MIRANDA, FRITZ CORTEZ BSN – 3C

STUDENT NOTES: ENDOCRINE SYSTEM SLIDE 5

2021 – 2022 Hormones are classified into four categories according to their
structure:
SLIDE 1 • Amines and amino acids (e.g., epinephrine, norepinephrine,
and thyroid hormones);
SLIDE 2 • peptides, polypeptides, proteins, and glycoproteins (e.g.,
INTRODUCTION thyrotropin-releasing hormone [TRH], follicle-stimulating
hormone [FSH], and growth hormone [GH]);
SLIDE 3 • Steroids (e.g., corticosteroids, which are hormones produced
by the adrenal cortex or their synthetic equivalents); and
SLIDE 4 • fatty acid derivatives (e.g., eicosanoid, retinoids)
Which brings us to the terms paracrine action and autocrine action.
There is a built-in negative feedback mechanism in the endocrine
We see, for example, system so that when there is an over abundance of hormones, a
the action of sex feedback is sent to either the pituitary or hypothalamus to stop the
hormones on the release of hormones.
ovaries. This is called
Paracrine, meaning, SLIDE 6
the hormones act
locally in the area So here is a picture familiar to all of us. You can appreciate how
where they are scattered the
released. endocrine
glands in the
Autocrine action refers to human body
when hormones act on the are. As
actual cells from which they mentioned
were released, as in when earlier, some
interleukin-1 is produced in hormones
response to external travel through
stimuli, where it binds to the blood
cell--surface receptors on stream to get
the same cell that produced to their target
it. glands.

This lecture will focus primarily on the pituitary and thyroid glands
and common disturbances that occur when things go out of whack.
SLIDE 7
The illustration gives you a snapshot of the pituitary gland and the
hormones it releases.
A brief description of your pituitary gland: it is a round structure,
about only half an inch in diameter, located on the inferior aspect of
the brain and is divided into anterior and posterior lobes.
The diagram clearly illustrates which hormones are released by the
anterior pituitary over the posterior pituitary. The hormones
released by the anterior pituitary enter the general circulation and
are transported to their target organs.
Special mention for TSH or your Thyroid Stimulating Hormone,
which in turn prods the thyroid to release its own set of hormones.
Notice these red lines? They represent the negative feedback
mechanism essential to maintain homeostasis.
SLIDE 8
Major hormones of as far as the pituitary and thyroid glands
Now although the pituitary gland, also called the hypophysis, is
referred to as the master gland, it cannot do much without signals
from the hypothalamus.
The hypothalamus is connected to the pituitary gland by the
pituitary stalk. It sends out releasing and inhibiting hormones to the
pituitary.
Releasing hormones include:
 Corticotropin Releasing Hormone
 Thyroid Releasing Hormone
 Growth Hormone Releasing Hormone
 Gonadotropin Releasing Hormone
Then we have the inhibiting hormones:
 Somatostatin inhibits GH and TSH
 Dopamine inhibits prolactin release from the pituitary and
inhibits FSH and LH
SLIDE 9
These are the actions of the major hormones of the pituitary:
Starting with the anterior pituitary:
 Gh or Growth hormone stimulates growth of bone and
muscle, promotes protein synthesis and fat metabolism, and
decreases carbohydrate metabolism.
  ACTH or Adrenocorticotropic hormone stimulates synthesis Remembering these concepts will help you better grasp the whys of
and secretion of adrenal cortical hormones, and the disturbances in ADH secretion which we will discuss later in this
 TSH or Thyroid-stimulating hormone stimulates synthesis lecture.
and secretion of thyroid hormones.
 Oxytocin stimulates contraction of the pregnant uterus, milk
ejection from breasts after childbirth.
SLIDE 10
Still by the anterior pituitary, we have: SLIDE 12
Assessment of a client with endocrine problems starts with a good
 FSH (Follicle-stimulating hormone) health history. We ask the patient if they have observed changes in:
 Energy level
- Female: stimulates growth of ovarian follicle and ovulation  Tolerance to heat or cold
 Weight
- Male: stimulates sperm production
 Thirst
 LH (Luteinizing hormone-)  Frequency of urination
 Fat and fluid distribution
- Female: stimulates development of corpus luteum,  Secondary sexual characteristics (e.g., loss or growth of hair,
release of oocyte, production of estrogen and progesterone menstrual cycle)
 Memory
- Male: stimulates secretion of testosterone, development  Concentration
of interstitial tissue of testes  Sleep patterns
 Mood
 Vision changes
 Joint pain
SLIDE 11
Also by the Anterior Pituitary, we have:  Sexual dysfunction

