomy or by deliberate surgical removal of the
parathyroid glands.
Idiopathic hypothyroidism can occur spontaneously. The exact cause is
unknown, but an autoimmune basis is suspected in many clients.
Hypoparathyroidism may occur with other autoimmune disorders such as
adrenal insufficiency, hypothyroidism diabetes mellitus, pernicious anaemia, and
vitiligo.
Hypomagnesaemia (decreased serum magnesium levels) may also cause
hypoparathyroidism. Hypomagnesaemia is seen in alcoholics and in clients with
malabsorption syndromes, chronic renal disease, and malnutrition. It causes
impairment of PTH secretion and may interfere with the effects of PTH on the
bones and kidneys.
Symptoms of hypoparathyroidism may include:
• Tingling in the lips, fingers, and toes
• Dry hair, brittle nails, and dry, coarse skin
• Muscle cramps and pain in the face, hands, legs, and feet
• Cataracts on the eyes
• Malformations of the teeth, including weakened tooth enamel and misshapen
roots of the teeth
• Loss of memory

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 • Headaches
• Severe muscle spasms (also called tetany) and convulsions

Treatment of hypoparathyroidism is to restore the calcium and phosphorus to

normal levels in the body.
If hypoparathyroidism is left untreated, complications can include a blocked
airway due to severe muscle spasms, stunted growth, malformed teeth,
development of cataracts, and calcium deposits in the brain.

Definition of Terms

1. Apathy – want of feeling, emotion or concern; indifference, insensibility. Seen

in patients with depression dementia, schizophrenia and certain organic
disorders – apathetic, apathetic.
2. Atrial Fibrilation – a heart rhythm disorder (arrhythmia). It usually involves a
rapid heart rate that is not regular.
3. Carpopedal Spasm – spasm of the hand or foot, or of the thumbs and great
toes, seen in tetany.
4. Cheilosis – fissuring and scaling of the lips, especially at the angles of the
mouth, usually resulting from riboflavin deficiency.
5. Chvostek’s sign – an indication of tetany in which a unilateral spasm of the
oris muscle is initiated by a slight tap over the facial nerve anterior to the
external auditory canal.
6. Cold intolerance – an abnormal sensitivity to a cold environment or cold
temperatures.
7. Delirium – a state of frenzy or uncontrollable excitement, characterized by
disorientation, mental confusion, impulsive behavior, incoherent speech;
often accompanied by delusions and hallucinations.

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8. Dementia – an organic mental disorder severe enough to prevent normal
social and occupational functioning; deterioration of one’s memory, judgment
and personality.
9. Digeorge syndrome – A genetic disorder characterized by hypocalcemia (due
to hypoplasia of the parathyroid glands that are needed to control calcium),
immunodeficiency (due to hypoplasia of the thymus) and congenital heart
disease.
10.Dysphagia – painful or difficulty swallowing.
11.Dysrhythmias – disorder or abnormal rhythm.
12.Emotional Lability - a condition of excessive emotional reactions and frequent
mood changes.
13.Exophthalmos – abnormal protrusion of the eyeballs.
14.Goiter – a noncancerous enlargement of the thyroid gland, visible as a
swelling at the front of the neck, that is often associated with iodine
deficiency.
15.Hashimoto’s Thyroiditis – a progressive disease of the thyroid gland
characterized by the presence of antibodies directed against the thyroid, and
by infiltration of the thyroid gland by lymphocytes.
16.Heat intolerance - the inability to be comfortable when external temperatures
rise.
17.HcG – Human chorionic gonadotropin, a human hormone made by chorionic
cells in the fetal part of the placenta. Human chorionic gonadotropin (hCG) is
directed at the gonads and stimulates them. Hence, the name
"gonadotropin."
18.HLA – the major human histocompatibility system. HLA-typing is done before
transplantation to determine the degree of histocompatibility. HLA is an
acronym for Human Leukocyte Antigens.
19.Hyperthyroidism – a condition in which the thyroid gland makes too much
thyroid hormone.
20.Hypoparathyroidism – Underfunction of the parathyroid glands with deficient
production of the hormone parathormone which leads to low blood calcium
(hypocalcemia). The parathyroid glands are located adjacent to the thyroid
gland. They may be missing due to a birth defect, impaired
by autoimmune disease, or surgically removed during thyroid surgery.
Treatment is with oral calcium supplements and oral vitamin D. Oral vitamin
D increases the gut absorption of calcium in the diet and helps to maintain
normal blood calcium levels.
21.Hypothyroidism – or underactive thyroid, develops when the thyroid gland
fails to produce or secrete as much thyroxine (T4) as the body needs.
Because T4 regulates such essential functions as heart rate, digestion,
physical growth, and mental development, an insufficient supply of this

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 hormone can slow life-sustaining processes, damage organs and tissues in
every part of the body, and lead to life-threatening complications.
22.Impetigo Herpetiformis – a very rare, acute dermatitis with symmetrically
ringed, pustular lesions, occurring chiefly in pregnant women and associated
with severe constitutional symptoms.
23.Jod-Basedow Effect – hyperthyroidism following administration of iodine or
iodide, either as a dietary supplement or as contrast medium. This
phenomenon is an iodine-induced hyperthyroidism, typically presenting in a
patient with endemic goiter that then relocates to an iodine-abundant
geographical area. It is named for Karl Adolph von Basedow, a German
physician and the German word for iodine, "jod."
24.Myxedema – a disease caused by decreased activity of the thyroid gland in
adults and characterized by dry skin, swellings around the lips and nose,
mental deterioration, and a subnormal basal metabolic rate.
25.Paranoia – an unfounded or exaggerated distrust of others, sometimes
reaching delusional proportions. Paranoid individuals constantly suspect the
motives of those around them, and believe that certain individuals, or people
in general, are "out to get them."
26.Polydipsia – chronic excessive thirst and fluid intake.
27.Psychosis – in the general sense, a mental illness that markedly interferes
with a person's capacity to meet life's everyday demands. In a specific sense,
it refers to a thought disorder in which reality testing is grossly impaired.
28.Riboflavin – an orange-yellow crystalline compound that is the principal
growth-promoting factor in the vitamin B complex, naturally occurring in milk,
leafy vegetables, fresh meat, and egg yolks.
29.Sheehan Syndrome – a condition affecting women who experience life-
threatening blood loss during or after childbirth. Severe blood loss deprives
your body of oxygen and can seriously damage vital tissues and organs. In
Sheehan's syndrome, the damage occurs to the pituitary gland — a small
gland at the base of your brain. The result is the permanent underproduction
of essential pituitary hormones (hypopituitarism).
30.Thyroxine – a chemical substance made by the thyroid gland The thyroid
gland uses iodine to make thyroid hormones. Thyroxine (T4), one of the most
important thyroid hormones, has four iodine molecules attached to its
molecular structure.
31.Triiodothyronine – a hormone made by the thyroid gland. It has three iodine
molecules attached to its molecular structure. It is the most powerful thyroid
hormone, and affects almost every process in the body, including body
temperature, growth, and heart rate.
32.Trousseau sign – a spasm in the muscles in the forearm when a tourniquet is
applied to the upper arm, which causes the index and middle fingers to

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 extend. It is a sign of latent tetany, showing that the blood contains too little
calcium.

Human Anatomy & Physiology

AUTONOMIC NERVOUS SYSTEM
The autonomic nervous system (ANS) is actually art of the peripheral
nervous system in that it consists of motor portions of some cranial and spinal
nerves. Because its functioning is so specialized, however, the autonomic nervous
system is usually discussed as a separate entity, as we will do here. Making up the

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autonomic nervous system are visceral motor neurons to smooth muscle, cardiac
muscle, and glands. These are the visceral effectors; muscle will either contract
or relax, and glands will either increase or decrease their secretions. The ANS has
two divisions: sympathetic and parasympathetic. Often, they function in
opposition to each other, as you will see. The activity of both divisions is integrated
by the hypothalamus, which ensures that the visceral effectors will respond
appropriately to the situation.

AUTONOMIC PATHWAYS
An autonomic nerve pathway from the central nervoussystem to a visceral
effector consists of two motor neurons that synapse in a ganglion outside the CNS.
The first neuron is called the preganglionic neuron, from the CNS to the ganglion.
The second neuron is called the postganglionic neuron, from the ganglion to the
visceral effector. The ganglia are actually the cell bodies of the postganglionic
neurons.

SYMPATHETIC DIVISION
Another name for the sympathetic division is thoracolumbar division, which
tells us where the sympathetic preganglionic neurons originate. Their cell bodies are
in the thoracic segments and some of the lumbar segments of the spinal cord. Their
axons extend to the sympathetic ganglia, most of which are located in two chains
just outside the spinal column. Within the ganglia are the synapses between
preganglionic and postganglionic neurons; the postganglionic axons then go to the
visceral effectors. One preganglionic neuron often synapses with many
postganglionic neurons to many effectors. This anatomic arrangement has
physiological importance: The sympathetic division brings about widespread
responses in many organs.
The sympathetic division is dominant in stressful situations, which include
anger, fear, or anxiety, as well as exercise. For our prehistoric ancestors, stressful
situations often involved the need for intense physical activity—the “fight or flight
response.” Our nervous systems haven’t changed very much in 50,000 years, and if
you look at Table 8–5, you will see the kinds of responses the sympathetic division
stimulates. The heart rate increases, vasodilation in skeletal muscles supplies them
with more oxygen, the bronchioles dilate to take in more air, and the liver changes
glycogen to glucose to supply energy. At the same time digestive secretions
decrease and peristalsis slows; these are not important in a stress situation.
Vasoconstriction in the skin and viscera shunts blood to more vital organs such as
the heart, muscles, and stay and fight or to get away from potential danger. Even
though we may not always be in life-threatening situations during stress (such as
figuring out our income taxes), our bodies are prepared for just that.

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ENDOCRINE SYSTEM
The endocrine system is made up of glands in many tissues and organs in a
variety of body areas, a key feature of all endocrine glands in the secretion of
hormones, Hormones are natural chemical that exert their effect on specific tissue
known as target tissues. Target tissues are usually located some distance from the
endocrine gland, with no direct physical connection between the endocrine gland
and its target tissue. For this reason the endocrine gland is called “ductless”
glands and must use the
blood to transport
secreted hormones to the
target tissues. Endocrine
glands include the
following:
•
Hypothalamus
• Pituitary
glalnds
Anterior pituitary
Posterior pituitary
• Adrenal glands
• Thyroid glands
• Islet cells of the
pancreas
• Parathyroid glands
• Gonads
Ovary
Testes

The control of cellular function by any hormone depends on a series of

reactions working through negative feedback control mechanism. The hormone
secretion is dependent on the need of the body for the final action of that hormone.
When a body starts to move away from normal range and specific action or

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response is needed to correct this change, secretion of the hormone capable of
causing the correcting action or response is stimulated until the need (demand) is
met. As the correction occurs, hormone secretion decreases (and may halt). This
type of control for hormone synthesis is “negative feedback” because the hormone
causes the opposite action of the initial condition change.
Some hormones that use negative feedback mechanism have more complex
interactions. These interactions involve a series of reaction in which more than one
endocrine gland, as well as the final target tissues, is stimulated. In such situation,
the first hormone in the series may have another endocrine gland as its target
tissue, for this type of mechanism to maintain homeostasis.