 Prolactin prepares female breast for breastfeeding SLIDE 13

The Posterior Pituitary produces only two very important hormones:
 ADH or Antidiuretic hormone. I call it the NO PEE hormone.
ADH also called Arginine Vasopressin or AVP increases water
reabsorption by the kidney tubules, hence you don’t pee so
much. Secretion of vasopressin is stimulated by an increase
in blood osmolality or by a decrease in blood pressure.
It is also important that we document:
 The severity of changes
 The length of time the client has experienced these changes
 The way in which these changes have affected the patient’s
ability to carry out activities of daily living
 The effect of the changes on the patient’s self-perception
 Family history
 hormone on other substances (e.g. the effect of insulin on
SLIDE 14 blood glucose levels)
Physical examination of the client should include:  They also help to determine if there is hypofunction or
 Vital signs hyperfunction of the endocrine system and where the site of
 Head-to-toe inspection the dysfunction is.
 Palpation of skin, hair, and thyroid
 Physical changes (appearance of SLIDE 16
facial hair in women, “moon
face”, “buffalo hump”, Urine Tests are performed:
exophthalmos)  To determine the amount of
 Mood and behavior changes hormones or the end products of
(nervousness, lethargy, fatigue) hormones excreted by the kidneys.
 Vision changes  It can be collected as one-time
 Edema specimens or as 24-hour urine
 Thinning of the skin specimens, depending on the
 Trunk obesity disorder
 Thinness of the extremities  Disadvantage: patient may be
unable to urinate at scheduled intervals and some
 Increased size of the feet and hands
medications or disease states may affect test results
 Hypo- or hyper- reflexia
SLIDE 17
SLIDE 15
Other Diagnostic Studies
Our role as nurses when it comes to diagnostic studies is to educate
the patient about the purpose of the study to be undergone, what
 Stimulation tests and Suppression tests
to expect, and any possible side effects related to these
examinations. Our nurses’ notes should reflect information about  Imaging studies
the progression of the disease and the patient’s response to  Genetic screening
therapy.
So diagnostic evaluation includes blood tests, urine tests, and other Stimulation and Suppression testing measures the response of
diagnostic studies. certain glands within the endocrine system to different types of
hormones. These are performed where a certain substance is
Blood Tests are done: measured both before and after the administration of another
 To determine levels of substance to determine if levels are stimulated or suppressed. These
circulating hormones, the tests are most commonly performed in the evaluation of possible
presence of autoantibodies, endocrine disorders.
and the effect of a specific
SLIDE 18
STIMULATION TESTS
Stimulation testing is used to confirm hypofunction of an endocrine
gland.
A few examples include:
 Growth Hormone Stimulation — used
to find out if a child’s pituitary gland is
producing enough growth hormone
 Glucose Tolerance — used to rule out
diabetes, hypoglycemia and insulin
resistance
 ACTH Stimulation — used to find out if
a child’s adrenal glands are producing enough cortisol and
to rule out congenital adrenal hyperplasia
SLIDE 19
SUPPRESSION TEST
Suppression testing on the other hand is used to detect
hyperfunction of an endocrine organ.
A common example would be:
1. Dexamethasone suppression test (DST) – used to assess
adrenal gland function by measuring how low cortisol levels
change in response to oral doses or an injection of
dexamethasone. It is typically used to diagnose Cushing’s
syndrome
* Dexamethasone is an exogenous steroid that provides
negative feedback to the pituitary gland to suppress
the secretion of ACTH
SLIDE 20
IMAGING STUDIES
These studies provide a picture
of the interior structures of the
body. Imaging is a great tool for
doctors to diagnose a disorder,
determine how severe the
disorder is, and monitor people
after the diagnosis of the
disorder is made. Most imaging tests are painless, relatively safe,
and noninvasive. Of course, this does not mean these studies are
not risk-free. (Cancer being a major risk)
Imaging studies use:
 Radiation, as in computerized tomography (CT), and
radionuclide scanning including positron emission
tomography (PET), bone density scan also called DEXA scan.
 Sound waves, as in ultrasonography
 Magnetic field, as in magnetic resonance imaging (MRI), and
 Substances, also called contrast agents, that are swallowed,
injected, or inserted to highlight or outline the tissue or
organ.
SLIDE 21
GENETIC SCREENING
Genetic screening is employed:
to identify specific genes associated with endocrine disorders
for selective targeting for drug development, and
for increased understanding of the function of the endocrine
system.
Genetic tests are done using a blood or spit sample. Other samples
may include hair, skin, amniotic fluid, or other tissue. These tests
help identify changes in genes, chromosomes, or proteins. Results
are usually ready in a few weeks. Now because we share DNA with
our family members, if you are found to have a genetic change, your
family members may have the same change.
I suggest you do your own SLIDE 23
research into these This slide presents a birds-eye view of the conditions that may result
different types of diagnostic from abnormalities in the pituitary gland whether it be the anterior
tests because although they or the posterior portion.
are pretty interesting, I
would be digressing from First, a quick review of the hormones before we proceed.
the main topic of my
lecture. The anterior pituitary hormones are:
That being said, let’s move  ACTH or adrenocorticotropic hormone stimulates the
on to the disorders. adrenal gland to release cortisol
 FSH and LH or follicle stimulating hormone and lutenizing
hormone impact sexual function and fertility
SLIDE 22  Prolactin stimulates milk production
Here is a closer look at your  TSH or thyroid stimulating hormone stimulates thyroid to
pituitary gland. You can see release hormone that impact metabolism
the vessels through which  GH or Growth hormone stimulate growth
hormones are secreted from both the anterior and posterior
portions. The posterior hormone are:
 ADH or antidiuretic hormone helps control water loss
When your pituitary gland oversecretes or undersecretes through the kidneys
horomones, this is when problems occur. Abnormalities of the  Oxytocin stimulates uterine contraction and release of milk
anterior and posterior portions of the gland may occur
independently. Again, keeping the functions of these hormones in mind, will help
you better understand their role in the development of disease.

We have conditions of hypersecretion in the anterior portion that

causes Cushing Syndrome, Gigantism, and Acromegaly.
Hyposecretion leads to dwarfism and panhypopituitarism.

There is a condition called SIADH that results from hypersecretion

of the posterior pituitary and Diabetes Insipidus from the
hyposecretion of such.
We first look into the disorders involving the • Dwarfism results from insufficient secretion of GH during
anterior pituitary. childhood.

SLIDE 24
So here are a few typical examples of persons with
the anterior pituitary disorders mentioned in the
previous slide:
• Cushing Syndrome is
most common since
disturbances in the secretion of
the anterior gland most
commonly involves ACTH.
• Panhypopituitarism is the term
applied when all anterior pituitary
hormones are undersecreted. This
results in the atrophy of the thyroid gland, the adrenal
cortex, and the gonads because of the loss of the tropic-
stimulating hormones.

• Acromegaly is a disorder caused by an

excess of GH in adults, and results in
enlargement of peripheral body parts
and soft tissue, after the fusion of the
epiphyseal plates has occurred,
without an increase in height.
• Gigantism on the other hand
occurs when there is oversecretion
of GH in children before the fusion
of epiphyseal plates. So when this happens, a
person may grow to be 7 or even 8 ft tall.
SLIDE 25
HYPERPITUITARISM (Anterior Pituirary)
SLIDE 26
As earlier mentioned, this condition happens when the pituitary
gland produces an excessive amount of growth hormone resulting
in an overgrowth of body tissues. You remember the pictures of the
people with conditions such as Cushing’s Syndrome, acromegaly and
gigantism, resulting in an overgrowth of all body tissues. Prolactin or
thyroid hormones may also be affected.
Excess secretion of growth hormone is often due to a benign
anterior pituitary adenoma. In some cases, the tissue overgrowth
may be a carcinoma.