HYPOTHALAMUS AND PITUITARY GLANDS

Structure:

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 The hypothalamus is a small area of nerve and glandular tissue located
beneath the thalamus on each side of the third ventricle in the brain. Nerve fibers
connect the hypothalamus to the rest of the central nervous system. The
hypothalamus shares a small, closed circulatory system with the anterior pituitary
gland. This system is known as the hypothalamic –hypophysial portal system and it
allows hormone produced in the hypothalamus to travel directly to the anterior
pituitary gland.
The pituitary gland is located at the base of the brain in a valley of the
sphenoid bone called the sella turcica. The oval pituitary gland is about 1 cm in
diameter and is divided into two lobes. The anterior lobe, or adenohyphosis, makes
up about 70% of the gland. The posterior lobe, or neurohyphosis, stores hormones
produced in the hypothalamus. Nerve fibers in the hypophysial stalk, a structure
extending from the hypothalamus, connect the hypothalamus to the posterior
pituitary.

Function:
The hypothalamus has both endocrine and nonendocrine functions. The
endocrine function is to produce regulatory hormones some of these hormones are
released into the blood and travel to the anterior pituitary, where they either
stimulate or inhibit the release of anterior pituitary hormones.
In response to the releasing hormones of the hypothalamus, the anterior
pituitary secretes tropic hormones, which stimulate other endocrine glands. The
hormones of the posterior pituitary vasopressin (anti-diuretic hormone) oxytocin,
are produce in the hypothalamus and sent through the nerve tracts that connect
the hypothalamus with the posterior pituitary. These hormones are stored in the
nerve endings of the posterior pituitary and are released into blood when needed.

ANTERIOR PITUITARY GLANDS

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POSTERIOR PITUITARY GLANDS

THYROID GLAND

16
Structure:
The thyroid gland is in the anterior neck, directly below the cricoids cartilage.
It has two lobes joined by a thin strip of tissue (isthmus) in front of the trachea.
The thyroid gland has a rich blood supply, and the right lobe is slightly larger
than the left lobe. It is composed of follicular and parafollicular cells. Follicular cells
produce the thyroid hormones thyroxine (T4) and triiodothyroxine (T3).
Parafollicular cells produce and secrete thyrocalcitonin (calcitonin), which helps to
regulate serum calcium levels.
The thyroid is stimulated by the pituitary hormone TSH to produce two
hormones, thyroxine (T4) and triiodothyronine (T3) in the presence of iodide.
Hormone production proceeds by six steps:
1. Dietary iodine is transported from the capillary through the epithelial cell into
the lumen.
2. Iodine is oxidized to iodide by the thyroid peroxidase enzyme (TPO) and is
bound to tyrosine residues on the thyroglobulin molecule to yield
monoiodotyrosine (MIT) and diiodotyrosine (DIT).
3. TPO further catalyzes the coupling of MIT and DIT moieties to form T4
and/or T3.
4. The thyroglobulin molecules carrying the hormones are taken into the
epithelial cells via endocytosis in the form of colloid drops.
5. Proteolysis of the iodinated hormones from thyroglobulin takes place via
protease/peptidase action in lysosomes and the hormones are released to the
capillaries.
6. Any remaining uncoupled MIT or DIT is deiodinated to regenerate iodide and
tyrosine residues.

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Function:
• CONTROL OF METABOLISM
Both T3 and T4 increase metabolism, which causes an increase in oxygen use
and heat production in all tissues. The two hormones differ in structure, but their
functions are the same. Most circulating T4 and T3 in bound to plasma proteins. The
portion of bound hormone is in balance with the free hormone. The free hormone
moves into the cell, where it binds to its receptor in the cell nucleus. Once in the
cell, T4 is converted to T3impaired by stress, starvation, dyes, bête blockers,
amiodarone, corticosteroid, and propylthiouracil. Cold temperatures increase the
conversion.
The secretion of the thyroid hormones T3 and T4 is controlled by the
hypothalamic-pituitary-thyroid gland axis, or feedbeck mechanism, the
hypothalamus secretes thyrotropin releasing hormone (TRH). TRH triggers the
anterior pituitary gland to secrete thyroid-stimulating hormone (TSH), which the n
stimulates the thyroid gland to make and release thyroid hormones. If thyroid
hormone level is high, TSH released is inhibited; if low, TSH release is increased.
This is an example of negative feedback mechanism system. Cold and stress are
two factors that cause the hypothalamus to secrete TRH, which then stimulates the
anterior pituitary to secrete TSH.
Thyroid hormone production involves a series of steps. Dietary inta1ke of
protein and iodine is needed to produce thyroid hormones. Iodine is absorbed from
the intestinal tract as iodide. The thyroid gland withdraws iodide from the blood and
concentrates it. After iodide is in the thyroid, it enters into a series of reactions to
form T4 and T3. These hormones bind to thyroglobulin and are stored in the
follicular cells of the thyroid gland. With stimulation, T4 and T3 break off from
thyroglobulin and are released into the blood. They may enter the cells to bind to
the nucleus, and turn on genes important inmetabolism. Thus the presence of T4
and T3 directly regulate basal metabolic rate (BMR).

• CALIUM AND PHOSPHORUS BALANCE

Calcitonin (also called thyrocalcitonin, or TCT) is another hormone produced
in the thyroid gland. Calcitonin lowers serum calcium serum calcium and serum
phosphorous levels by reducing bone desorption (breakdown). It works in opposition
to parathyroid hormone (PTH).

18
 The serum calcium level determines calcitonin secretion. Low serum calcium
levels suppress the release of calcitonin; elevate serum calcium levels increase its
secretion. Other factors that increase calcitonin release are pregnancy, a high
calcium diet, and an increase secretion of gastrin.