SLIDE 27
HALLMARK SIGNS AND SYMPTOMS

 Increased body size caused by overproduction of growth

hormone
  Hypertension
 Orthopedic complaints such as arthritis and carpal tunnel
syndrome
 Cardiovascular changes such as heart enlargement, heart
failure, arteriosclerosis, or hypertension
 Hypogonadism causing delayed or arrested puberty
SLIDE 28
COMMON TEST RESULTS
 Increased serum growth hormone as the pituitary gland is
producing an excess of growth hormone.
 Increased prolactin; most pituitary tumors will cause on
overproduction of one or more of the pituitary hormones.
 Increased glucose; diabetes is
common in acromegaly.
SLIDE 29
PROGNOSIS
 Successful treatment can stop progression of the disease;
however, physical changes that occur before treatment
begins are permanent.
SLIDE 30
Treatment
 Administer dopamine agonists such as bromocriptine and
cabergoline to decrease the tumor size.
 Long-acting octreotide (an octapeptide) may be
administered to help control acromegaly.
 Surgical removal of the pituitary tumor.
 Radiation (either external or gamma knife) to reduce
adenoma size.
 Hormone replacement therapy following surgery.
 Antihypertensive medications to control blood pressure.
SLIDE 31
NURSING DIAGNOSES
 Disturbed body image related to illness or illness treatment
SLIDE 32
NURSING INTERVENTIONS
 Monitor blood pressure.
 Perform range of motion exercise to assure joint mobility.
 Provide emotional support.
 Explain to the patient:
- Action of medications
- Do not stop taking hormone replacement suddenly.
Let’s move on to hypopituitarism.
SLIDE 33
HYPOPITUITARISM (Anterior Pituitary)
First off, HYPOPITUITARISM, which is the hypofunction of the
pituitary gland can result from disease of the gland itself or disease
of the hypothalamus. Either way, the result is the same. This means
that the pituitary gland is unable to secrete a normal amount of
pituitary hormones. Again, common disorders here are your
dwarfism and panhypopituitarism.
SLIDE 34
So what can cause hypopituitarism? Primary causes are pituitary
tumors, inadequate blood supply to the pituitary gland, head
trauma, infection, stroke, increased intracranial pressure (as in a
bleed), radiation therapy, brain surgery, or surgical removal of a
portion of the pituitary gland. Secondary causes affect the
hypothalamus, which regulates the pituitary gland.
SLIDE 35
HALLMARK SIGNS AND SYMPTOMS
 Decreased caused by a decreased production of ACTH
 Lethargy and diminished cognition caused by a decreased
production of TSH
 Sensitivity to cold due to low TSH, which stimulates thyroid
hormone
 Decreased appetite and unintentional weight gain because
of TSH deficiency
 Infertility owing to decreased luteinizing hormone (LH) and
follicle—stimulating hormone (FSH) production
 Short stature due to diminished secretion of the growth
hormone.
 Menstrual irregularities or amenorrhea
caused by decreased production of FSH
and LH
 Loss of libido because of decrease in sex
hormones
SLIDE 36
COMMON TEST RESULTS
 Decreased ACTH usually due to a lesion of the pituitary.
 TSH deficiency owing to a mass, trauma, surgery, or
idiopathic.
 Decreased Prolactin due to a mass, causing diminished or
lack of prolactin from the anterior pituitary.
 Presence of a pituitary tumor is shown on MRI.
SLIDE 37
PROGNOSIS
Patients will require lifelong treatment, they can expect a normal
lifespan.
SLIDE 38
TREATMENT involves the:
 Administration of replacement hormones (estrogen,
testosterone, corticosteroids, growth hormone, and/or
thyroid hormone).
 Surgical removal of the pituitary tumor if it exists.
SLIDE 39
NURSING DIAGNOSES you may formulate would be
 Disturbed body image associated with illness
 Sexual dysfunction related to disease
SLIDE 40
NURSING INTERVENTIONS
 Monitor weight daily because ADH and ACTH, from the
pituitary, regulate fluid retention and excretion in the body.
 Monitor intake and output to ensure the balance is equal
due to hormone regulation.
 Explain to the patient:
- The need to take medication for the rest of the patient’s
life.
- The need for frequent laboratory tests.
This slide concludes our discussion of the disorders of the pituitary
gland in general. Let’s now move on to the disorders of specific to
the posterior pituitary.
SLIDE 41
We shall now look into the disorders SIADH resulting from
hypersecretion, and Diabetes Insipidus resulting from
hyposecretion of the posterior pituitary gland.
SLIDE 42
SIADH (Syndrome of Inappropriate Antidiuretic Hormone
Secretion)
Posterior Pituitary
If you recall, the antidiuretic hormone or ADH is responsible for
controlling the amount of water reabsorbed by the kidney, and this
prevents the loss of too much fluid. When too much water in the
body is detected, ADH production or secretion is halted (because the
body needs to get rid of that excess water)
Syndrome of inappropriate secretion of antidiuretic hormone
(SIADH) is caused by too much ADH being secreted by the posterior
pituitary gland even in the face of subnormal serum osmolality
(meaning, there is more water than normal compared to solutes).
SLIDE 43
SIADH is often of nonendocrine origin. Disorders of the CNS, such as
head injury, brain surgery or tumor, and infecton are thought to
produce this condition by direct stimulation of the pituitary gland.
Also, some such as carbamazepine (used to treat certain seizures
and pain), cyclophosphamides (given for certain types of cancer)
may directly stimulate the pituitary gland.
Certain cancers, especially small cell carcinoma of the lung, may
produce ADH.
SLIDE 44
HALLMARK SIGNS AND SYMPTOMS
S/S of SIADH include excessive ADH secretion from the pituitary
gland, sticky thick urine, fluid retention, and a sodium deficiency
known as euvolemic (meaning, normal volume) dilutional
hyponatremia. This means there is a low sodium
level with normal fluid volume.
The following signs and symptoms are all due to
euvolemic dilutional hyponatremia.
 Headaches
 Nausea and vomiting
 Confusion
 Personality changes or confusion
 And in a worse-case scenario, coma, seizures, or death
SLIDE 45
COMMON TEST RESULTS
 Hyponatremia (low serum sodium) due to the dilution.
 Urine osmolality is elevated (> 150 mOsmol/kg) because of
inappropriate concentration of urine.
 Urine sodium is greater than 20 mEq/L.
 BUN and creatinine levels are low to normal.
SLIDE 46
PROGNOSIS
For patients with SIADH, if sodium (Na)
levels are kept within normal limits,
prognosis is excellent.
SLIDE 47
MEDICAL INTERVENTIONS include eliminating the underlying cause,
if possible, and restricting fluid intake. Diuretics like furosemide
may be given alongside fluid restriction if severe hyponatremia is
present. (This increases the excretion of free water --- water that
must be removed to correct hyponatremia)
SLIDE 51
DI may occur following surgical treatment of a brain tumor. It may
also occur secondary to nonsurgical brain tumors, traumatic brain
injury or infections of the nervous system.

SLIDE 48 Also, DI may result post hypophysectomy (removal of pituitary

NURSING DIAGNOSES gland), and failure of the renal tubules to respond to ADH, elevated
 Risk for imbalanced fluid volume calcium levels, and the use of certain medications.
 Excess fluid volume

SLIDE 49
NURSING INTERVENTIONS include: SLIDE 52
 Close monitoring of daily weight.
To review, ADH is a substance that regulates water balance in the
(Weigh the patient daily using the same scale,
body by controlling water loss in the urine.
at the same time of day with similar clothing)
 Monitoring of urine and blood
chemistries (check electrolytes to determine
sodium levels)
 Close monitoring of I & O
 Restriction of fluid because excess fluid dilutes sodium levels.
 Monitoring of neurologic status
 Supportive measures and explanations of procedures and
treatments to assist the patient in managing his disorder.

SLIDE 50
DIABETES INSIPIDUS (Posterior Pituitary)
The most common disorder related to the posterior lobe
dysfunction is diabetes insipidus or DI. This is a condition in which
abnormally large volumes of dilute urine are excreted as a result of
deficient production of vasopressin.
Antidiuretic hormone (ADH) is produced within the hypothalamus
and then stored in the pituitary until needed. Whether it is a
decrease in the production of ADH by the hypothalamus or a
decrease in the release of ADH by the pituitary, the ability of the
kidneys to concentrate urine gets compromised. Also, as mentioned
in the previous slide, a condition referred to as nephrogenic
diabetes insipidus, where the renal tubules fail to respond to ADH,
contributes to the disorder.
All of these result in the excretion of large amounts of diluted urine.
The patient then drinks large volumes of fluid to replace the fluids
lost due to increased urine output.
SLIDE 53
HALLMARK SIGNS AND SYMPTOMS
 increase urine volume as the kidneys fail to concentrate
urine.
 increase thirst as the body attempts to replace lost fluid.
The patient experiences intense thirst and can drink to to 20
liters daily.
SLIDE 54
COMMON TEST RESULTS
URINE:
 There are no abnormal substances such as glucose or
albumin in the urine; the kidneys just cannot concentrate
urine.
 Specific gravity in urine is very low at 1.001 to 1.005. The
normal range for urine specific gravity is 1.005 to 1.030. This
is due to increased fluid in the urine where urinary output
can go to as much as more than 250 ml per hour.
 Fluid deprivation test. This is carried out by withholding
fluids for 8 to 12 hours or until 3% or 5% of body weight is
lost. The patient is weighed frequently during the test.
If the patient has DI, they will continue to pee large amounts
of dilute urine wherein the specific gravity and osmolality of
the urine does not increase despite the lack of fluid intake.
(Normally, if a person lacks fluid, osmolality should increase
and the person excretes a small amount of concentrated
urine).
 Vasopressin challenge test . After the water deprivation test,
the patient may be given a small dose of ADH, usually as an
injection to see how the body reacts to the hormone. This
test helps identify the type of diabetes insipidus.
If the dose of ADH stops the person from urinating, it is likely
the condition is a result of a shortage of ADH from the
pituitary and the kidneys are fine. In this case, the patient
may be diagnosed with cranial diabetes insipidus. However,
if the patient continues to pass urine despite the dose of ADH
given, this suggests there already is enough ADH in the body,
but the kidneys are not responding to it. In this case, the
patient may be diagnosed with nephrogenic diabetes
insipidus. I mentioned this term in an earlier slide.
SLIDE 55
BLOOD: in the blood,
 There is also an increased serum osmolality and
elevated levels of sodium. Since electrolytes indicate
dehydration, Na and Cl will rise as the concentration
increases.
 Increased BUN, again indicating dehydration because the
concentration of solutes to fluid is rising.
 There is normal blood glucose which indicates that diabetes
insipidus is not a complication of diabetes mellitus.
 A blood test may be done to assess the levels of ADH in the
blood.
MRI:
 May reveal the presence of a pituitary tumor or
hypothalamus tumor.

SLIDE 56
PROGNOSIS
Treatment will eliminate the symptoms of diabetes insipidus and the
patient can expect a normal lifespan.
SLIDE 57
TREATMENT
 Administer replacement ADH hormone (so they don’t keep
peeing) such as vasopressin or desmopressin to return
normal urination.
 Administer a diuretic such as hydrochlorothiazide to
decrease urination.
 Place the patient on a low-salt diet to reduce urine
production in the kidneys.
 Increase fluid intake until urination returns to normal.
 Limiting fluid intake in an attempt to lessen urinary output
will not work since the patient will still continue to excrete
large amounts of urine. If we restrict fluids this will cause the
patient to have an even more insatiable craving for fluid and
will result in Hypernatremia and Severe dehydration.
 Monitor for signs of dehydration.
 Weigh the patient each day using the same scale, at the
same time of day, wearing similar clothing.
 Explain to the patient:
- Medication must be taken every day.
- Wear a medical alert necklace/bracelet to
alert healthcare
providers that you have diabetes insipidus
This slide concludes the lecture on the disorders of the pituitary
gland.
We proceed to the next endocrine gland…
SLIDE 60
THYROID GLAND
SLIDE 61
Your thyroid gland, which by the way, is the largest endocrine
gland, is a butterfly-shaped organ located in the lower neck, anterior
to the trachea. It consists of two lateral lobes connected by an
isthmus. This gland is about 3 cm long and 3 cm wide and it weighs
about 30 gms.

SLIDE 58
NURSING DIAGNOSES
 Risk for impaired urinary elimination
 Impaired oral mucous membrane related to inadequate oral
secretions
 Deficient fluid volume due to excessive fluid loss or
inadequate fluid intake