PARATHYROID GLAND
Structure:
The parathyroid glands consist of four small glands located close to,
embedded in, or attached to the back surface of the thyroid gland. The chief cells of
the parathyroid glands produce and secrete PTH.
Parathyroid hormone (PTH) is an antagonist to calcitonin and is important
for the maintenance of normal blood levels of calcium and phosphate. The target
organs of PTH are the bones, small intestine, and kidneys.
PTH increases the reabsorption of calcium and phosphate from bones to the
blood, thereby raising their blood levels. Absorption of calcium and phosphate from
food in the small intestine, which also requires vitamin D, is increased by PTH. This
too raises the blood levels of these minerals. In the kidneys, PTH stimulates the
activation of vitamin D and increases the reabsorption of calcium and the excretion
of phosphate (more than is obtained from bones). Therefore, the overall effect of
PTH is to raise the blood calcium level and lower the blood phosphate level.
Secretion of PTH is stimulated by hypocalcemia, a low blood calcium level,
and inhibited by hypercalcemia. Together, these hormones maintain blood calcium
within a normal range. Calcium in the blood is essential for the process of blood
clotting and for normal activity of neurons and muscle cells.
As you might expect, a sustained hypersecretion of PTH, such as is caused by
a parathyroid tumor, would remove calcium from bones and weaken them. It has
been found, however, that an intermittent, brief excess of PTH, such as can occur
by injection, will stimulate the formation of more bone matrix, rather than matrix
reabsorption. This may seem very strange—the opposite of what we would expect—
but it shows how much we have yet to learn about the body. PTH is being
investigated as a possible way to help prevent osteoporosis.

19
 HYPERTHYROIDISM
General Appearance: Irritable, profuse sweating, flushed skin with salmon color, nervous, enlarged thyroid gland, protruding eyes, weight loss.

Subjective
System Objective (Patient may Problem Identified Nursing Diagnosis
verbalize)
Head:
• Head is normocephalic and
symmetrical
“nangalagas akong
Head/Hair/Face Hair: Hair loss Disturbed Body Image
buhok”
• Hair loss
Face:
• Symmetrical facial features
Eyes:
• Abnormal eye
appearance/function
(ophthalmopathy)
• Wide eyed/startled look Risk for Injury
Exophthalmia
(exophthalmos) “dili man sakit akong Staring gaze
Eyes/Ears/Nose Ears: Risk for Infection
mata”
• Symmetrical Blurred vision
Disturbed Body Image
• No discharges noted
Nose:
• Symmetrically aligned
• No discharges noted
• Enlarged thyroid gland
Neck “nagdako akong li-og” Enlarged thyroid gland Disturbed Body Image
(goiter)
• Shortness of breath with or
without exertion
“ galisod ko og
Mouth/Thorax/Lungs • Rapid, shallow respirations Shortness of breath Ineffective Breathing Pattern
ginhawa”
• ed vital capacity
• Tachypnea
“wala man nagsakit
Back • No deformities noted No problem identified
akong likod”
Breast and axilla • No discharges “wala may sakit akong No problem identified

19
 • No lumps or swelling
totoy"
• No nodules
• Palpitations
• Chest pain
• Atrial fibrilation Acute pain
Cardiovascular/Peripheral
• Tachycardia “sakit akong dughan” Acute Pain
Vascular
• Dysrhythmias Hypertension
• Arrhythmia
• Hypertension
• Weight loss Imbalanced Nutrition: Less then
• Voracious Appetite “gana man ko Body Requirements
Imbalance nutrition
mukaon”
GIT • Increased bowel sound
Diarrhea
• Polydipsia Diarrhea
“uhaw permi”
• ↑ed BM Risk for Deficient Fluid Volume
• Polyuria
• ed libido
Male “hinay na akong dugo Increased Urine Output Risk for Deficient Fluid Volume
GUT/Reproductive • Impotence pero dili man pud ko
Female magdismenorya” Increased libido Sexual Dysfunction
• Amenorrhea
• ed menstrual flow
• Muscle weakness especially Fatigue
in the upper arms and Fatigue
Musculoskeletal thighs “kapoy akong lawas” Impaired Physical Mobility
• Tremor of the fingertips Muscle weakness/Tremor
• Fatigue Risk for Injury
“nangalagas akong Disturbed Body Image
• Excessive sweating buhok” Hair loss
(diaphoresis) Hyperthermia
• Smooth, warm, moist skin “sige lang pud ko Altered body temperature
Integumentary/ Metabolic • Thinning of scalp hair sington” Ineffective Thermoregulation
• Heat intolerance Heat Intolerance
• Low grade fever “dali rako sington Risk for Deficient Fluid Volume
• ↑ed basal metabolic rate maski ang uban Diaphoresis
gitugnaw” Risk for impaired skin integrity
Neurologic • Blurred or double vision “blurred akong panan- Inability to sleep well Disturbed Sleep Pattern
aw”

20
 • Eye fatigue
• Photophobia
• Eyelid retraction, eyelid lag Fatigue
• Hyperactive deep tendon
reflexes Anxiety Fatigue
“dili ko katulog og
• Insomnia
tarong or dili ko
• Irritable Tremors Anxiety
katulog”
• Mood swings
• Manic behaviour Mood swing Risk for Injury
• Agitated
• Anxiety Insomnia
• Emotional lability
• Restlessness
• Enlarged thyroid gland
Endocrine “nagdako akong li-og” Enlarged thyroid gland Disturbed Body Image
• Thyroid bruit

21
 HYPOTHYROIDISM
General Appearance: thickened tongue, periorbital edema, dry skin, enlarged thyroid gland.

Subjective
System Objective (Patient may Problem Identified Nursing Diagnosis
verbalize)
Head:
• Head is normocephalic and
symmetrical
“nanghupong man
Head/Hair/Face Hair: Edema Excess Fluid Volume
akong nawong”
• Evenly distributed hair
Face:
• Facial puffiness
Eyes:
• Periorbital Edema
Ears: “dili man sakit akong
• Symmetrical mata” Excess Fluid Volume
Edema
Eyes/Ears/Nose • No discharges noted
“unsa day? Dili ko Disturbed Sensory Perception
• Loss of hearing Loss of hearing
kaklaro sa imong (Auditory)
Nose:
gisulti”
• Symmetrically aligned
• No discharges noted
• Enlarged thyroid gland
Neck “nagdako akong li-og” Enlarged thyroid gland Disturbed Body Image
(goiter)
• Cheilosis
Shortness of breath
• Hypoventilation Ineffective Breathing Pattern
Mouth/Thorax/Lungs • Pleural effusion “galisod ko ginhawa”
Scaling of skin (angles of
• Dyspnea Risk for Impaired Skin Integrity
mouth)
• Hoarseness
“wala man nagsakit
Back • No deformities noted No problem identified
akong liko”
• No discharges
“wala may sakit akong
Breast and axilla • No lumps or swelling No problem identified
totoy"
• No nodules
Cardiovascular/Peripheral • Bradycardia “dali rako kapoyan” Bradycardia Activity Intolerance
Vascular • Dysrhythmias

22
 • Enlarged heart
• ed activity tolerance
• Hypertension
• Anorexia
• Indigestion
GIT • Weight gain
• Constipation
• Abdominal distention
• ed libido
• Impotence
• ed urine output
GUT/Reproductive Female
• Anovulation
• Changes in menses
(amenorrhea or prolonged
menstrual periods)
• Muscle aches and pains
• Delayed contraction &
Musculoskeletal relaxation of muscles
• Non-pitting edema
(hands)
• Cool, pale or yellowish, dry,
coarse, scaly skin
• Thick, brittle nails
Integumentary/ Metabolic • Dry, coarse, brittle hair
• Poor wound healing
• Skin thickness (Myxedema)
• Cold intolerance
Neurologic • Slowing of intellectual
functions (slowness or
slurring of speech, impaired
memory, inattentiveness)
• Lethargy or somnolence
• Confusion
• Hearing loss
• Numbness & tingling of the
extremities (paresthesia)
Dyrhythmias Risk for Decreased Cardiac
Output
Imbalance nutrition
“maglisod ko og Risk for Imbalance Nutrition:
libang” More than Body Requirements
Constipation
Constipation
“hinay na akong dugo
pero dili man pud ko Increased libido Sexual Dysfunction
magdismenorya”
Acute Pain
“nanghupong man ko” Muscle weakness/Tremor
Activity Intolerance
“sakit akong muscles” Edema
Excess Fluid Volume
“gauga lang akong Dry skin Risk for Impaired Skin Integrity
panit sauna dili man”
Poor wound healing Risk for Infection
“dugay maau akong
samad na” Decreased hair growth Disturbed Body Image
“unsa day? Dili ko Loss of hearing Disturbed Sensory Perception
kaklaro sa imong (Auditory)
gisulti” Confusion
Disturbed Thought Process
23
 • ed tendon reflexes
• Apathy
• Depression
• Paranoia
• Withdrawal
• Dementia
• Irritable
• Excessive sleepiness
Infant
• Mental retardation
• ↑ed sensitivity to opiods &
tranquilizers
Endocrine • enlarged thyroid gland “nagdako akong li-og” Enlarged thyroid gland Disturbed Body image

24
 HYPOPARATHYROIDISM
General Appearance: Irritable, depressed, muscle twitching in some areas, muscle cramps, tremor, photophobia.

Subjective
System Objective (Patient may Problem Identified Nursing Diagnosis
verbalize)
Head:
• Head is normocephalic and
symmetrical Muscle twitching
“wala raman naglabad
Head/Hair/Face Hair: Disturbed Body Image
akong ulo”
• Thin hair Thin hair
Face:
• Muscle twitching
Eyes:
• Presence of twitching
• Cataracts on the eye
• Blurring of vision (diplopia)
Ears:
”halap-halap man
Eyes/Ears/Nose • Symmetrical Blurring of vision Risk for Injury
akong tan-aw”
• No discharges noted
• Loss of hearing
Nose:
• Symmetrically align
• No discharges noted
• No lumps or lesions “wala raman nagsakit
Neck No problem identified
noted upon palpation akong li-og”
• Twitching, tingling and
numbness around the Bronchospasm & Laryngeal
mouth spasm
Mouth/Thorax/Lungs “lisod ko ginhawa” Impaired Gas Exchange
• Bronchospasm
Muscle twitching
• Laryngeal spasm
“wala man nagsakit
Back • No deformities noted No problem identified
akong likod”
Breast and axilla • No discharges “wala may sakit akong No problem identified

25
 • No lumps or swelling
totoy"
• No nodules
Cardiovascular/Peripheral • Cardiac dysrhythmias
“dali rako kapoyan” Altered heart rhythm
Risk for Decreased Cardiac
Vascular • Hypotension Output
• Dysphagia “maglisod ko og tulon”
GIT • ↑ed gastric motility Diarrhea Diarrhea
• Abdominal cramping
GUT/Reproductive • ↓ed urine output ”painful urination” Acute pain Acute Pain
• General muscle
hypertonia
• Tremor
• Spasmodic or
uncoordinated contractions
• Muscle cramps in the “sakit akong muscles” Muscle cramps Impaired Physical Immobility
Musculoskeletal extremities
• Stiffness in the hands “naa koy cramps” Risk for Injury
and feet
• Carpopedal spasm
• Chvostek and trousseau
sign
• s/s of hypocalcemia
• Dry skin
• Enamel hypoplasia
• Shortened premolar roots Risk for Impaired Skin Integrity
• Thickened lamina dura Dry skin
“gauga lang akong
Integumentary/ Metabolic • Delayed tooth eruption Risk for Infection
panit sauna dili man”
• Increased dental caries Alopecia
• Psoriasis Disturbed Body Image
• Exfoliative dermatitis
• Impetigo herpetiformis
Neurologic • Irritability “I’m depressed” Confusion Disturbed Thought Process
• Anxiety
• Depression Risk for Injury
• Delirium
Anxiety
• Seizure
• Numbness