SLIDE 59
NURSING INTERVENTION
 Maintain fluid and electrolyte balance.
 Monitor intake and output.
The blood flow to the thyroid is about 5ml/min per gram of thyroid
tissue, which, amazingly, is about five times the blood flow to the
liver!
SLIDE 62
Several hormones and chemicals are responsible for normal thyroid
function. The thyroid hormone, Calcitonin, and Iodine play key
roles in this.
Thyroid hormone is actually
comprised of two separate
hormones, which are T3 or
Triiodothyronine and T4 or
Thyroxine. These two hormones are amino acids that contain iodine
molecules bound to the amino acid structure. T4 has four iodine
atoms in each molecule, and T3 has, you guessed it – 3.
These hormones are synthesized and stored bound to proteins in
the cells of the thyroid gland until they are released into the
bloodstream in response to a need or stimulus. However, in order
for T3 and T4 to travel through the bloodstream, they need what we
call three thyroid-binding hormones. These are thyroxine-binding
globulin (TBG), transthyretin, and Albumin.
SLIDE 63
Iodine is essential to the thyroid gland for it to synthesize its
hormones. The thyroid uses up most of the iodine in the body and
the lack of iodine is a major factor in the alteration of thyroid
function. We get our iodine in the form of Iodide from food. Iodide
is absorbed into the blood in the GI tract. It is then taken up by the
thyroid gland from the blood, concentrating this iodide within the
cells where iodide ions are converted to iodine molecules. Iodine
then reacts to tyrosine (an amino acid) to form the thyroid
hormones.
Euthyroid is the term which refers to the thyroid hormone
production being normal. In other words, there is homeostasis when
a euthyroid state is achieved and maintained. This brings us to the
hypothalamic – pituitary – thyroid axis.
SLIDE 64
Hypothalamic-Pituitary-Thyroid Axis
The hypothalamus releases TRH (Thyrotropin-releasing hormone)
that in turn influences the pituitary gland to release TSH (Thyroid-
stimulating hormone) or Thyrotropin. TSH controls the rate that the
thyroid releases thyroid hormone through a negative feedback
mechanism as seen by the dotted lines. If there is a decrease of
thyroid hormone concentration in the blood, the release of TSH
increases, which in turn results in an increased output of T3 and
T4.
Environmental factors, such as a decrease in temperature, may lead
to an increased TRH secretion which inevitably results in an
elevation of thyroid hormones.
SLIDE 65
Let’s just quickly touch on the hormones of the thyroid before
proceeding.
Thyroid Hormones
The main function of thyroid hormone is to control cellular
metabolic activity.
T4 is a relatively weak hormone and maintains body metabolism in
a steady state.
T3 on the other hand is about five times as potent as T4 and has a
more rapid metabolic action.
These hormones accelerate metabolic processes by increasing the
level of specific enzymes that contribute to the oxygen consumption
and altering the responsiveness of tissues to other hormones.
The thyroid hormones cell replication and are important in brain
development. Your thyroid hormone is also necessary for normal
growth.
Thyroid hormones affect virtually every major organ system and
tissue function, including basal metabolic rate, tissue
thermogenesis, serum cholesterol levels, and vascular resistance.
Calcitonin, or thyrocalcitonin, is
another hormone secreted by the
thyroid gland which lowers blood
calcium and phosphate levels. It is
secreted in response to high
plasma levels of calcium and it
reduces the plasma level of calcium
by increasing deposition in the
bone.
Now all these hormones, including those of the other endocrine
glands, all have to be kept in proper balance.
For example, oversecretion of thyroid hormones or
hyperthyroidism, is manifested by a greatly increased metabolic
rate. Oversecretion is usually associated with an enlarged thyroid
gland known as goiter.
Goiter also commonly occurs with iodine deficiency. A lack of iodine
results in low levels of circulating thyroid hormones, which causes
increased release of TSH in an effort to compensate for these low
levels. The elevated TSH then causes overproduction of
Thyroglobulin, a precursor of T3 and T4 and eventually
hypertrophy of the thyroid gland.
SLIDE 66
The thyroid gland is inspected and palpated routinely in all patients.
Inspection begins with identification of landmarks. The lower neck
region is inspected for swelling or asymmetry. The thyroid is
palpated for size, shape, consistency symmetry, and the presence
of tenderness.
If palpations presents an enlarged thyroid gland, both lobes are
auscultated to identify localized audible vibration of a Bruit, which is
indicative of increased blood flow through the thyroid gland and this
is associated with hyperthyroidism.
Other abnormal findings may include a soft texture (indicative of
Grave Disease), firmness (Hashimoto thyroiditis or malignancy), and
tenderness (for Thyroiditis).
SLIDE 67
In addition to inspection, palpation and auscultation, thyroid
function tests may be ordered. These include:
 Lab measurement of thyroid hormones
 Thyroid scanning
 Biopsy
 Ultrasonography
 Serum immunoassay for TSH and free T4
 Ultrasound, CT, and MRI
Let’s explore these thyroid tests more…
SLIDE 68
Serum Thyroid-Stimulating Hormone is the primary screening test for
thyroid function. It is used to confirm clinically suspected thyroid
disease, for monitoring thyroid hormone replacement therapy, and
for differentiating between disorders of the thyroid gland itself and
disorders of the pituitary or hypothalamus.
In hyperthyroidism T3 and T4 are high, hence TSH is decreased since
the pituitary is reacting to the increase of circulating thyroid
hormones. Conversely, in hypothyroidism, TSH is ↑ since T3 and T4
are low and the pituitary is trying to stimulate the thyroid to
produce more thyroid hormone,
Serum T3 and T4 test is a direct measurement of your free or