26
 • Tingling
• increased DTR
• Psychosis
Endocrine • ↓ed PTH

27
 Hypothyroidism and Hyperthyroidism
DAGNOSTIC PURPOSE NORMAL VAUES INTERPRETATION SIGNIFICANCE NURSING
TEST CONSIDERATION
Serum Thyroid- • To confirm or Increased • TSH levels may be PREPARATION
Stimulating rule out Undetectable to slightly increased in
Hormone primary 15µIU/mL euthyroid patients with • Explain to the
hypothyroidis thyroid cancer. patient that this test
m and • Levels >20µIU/mL helps assess thyroid
distinguish it suggest primary gland function.
from hypothyroidism or, • Tell the patient
secondary possibly, endemic that the test requires a
hypothyroidis goiter. blood sample. Explain
m. who will perform the
Deceased venipuncture and
• To monitor • Decreased TSH when.
drug therapy levels may also result • Explain to the
in the patient from hyperthyroidism patient that he may
with primary (graves’ disease) and feel slight discomfort
hypothyroidis thyroiditis; both are from the tourniquet
m. marked by and needle puncture.
hypersecretion of • Inform the patient
thyroid hormones, that he need not
which suppresses TSH restrict food and fluids.
release. Provocative
testing with TRH is PATIENT CARE
necessary to confirm
the diagnosis.
• After getting the
sample, apply direct
pressure to the
venipuncture site until
bleeding stops.
• Instruct the
patient that he may

28
 resume medications
stopped before the
test, as ordered.
Free Thyroxine • To Normal range for Increased • High FT4 and FT3 PREPARATION
and Free measure the FT4 is 0.9 to levels indicate
Triiodothyronine metabolically 2.3ng/dl (SI, 10- hyperthyroidism, unless • Explain to the
active form of 30nmol/L); for FT3 the patient has patient that this special
thyroid peripheral resistance to test helps evaluate
0.2 to 0.6ng/dl (SI,
hormones thyroid hormone. thyroid function.
0.003-0.009 nmol/L)
• High FT3 with • Tell the patient
• To aid normal or low FT4 levels that the test requires a
diagnosis of indicate T3 toxicosis, a blood sample. Explain
hyperthyroidis distinct form of who will perform the
m and hyperthyroidism. venipuncture and
hypothyroidis Decreased when.
m when TBG • Low FT4 levels • Explain to the
levels are usually indicate patient that he may
abnormal hypothyroidism, except feel slight discomfort
in patients receiving from the tourniquet
replacement therapy and needle puncture.
with T3.
• FT4 and FT3 levels PATIENT CARE
may vary in patients
receiving thyroid
therapy, depending on • After getting the
the preparation used sample, apply direct
and the time of sample pressure to the
collection. venipuncture site until
bleeding stops.
Triiodothyronine • To aid in 25% to 35% Increased • A high T3 uptake PREPARATION
Uptake the diagnosis percentage with
of increased T4 levels • Explain to the
hypothyroidis indicates patient that this test
m and hyperthyroidism helps evaluate thyroid
hyperthyroidis (implying few TBG free function.
m when TBG binding sites and high

29
 is normal FT4 levels). • Tell the patient
• To aid in • A high T3 uptake that the test requires a
the diagnosis percentage with a blood sample. Explain
of primary decreased or normal who will perform the
disorders of FT4 levels suggests venipuncture and
TBG levels. decreased TBG levels. when.
Such decreased levels • Withhold drugs
may be caused by that may interfere with
protein loss, decrease test results, such as
production or estrogens, androgens,
competition for T4 phenytoin, salicylates,
binding sites by certain and thyroid
drugs preparations. If the
Decreased
patient must continue
• A low T3 uptake them, note this on the
percentage with laboratory request.
decreased T4 levels • Explain to the
indicates levels patient that he may
indicates feel slight discomfort
hypothyroidism from the tourniquet
(implying more TBG and needle puncture.
free binding sites and • Tell the patient
low FT4 levels). that the laboratory
• A low T3 uptake requires several days
percentage with an to complete the
increased or normal FT4 analysis.
levels suggests
increased TBG levels. PATIENT CARE
Such increased levels
may result from
• After getting
exogenous or
the sample, apply
endogenous estrogen
direct pressure to the
levels or from idiopathic
venipuncture site until
causes.
bleeding stops.
• Instruct the

30
 patient that he may
resume medications
stopped before the
test, as ordered.
Serum Thyroxine • To Total T4 levels,5 to Increased • Increased T4 PREPARATION
evaluate 13.5 g/dl (SI, 60 to levels are consistent
thyroid 165 mmol/L) with primary and • Explain to the
function secondary patient that this test
• To aid hyperthyroidism, helps evaluate thyroid
in the including excessive T4 function.
diagnosis of (levothyroxine) • Tell the patient
hyperthyroidis replacement therapy that he need not fast or
m and (fractitious or iatrogenic restrict activity.
hypothyroidism hyperthyroidism).
• Tell the patient
• To • Overt signs of that the test requires a
monitor the Decreased hyperthyroidism require blood sample. Explain
patient’s further test. who will perform the
response to venipuncture and
antithyroid • Subnormal when.
medication in levels suggest primary • Withhold drugs
the or secondary that may interfere with
hyperthyroidis hypothyroidism or may test results. If they
m or to thyroid be caused by T4 must be continued,
replacement suppression by normal, note this on the
therapy in elevated or laboratory request.
hypothyroidism replacement T3 levels. • If this test is to
(TSH estimates • When monitor thyroid
needed to hypothyroidism can’t therapy, the patient
confirm be confirmed, it may be should continue to
hypothyroidism necessary to measure receive daily thyroid
) TSH levels. supplements.

• Normal T4 levels PATIENT CARE

don’t guarantee
euthyroidism; for
• After getting the

31
 example, normal sample, apply direct
readings occur in T3 pressure to the
toxicosis. venipuncture site until
bleeding stops.
• Instruct the
patient that he may
resume medications
stopped before the
test, as ordered.
Antithyroid • To detect The normal titer is Abnormal Results • The presence of PREPARATION
Antibodies circulating less than 1:00 for antithyroglobulin or
antithyroglobul antithyroglobulin antimicrosomal • Explain to the
in antibodies and antimicrosomal antibodies in serum can patient that this test
when clinical indicate subclinical helps evaluate thyroid
antibodies.
evidence autoimmune thyroid function.
indicates disease, Graves’ • Inform the patient
Hashimoto’s disease, or idiopathic that he need not
thyroiditis, myxedema. restrict food and
Graves • Titers of 1:400 or fluids.
disease, or greater suggest • Tell the patient
other thyroid Hashimoto’s thyroiditis that the test requires
disease. • Antithyroglobulin a blood sample.
antibodies may also Explain who will
occur in some patients perform the
with other autoimmune venipuncture and
disorders, such as when.
systemic lupus • Explain to the
erythematous, patient that he may
rheumatoid arthritis, feel slight discomfort
and autoimmune from the tourniquet
haemolytic anemia. and needle puncture.

PATIENT CARE

32
 • After getting the
sample, apply direct
pressure to the
venipuncture site until
bleeding stops.
Radioactive Iodine • To • At 2 hours, Above normal • Above normal PREPARATION
Uptake Test evaluate 4% to 12% of the uptake may indicate
thyroid radioactive iodine hyperthyroidism, early • Explain to the
function accumulates in Hashimoto’s thyroiditis, patient that this test
• To aid in the thyroid; after hypoalbunemia, lithium helps evaluate thyroid
the diagnosis 6 hours, 5% to ingestion, or idodine function.
of 20% at 24 hours, deficient goiter. • Instruct the
hyperthyroidis 8% to 29% • In hyperthyroidism, patient to begin fasting
m and the rate of turnover at midnight the night
hypothyroidism • The may be so rapid that a before the test.
• To remaining falsely normal • Explain to the
distinguish radioactive iodine measurement occurs at payient that he’ll
between is excreted in the 24 hours. receive radioactive
primary and urine. Local iodine (capsule or
secondary variations in the liquid) and that he’ll
thyroid normal range of Below normal
• Below normal then be scanned after 2
disorders (in iodine uptake uptake may indicate hours, 6 hours, and 24
combination may occur hypothyroidism, hours.
with other because of subacute thyroiditis, or • Assure the patient
tests). regional iodine overload. that the test is painless
difference in and that the small
dietary iodine amount of radioactivity
intake and is harmless.
procedural • Check the
differences patient’s history for
among iodine exposure, which
laboratories. may interfere with test
results.
• Note previous
radiologic test using

33
 contrast media, nuclear
medicine procedures,
or current use of iodine
preparations or thyroid
drugs on the film
request slip.
• Iodine
hypersensitivity isn’t
considered a
contraindication
because the amount of
idodine used is similar
to the amount
consumed in a normal
diet.
• Make sure the
patient or a responsible
family member has
signed an informed
consent form, if
required.

PATIENT CARE

• Instruct the
patient to resume a
light diet 2 hours after
taking the oral dose of
radioactive iodine.
When the study is
complete, the patient
may resume his usual
diet.
Thyroid- • To aid in • TSI doesn’t Increased • Increased TSI levels PREPARATION
stimulating the evaluation normally appear are linked to

34
immunoglobulin of suspected in serum, but it’s exophthalmus, graves’ • Explain to the pt.
thyroid disease considered disease (thyrotoxicosis) that this test evaluates
normal at < and recurrence of thyroid function as
• To aid in 130% of basal hyperthyroidism. appropriate.
the diagnosis activity. Implementation:
os suspected
• Perform a
thyrotoxicosis,
venipuncture and
especially in
collect the sample in a
pt’s. w/
5ml clot activator tube
exophthalmus
handle the sample
• To monitor gently to prevent
treatment of hemolysis and send it
thyrotoxicosis to the laboratory
immediately.
Thyroxine-binding
globulin, serum
• To evaluate
abnormal
thyrometabolic states
that don’t correlate w/
thyroid hormone (T3 or
T4)
• To identify TBG
abnormalities.
• TBG by
immunoassay, 16 to
32mg/dl
• Elevated TBG
levels may indicate
hypothyroidism or
congenital (genetic)
excess, some forms of
hepatic disease
• Suppressed levels
may indicate

35
 hyperthyroidism or
congenital deficiency.

PATIENT CARE
• Instruct the pt.
that he may resume
medications stopped
before the test.

OTHER DIAGNOSTIC TESTS

DAGNOSTIC PURPOSE NORMAL VAUES INTERPRETATION SIGNIFICANCE NURSING

TEST CONSIDERATION
Thtroid • To • A uniform Abnornal • Smooth-bordered, PREPARATION
Ultrasonography evaluate the echo pattern echo-free areas with
thyroid throughout the enhanced sound • Make sure the
structure. gland transmission suggest patient has signed an
• To cysts. appropriate consent
differentiate form.
between a • Solid and well- • Note and report all
cyst and a demarcated areas with allergies.
solid tumor. identical echo patterns • Tell the patient
• To monitor suggest adenomas and that he need not
the size of the carcinomas. restrict food and fluids
thyroid gland before the test.
during • Explain that the
suppressive study is painless and
therapy. safe.
• To allow
accurate
PATIENT CARE
measurement
of a nodule.

36
 • To aid in • Thoroughly clean
the the patients neck to
performance remove the contact
of thyroid solution
needle biopsy
Thyroid Scan • To aid in • 80-200 Abormal • In T3 toxicosis, T3 • Pregnancy,
the diagnosis nanograms/dl levels rise, while total however, should be
of thyroid and free T4 levels ruled out before the
disorders remain normal scan is performed.