unbound thyroxine, the only metabolically active fraction of T4. Free
T4 levels correlate with metabolic status; they are elevated in
hyperthyroidism and decreased in hypothyroidism.
Serum T3 and T4 test measures total T3 or T4 which includes
protein-bound and free hormone levels that occur in response to
TSH secretion. In hyperthyroidism, T3 levels appear to be a more
accurate indicator of the presence or severity of the disorder since
T4 levels are often within normal range.
T3 Resin Uptake Test is an indirect measure of unsaturated TBG
(thyroxine-binding globulin). It is used to determine the amount of
thyroid hormone bound to TBG and the number of available binding
sites. If the number of free or unoccupied binding sites is low, as in
hyperthyroidism, the T3 uptake is greater than normal (the normal
T3 uptake being 25% to 35%). Conversely, if the number of available
sites is high, as in hypothyroidism, the test result would be less than
25%. T3 uptake is useful in evaluating thyroid hormone levels in
patients who have received diagnostic or therapeutic doses of
iodine.
Thyroid Antibodies Test are used for both hypothyroid and
hyperthyroid conditions. Results of testing by immunoassay
techniques for antithyroid antibodies are positive, in varying
degrees, in chronic autoimmune thyroid disease, Hashimoto
thyroiditis, Graves disease, and other organ specific autoimmune
diseases such as systemic lupus erythematosus or SLE and
rheumatoid arthritis.
SLIDE 69
Radio Iodine Uptake measures the rate of iodine uptake by the
thyroid gland. Patients with hyperthyroidism exhibit a high uptake of
iodine 123. The opposite is seen with patients with hypothyroidism.
Fine-Needle Aspiration Biopsy uses a small-gauge needle to sample
thyroid tissue for biopsy. It is a safe and accurate method for
detecting malignancy. Results are reported as (1) negative (benign),
(2) positive (malignant), (3) indeterminate (suspicious), and (4)
inadequate (nondiagnostic)
Thyroid Scan, Radioscan, or Scintiscan takes visual images of the
distribution of radioactivity in the area being scanned. _________
and Iodine 131 are the most
commonly used isotopes of iodine.
Scans are helpful in determining the
location, size, shape, and anatomic
function of the thyroid gland,
especially when thyroid tissue is
substernal or large. Areas of increased
function are called “Hot” areas while
areas of decreased function are called “Cold” areas. Lack of function
noted increases the likelihood of a malignancy.
 Serum Thyroglobulin (Tg) can be measured reliably in the
serum by radioimmunoassay. It is used to detect the
persistence or recurrence of Thyroid Garcinoma.
  Document significant information in the patient’s medical
record and laboratory requisition
SLIDE 70
For nursing implications, SLIDE 71
when thyroid tests are HYPERTHYROIDISM
ordered and scheduled, it is Hyperthyroidism is a common
necessary to first determine endocrine disorder and is a form of
if the patient is allergic to thyrotoxicosis which results from an
iodine (shellfish), and excessive synthesis and secretion of
whether the patient has endogenous or exogenous thyroid
taken medications or agents hormones by the thyroid.
that contain iodine as these
may alter test results. SLIDE 72
As shown in the picture, because there is an increase in thyroid
Obvious sources of iodine-containing medications include contrast hormones T3 and T4, there is a decrease in TSH in an attempt to
agents and those used to treat thyroid disorders such as radioactive achieve equilibrium.
iodine. Less obvious sources are topical
antiseptics, multivitamins, food
supplements that may contain kelp and SLIDE 73
seaweed, and an antiarrythmic agent Causes of hyperthyroidism include Graves disease, toxic
called Amiodarone. multinodular goiter, toxic adenoma, thyroiditis, and excessive
ingestion of thyroid hormone.
Estrogens, salicylates, amphetamines,
chemotherapeutic agents, antibiotics, Graves Disease, the most common cause of hyperthyroidism, is an
corticosteroids, and diuretics may also autoimmune disorder that results from an excessive output of
affect test results. thyroid hormones due to abnormal stimulation of thyroid gland by
Lastly, the nurse has to document circulating immunoglobulins. This disease affects women eight
significant information in the patient’s times more frequently than men, with onset usually between the
medical record and laboratory second and fourth decades.
requisition.
 Graves disease
 Check if patient is allergic to iodine  Toxic multinodular goiter
 Ask if the patient has taken medications or agents that  Toxic adenoma
contain iodine  Thyroiditis
 Excessive ingestion of thyroid hormone
 The prognosis is good if the cause of hyperthyroidism is treated;
however, hyperthyroidism is a chronic disease.
SLIDE 74
HALLMARK SIGNS AND SYMPTOMS
 Enlarged thyroid gland (goiter)possibly Signs such as bulging eyes (exophthalmos) are not reversible.
caused by tumor Furthermore, thyroid surgery may result in complications.
 Protrusion of the eyeballs (exophthalmos) due to
lymphocytic infiltration which pushes out the eyeball
 Sweating (diaphoresis); excess thyroid hormone raises the SLIDE 77
metabolic rate TREATMENT
 Increased appetite owing to increased metabolism Objective of medical management of hyperthyroidism is: To restore
 Nervousness because of high levels of thyroid hormone reduce thyroid hyperactivity to relieve symptoms and prevent
 Weight loss due to increased metabolism complications
 Menstrual changes owing to elevated levels of thyroid  Pharmacologic therapy: There are two forms available for
hormone treating hyperthyroiditis and controlling excessive thyroid
 Difficulty concentrating activity: 1 is the use of Irradiation by administration of the
 Restlessness radioisotope 131I as it has destructive effects on the thyroid
 Diarrhea gland, and 2 are antithyroid medications that interfere with
the synthesis of thyroid hormones and other agents that
 Elevated blood pressure
control manifestations of hyperthyroidism.

 Radioactive Iodine Therapy. This therapy is contraindicated

SLIDE 75 during pregnancy and women are instructed not to conceive
COMMON TEST RESULTS at least 6 months following treatment. Also, radioactive
iodine should not be given until at least 6 weeks after
 Increased serum T3.
lactation stops. The goal here is to eliminate the
 Increased serum T4.
hyperthyroid state with the administration of sufficient
 Low TSH
radiation in a single dose.
 Increased TRH and TSH if pituitary gland is the cause of
hyperthyroidism.
So the way this works is most of the iodine that enters and
 Presence of antibodies if cause is Graves’ disease. stored in the body becomes concentrated in the thyroid gland.
 Thyroid scan reveals enlarged thyroid. Ergo, the radioactive isotope of iodine enters and stays in the
thyroid gland where it does its job to destroy thyroid cells
SLIDE 76 without harming other radiosensitive tissues. Eventually, over
PROGNOSIS several weeks, the thyroid cells exposed to the radioactive
 iodine are destroyed, resulting in reduction of the hyperthyroid
state and eventually hypothyroidism.
Methimazole (MMI and Tapazole (MMI) is given 4 to 6 weeks
prior to this treatment in patients at high risk for complications
of hyperthyroidism (like older adults and patients with
cardiovascular disease. MMI is stopped 3 days before and
restarted 3 days post radioactive iodine is given. MMI is tapered
over 4 to 6 weeks.
The irony is that in an effort to treat hyperthyroidism, we end
up with hypothyroidism. Hence thyroid hormone replacement is
started 4 to 18 weeks after your antithyroid meds have been
stopped. Of course, with reference to lab values of TSH, serum
free T4 and total T3 at varying points during the treatment.
Eventually, and hopefully euthyroid state can be achieved.
Caution: Patients who receive radioactive iodine should be advised
that they can contaminate their household and other family
members through body secretions or radiation emitting from their
body. Sexual contact and even sleeping in the same bed is to be
avoided. Children and pregnant women should also stay away from
these patients.
 Antithyroid medications. Most commonly used are
methimazole (MMI and Tapazole) or propylthiouracil (PTU).
What these medications do is they block the utilization of
iodine by interfering with the iodination of tyrosine and the
coupling of iodotyrosines in the synthesis of thyroid
hormones. These meds are used till the patient is euthyroid.
 Adjunctive therapy comes in the form of iodine or iodide
solutions which used to be the only therapy available for
patients with hyperthyroidism. Iodine solutions, in the short
term, are considered effective, especially when treating
patients with thyroid storm or those requiring surgery for
hyperthyroidism.
 Surgical management: Candidates for surgery are Pregnant
women who are allergic to antithyroid meds, patients with
large goiters, or patients
unable to take antithyroid agents. Or surgery is also performed
for patients with obstructive symptoms, for women in their
second trimester of pregnancy, and for those who need their
thyroid function to be rapidly normalized. Before surgery,
though, antithyroid medications are given until signs of
hyperthyroidism have subsided. Aspirin should be withheld
several weeks before surgery to avoid post-operative bleeding.
Subtotal thyroidectomy has an 8% recurrence rate at 5 years, as
opposed to almost 0% in patients who have total
thyroidectomies.
SLIDE 78
NURSING DIAGNOSES
 Imbalanced nutrition: less than what body requires related
to inadequate intake in relation to metabolic needs
 Fatigue related to sleep deprivation
 Hyperthermia related to increased metabolic rate
 Ineffective coping
 Situational low self-esteem
Collaborative Problems / Potential Complications
 Thyrotoxicosis or thyroid storm
 Hypothyroidism
Gerontologic Considerations. Although hyperthyroidism is much
less seen in older adults as compared to hypothyroidism, patients 65
years and older must be assessed carefully because they may
present with atypical and sometimes subtle signs and symptoms of
the disease and may be attributed to another source instead of
hyperthyroidism itself.
Thorough nursing assessment and history taking, coupled with labs
such as serum TSH and free T4 and T3 will help ensure that thyroid
disorders are not missed.
SLIDE 79
NURSING INTERVENTIONS
 Monitor vital signs.
 Provide cool environment.
 Protect the patient’s eyes with dark
glasses and artificial tears if the
patient has exophthalmos.
 Provide a diet high in carbohydrates,
protein, calories, vitamins, and
minerals.
 Monitor for laryngeal edema following surgery (hoarseness
or inability to clearly speak).
 Keep oxygen, suction, and a tracheotomy set near bed in
case the neck swells and breathing is impaired.
 Keep calcium gluconate near the patient’s bed following
surgery. This is the treatment for tetany and is used to
maintain the serum calcium level in normal range.
SLIDE 80
NURSING INTERVENTIONS (continued)
 Place the patient in a semi-Fowler’s position to decrease
tension on the neck following surgery.
 Support the patient’s head and neck with pillows.
 Monitor for muscle spasms and tremors (tetany) caused by
manipulation of the parathyroid glands during surgery.
 Check drainage and hemorrhage from incision line; red flags
are frank hemorrhage and purulent, foul-smelling drainage.
 Monitor for signs of hypocalcemia (tingling of hands and
fingers).
 Check for Trousseau’s sign (inflate blood pressure cuff on the
arm and muscles contract).
 Check for Chvostek’s sign (tapping over the facial nerve
causes twitching of the facial muscles). Both this sign and
Trousseau’s sign are positive when the parathyroid glands
have been manipulated during thyroid surgery, in which case
they secrete too much phosphorus and not enough calcium.
Since muscles, that is the heart, need calcium for work, a low
calcium level may cause muscle spasms which are easily
detected by Chvostek’s sign and Trousseau’s sign. The treatment
is IV calcium, administered quickly.
SLIDE 81
THYROID STORM / THYROTOXICOSIS / THYROTOXIC CRISIS
So what is thyroid storm, aka thyrotoxicosis, aka Thyrotoxic crisis
This is a sudden onset of severe hyperthyroidism. If left untreated, it
is almost always fatal. Hence it is imperative that immediate
treatment be instituted.
SLIDE 82
PRECIPITATING FACTORS
Precipitating factors include stress, both physical and emotional.
Examples of physical stress are injuries, infection, diabetic
ketoacidosis, among others.
SLIDE 83
HALLMARK SIGNS AND SYMPTOMS
Clinical manifestations of thyroid storm include:
• Hyperpyrexia (> than 38.5C)
• Extreme Tachycardia (>130 bpm)
• Exaggerated symptoms of hyperthyroidism with
disturbances of a major system (for example, cardiovascular:
edema, chest pain, dyspnea, palpitations)
• Altered neurologic or mental state, which often appears as
delirium psychosis, somnolence, or coma.
 methimazole.
• Treat shock or adrenal insufficiency by giving
Hydrocortisone.
• Decrease output of T4 from the thyroid
SLIDE 84 gland by giving iodine.
PROGNOSIS • Treat severe cardiac symptoms (atrial
Thyroid storm is an Acute, life-threatening emergency. fibrillation, dysrhythmias, heart failure, etc) with
If untreated, thyroid storm sympatholytic agents like Propranolol combined with
is almost invariably fatal in digitalis.
adults (90% mortality rate) and
is likely to cause a similarly SLIDE 86
severe outcome in children. HYPOTHYROIDISM
We have finally come to our last topic for this lecture.
SLIDE 85
TREATMENT SLIDE 87
Immediate objectives are Hypothyroidism results from a decrease from normal levels of
reduction of body temperature and heart rate and prevention of thyroid hormone, your T4 and T3. When this happens, all body
vascular collapse thru the following: functions can be affected and can range from mild to life
• Reduction of body temperature with blankets, ice packs, threatening, as in the case of myxedema a severe deficiency.
cool environment, hydrocortisone, and acetaminophen
(Tylenol), We do not give salicylates (e.g. aspirin) since they As you see in the picture, when thyroid hormone levels go down,
displace thyroid hormone from binding proteins and worsen there is an increase in TSH. This increased TSH is a compensatory
the hypermetabolism. mechanism of the pituitary gland to try and get the thyroid to
• Improve tissue oxygenation and meet high metabolic produce more thyroid hormone. However, if the problem lies in the
demands by administering hypothalamus, TSH levels would be low as well because of the
humidified oxygen and obtaining decreased stimulation of TRH from the hypothalamus.
ABG levels and pulse oximetry to
monitor respiratory status SLIDE 88
• Replace liver glycogen stores TYPES