Hypoparathyroidism and Hyperparathyroidism

DAGNOSTIC PURPOSE NORMAL VAUES INTERPRETATION SIGNIFICANCE NURSING
TEST CONSIDERATION
Parathyroid • To aid in the • Levels vary, Elevated • Measures along PREPARATION
Hormone Test defferential depending on with serum calcium
diagnosis of the laboratory levels, abnormally • Explain to the
hyperparathyroi they must be elevated PTH values may patient that this test
dism and interpreted on indicate primary, help evaluate
hyperparathyroi calcium levels. secondary, or tertiary parathyroid function.
dism • Intact PTH hyperparathyroidism. • Instruct patient to
• C-terminal levels are 10-50 observe overnight fast
PTH assay; to pg/ml because food may
diagnose chronic • N-terminal affect PTH levels and
disturbances in fraction is 8-24 interfere with results
PTH metabolism, pg/ml • Tell the patient
such as • Abnormally low PTH
• C-terminal Abnormally Low values may result from that the test requires

37
 secondary and fraction is 0-340 Results hypoparathyroidism and a blood sample.
tertiary pg/ml hyperparathyroidism and Explain who will
hyperparathyroi from certain malignant perform the
dism; to diseases venipuncture and
differentiate when.
ectopic from • Explain to the
primary patient that he may
hyperthparathyr feel slight discomfort
oidism from the tourniquet
and needle puncture.

PATIENT CARE
• After getting the
sample, apply direct
pressure to the
venipuncture site until
bleeding stops.
Serum Calcium • Evaluate • In adults, Increased • Abnormally high PREPARATION
endocrine 8.2 to 10.2 serum calcium levels
function, mg/dl (hypercalcemia) may • Explain to the
calcium • In children, occur in patient that the serum
metabolism and 8.6 to 11.2 hyperparathyroidism and calcium test
acid base mg/dl parathyroid tumors, determines blood
balance pagets disease of the calcium levels.
• To guide bone, multiple myeloma, • Instruct patient to
therapy in metastatic carcinoma, observe overnight fast
patient with multiple fracture and because food may
renal failure, prolonged affect PTH levels and
renal transplant, immobilization. interfere with results
endocrine • Tell the patient
disorder, • Low calcum levels that the test requires
malignancies, or (hypocalcemia) may a blood sample.
cardiac disease result to Explain who will
and skeletal Decreased hyperparathyroidism perform the
disorder. total parathyroidectomy venipuncture and

38
 and malabsorption
• In the patient with
hypocalcemia, be alert
for circumoral and
peripheral numbness
and tingling, muscle
twitching, chvosteks
sign(facial muscle
spasm), tetany muscle
cramping trosseus sign
seizures, arrhythmias,
prolonged bleeding time,
and prolonged QT
interval
Serum phosphate • To aid in the • In adults, Increased • Increased levels or
diagnosis of 2.7-4.5 mg/dl hyperphosphatemia may
renal disorders • In children result to
and acid-base 4.5-6.7 mg/dl. hypoparathyroidism
imbalance
• To detect • Decreased
Decreased
endocrine, phosphate level or
skeletal, and hypophophatemia may
calcium result to
disorders hyperparathyroidism
39
when.
• Explain to the
patient that he may
feel slight discomfort
from the tourniquet
and needle puncture.
• Inform patient
that he need restrict
food and fluids.
PATIENT CARE
• After getting the
sample, apply direct
pressure to the
venipuncture site until
bleeding stops.
PREPARATION
• Explain to the
patient that the serum
phosphate test
measure phosphate
levles in the blood
• Tell the patient
that the test requires
a blood sample.
Explain who will
perform the
venipuncture and
when.
• Explain to the
patient that he may
feel slight discomfort
from the tourniquet
 and needle puncture.
• Inform patient
that he need restrict
food and fluids.
• Notify the
laboratory and
physician of drugs the
patient is taking that
may affect test result
it may be necessary
to restrict them.

PATIENT CARE
• After getting the
sample, apply direct
pressure to the
venipuncture site until
bleeding stops.
Alkaline • To detect • 45 to 115 Below normal • Below phosphatase PREPARATION
phosphatase and identify IU/ml ( SI, 45 to levels may occur in • Explain to the pt.
skeletal 115 U/L) hypoparathyriodism that this test assesses
diseases liver and bone
primarily function
characterized • Instruct the pt.
by marked too fast for at least
Above normal • High phosphatase
osteoblastic 8hrs. before the test.
level may occur in
activity Implementation:
hyperthyroidism
• To detect • Perform a
focal hepatic venipuncture and
lesions causing collect the sample in
biliary a 4ml clot-activator
obstruction, tube
such as a tumor
• Apply direct
or an abscess.
pressure to the

40
 venipuncture site
until bleeding stops
• Handle the
sample gently to
prevent hemolysis

PATIENT CARE
• Instruct the pt.
that he may resume
his usual diet.
Electrocardiograp • To identify • cardiac rate Abnormal Results • Increased QT and PREPARATION
hy conduction is 60-100bpm ST intervals because of
abnormalities • cardiac hypercalcemia • Explain to the
cardiac rhythm is patient the need to lie
arrhythmias, normal sinus still, relax and breath
myocardial rhythm normally during the
ischemia or • P wave procedure
infarction precedes each • Note current
• To monitor QRS complex cardiac drug therapy
recovery from • PR interval in the test request
MI lasts 0.12- 0.20 form as well as any
• To seconds other pertinent clinical
document • QRS information such as
pacemaker complex last pain or pacemaker
performance 0.06- 0.10 sec • Explain that the
• ST segment test in painless and
is not more than takes 5-10 min.
0.1mV
• T wave is PATIENT CARE
rounded and • disconnect the
smooth and is equipment, remove
positive leads I, the electrodes and
II, V3, V4,V5,V6 remove the gel with a
• QT interval moist cloth towel
duration varies

41
but usually last • if the patient is
0.36-0.44 sec having the recurrent
chest pain or if serial
ECGs are ordered, live
the electrode patches
in place.

42