depleted by the hyperthyroid state Hypothyroidism can involve failure of the pituitary gland, the
thru IV fluids containing dextrose hypothalamus, or both. When this happens, it is called
• Impede formation of thyroid Central Hypothyroidism. If only the pituitary is involved, it is
hormone and block conversion of T4 referred to as pituitary or secondary hypothyroidism. If the
to T3 by administering problem lies in the hypothalamus, which results in inadequate
propylthiouracil (PTU) or secretion of TSH because of a decreased stimulation of TRH, it is
called Hypothalamic or tertiary hypothyroidism. Neonatal  Extreme fatigue
hypothyroidism means thyroid deficiency is present at birth. In  Hair loss, brittle nails, dry skin
cases like this, the mother herself may also have thyroid deficiency.  Numbness and tingling of fingers
 Voice becomes husky
 Menstrual disturbances/Loss of libido
This decrease in thyroid hormone, has several causes as we shall see  Subnormal body temperature and pulse rate
in the next slide.  Weigh gain / cachexia
 Thickened skin
SLIDE 89  Mask-like appearance
CAUSES
 Apathetic
 The most common cause of hypothyroidism in adults is
 Constipation
Autoimmune disease (Hashimoto thyroiditis, post-Graves
 Personality / cognitive changes (dementia)
disease) Hashimoto disease occurs when the immune system
 Inadequate ventilation
attacks the thyroid gland. Hashimoto’s is more likely to occur
 Sleep apnea
in women than men and commonly appears between the
ages of 30 and 50 and tends to run in families. Development  Pleural and pericardial effusion, respiratory muscle weakness
of a goiter is a common first sign of Hashimoto’s disease.  Elevated serum cholesterol
 Atrophy of thyroid gland with aging  Atherosclerosis
 Therapy for hyperthyroidism using radioactive iodine or  Coronary artery disease
having a thyroidectomy  Poor left ventricular function
 Medications like Iodine compounds (such as amiodarone  Risk for intraoperative hypotension, postoperative heart
and lithium) and antithyroid medications (such as failure, altered mental status
propylthiouracil or PTU and methimazole)  Myxedema coma
 Radiation to head and neck to treat head and neck cancers,
or lymphoma SLIDE 91
 Infiltrative diseases of the thyroid like amyloidosis and COMMON TEST RESULTS
lymphoma  Increased TSH unless the cause is due to a decreased
 Iodine deficiency and iodine excess production of TSH by the pituitary gland.
 Decreased T3 and T4.
SLIDE 90  Presence of thyroglobulin, indicating Hashimoto’s
HALLMARK SIGNS AND SYMPTOMS thyroiditis.
All bodily systems get affected when there are thyroid issues.  Presence of peroxidase autoantibodies in serum, indicating
Hashimoto’s thyroiditis.
Some of these are found in mild cases of hypothyroidism and others  Increased cholesterol levels.
in more severe cases as in myxedema coma.
SLIDE 92
PROGNOSIS
Prognosis is excellent with replacement of thyroid hormones.
SLIDE 93
TREATMENT
The objective of medical management is, of course, to restore the
body to a normal metabolic state by hormone replacement and to
prevent progression of disease and further complications. This is
achieved through:
 Pharmacologic therapy: Commonly prescribed would be
synthetic Levothyroxine (Synthroid or Levothroid) to treat
the hypothyroidism and to suppress nontoxic goiters. If
patient deteriorates into myxedema coma, IV administration
of T4 and T3 are recommended.
High-dose glucocorticoids (hydrocortisone) tapered to low-
dose therapy if until coexisting adrenal insufficiency is ruled
out.
 Prevention of cardiac dysfunction: When thyroid
replacement is initiated, angina or dysrhythmias may occur
because thyroid hormones enhance the effects of
Catecholamines on the cardiovascular system (increased HR,
BP, RR, muscle strength and mental alertness). If this
happens, thyroid hormone administration must be
immediately discontinued and later resumed with caution
and with dosage adjustments and with close monitoring by
the primary provider and the nurse.
 Prevention of medication interactions: Oral thyroid
hormones interact with many other medications.
Magnesium containing antacids decrease thyroid hormone
absorption. And thyroid hormones may also decrease the
pharmacologic effects of digitalis
glycosides (Digoxin). When
beginning thyroid replacement, if
anticoagulants are also indicated, there
may be increased risk of bleeding so the dosage of
anticoagulants need to be decreased.
Caution must also be observed when concomitantly
administering thyroid hormones and hypnotics and
sedatives IV as effects of the later are potentiated by the
thyroid hormones. Risk of respiratory depression can be
fatal. Hence, hypnotics and sedatives are given at lower
doses, about ½ or 1/3 of that typically prescribed for patients
with similar age and weight with normal thyroid function.
 Supportive therapy: Severe hypothyroidism and myxedema
coma require immediate and aggressive treatment to
maintain vital functions. ABGs, O2 saturation must be closely
monitored. Fluids are given with caution because of the
danger of water intoxication. Passive rewarming with a
blanket over active rewarming is recommended to prevent
increased oxygen demands and hypotension.
SLIDE 94
NURSING DIAGNOSES
Here are some of the nursing diagnosis that may be identified in the
care of patients with hypothyroidism:
 Activity intolerance related to insufficient physiologic or
psychological energy
Goal: Increased participation in activities and increased
independence.
 Ineffective breathing pattern related to depressed
ventilation.
Goal: Improved respiratory status and maintenance of
normal breathing pattern
 Acute confusion related to depressed metabolism and
altered cardiovascular and respiratory status.
Goal: Improved thought processes.
 Risk for imbalanced nutrition: more than what body requires
 Goal: Provide a tailored and achievable diet plan
 Risk for constipation related to decreased motility of the GI And this wraps up my looong lecture. I hope you learned something.
tract Thank you.
Goal: Return to normal bowel function.
 Risk for imbalanced body temperature
Goal. Maintenance of normal body temperature REFERENCES:
 Deficient knowledge about therapeutic regimen for lifelong
thyroid replacement therapy. BOOKS
Goal: Knowledge and acceptance of the prescribed
therapeutic regimen. Hinkle, J., & Cheever, K. (2018). Brunner & Suddarth’s Textbook of
 Myxedema and myxedema coma
Goal: Evidence of progression to pre-coma baseline without Medical-Surgical Nursing (4th ed) (14th ed.). Wolter Kluwer
incurring additional complications.
Health/Lippincott, Williams & Wilkins.
SLIDE 95
NURSING INTERVENTION
James Edward Keogh. (2019). Medical-surgical nursing demystified.
 Monitor vital signs.
 Provide a warm environment. Mcgraw-Hill Education.
 Low-calorie diet.
 Increase fluids and fiber to prevent constipation. JOURNALS
 Take thyroid replacement hormone each morning to avoid
insomnia.
Beta cells in type 2 diabetes: Science explained. (2021, October 25).
 Monitor for signs of thyrotoxicosis (an increase in T3):
nausea, vomiting, diarrhea, sweating, tachycardia, and Www.medicalnewstoday.com.
palpitations.
 Explain to the patient: https://www.medicalnewstoday.com/articles/beta-cells-in-
 Side effects of thyroid hormone replacement. type-2-diabetes#explanation
 Review the signs of hyperthyroidism and hypothyroidism.
 Contact healthcare provider if signs change. VIDEOS
Quality and Safety Nursing Alert:
 Medications are given to the patient with hypothyroidism
with extreme caution because of the potential for altered Hyperthyroidism vs. Hypothyroid RN LPN NCLEX. (n.d.).
metabolism and excretion, as well as depressed metabolic Www.youtube.com.
rate and respiratory status.
https://www.youtube.com/watch?v=YyHM9xQyyas&t=16s
Immunology - Interleukin 1 (IL1) physiology and IL1 antagonist services/endocrinology/resources/endocrinology-patient-

pharmacology. (n.d.). Www.youtube.com. procedures/stimulation-testing

https://www.youtube.com/watch?v=T3rzJKxE6BU

SIADH vs DI (Diabetes Insipidus) for nursing RN PN NCLEX - YouTube.

(n.d.). Www.youtube.com.

https://www.youtube.com/watch?v=hKFGGv0E-5A

The Endocrine System. (n.d.). Www.youtube.com. Retrieved

February 27, 2022, from

https://www.youtube.com/watch?v=-S_vQZDH9hY&t=25s

WEBSITES

ACTH stimulation test: MedlinePlus Medical Encyclopedia. (n.d.).

Medlineplus.gov.
https://medlineplus.gov/ency/article/003696.htm

Evocative/suppression testing. (2020, February 19). Wikipedia.

https://en.wikipedia.org/wiki/Evocative/suppression_testing

NHS Choices. (2019). Diagnosis - Diabetes insipidus.

https://www.nhs.uk/conditions/diabetes-

insipidus/diagnosis/
Stimulation Testing. (n.d.). Children’s Hospital of Pittsburgh.

https://www.chp.edu/our-