Republic of the Philippines

UNIVERSITY OF EASTERN PHILIPPINES

University Town, Northern Samar
Web: uep.edu.ph Email: ueppres06@gmail.com

COLLEGE OF NURSING AND ALLIED HEALTH SCIENCES

Endocrine Disorders

Submitted by:
AGUILANDO, ANTHONY SETH T.
BSN-III

Submitted to:
Jeanette J. Rojo, MAN
Clinical Instructor
 Endocrine System Disorders

GIGANTISM
Gigantism is a rare condition that causes abnormal growth in children. This
change is most notable in terms of height, but girth is affected as well. It occurs when
your child’s pituitary gland makes too much growth hormone, which is also known as
somatotropin.
The most common cause of too much GH release is a noncancerous (benign)
tumor of the pituitary gland. Other causes include:

● Genetic disease that affects the skin color (pigmentation) and causes
benign tumors of the skin, heart, and endocrine (hormone) system
(Carney complex)
● Genetic disease that affects the bones and skin pigmentation
(McCune-Albright syndrome)
● Genetic disease in which one or more of the endocrine glands are
overactive or form a tumor (multiple endocrine neoplasia type 1 or type
4)
● Genetic disease that forms pituitary tumors
● Disease in which tumors form on the nerves of the brain and spine
(neurofibromatosis)

Signs And Symptoms

Some parts of their body may be larger in proportion to other parts. Common
symptoms include:

● Very large hands and feet

● Thick toes and fingers
● A prominent jaw and forehead
● Coarse facial features

Children with gigantism may also have flat noses and large heads, lips, or tongues.
 The symptoms your child has may depend on the size of the pituitary gland
tumor. As the tumor grows, it may press on nerves in the brain. Many people
experience headaches, vision problems, or nausea from tumors in this area. Other
symptoms of gigantism may include:

● Excessive sweating
● Severe or recurrent headaches
● Weakness
● Insomnia and other sleep disorders
● Delayed puberty in both boys and girls
● Irregular menstrual periods in girls
● Deafness

Pathophysiology
Diagnostic Examination

Diagnosis can be made from the characteristic clinical findings. MRI of the
sella is the imaging test of choice for diagnosis of pituitary adenoma. CT, MRI, or
skull x-rays disclose cortical thickening, enlargement of the frontal sinuses, and
enlargement and erosion of the sella turcica. X-rays of the hands show tufting of the
terminal phalanges and soft-tissue thickening.

● Serum IGF-1 should be measured in patients with suspected acromegaly;

IGF-1 levels are typically substantially elevated (3-fold to 10-fold), and
because IGF-1 levels do not fluctuate like GH levels do, they are the simplest
way to assess GH hypersecretion. IGF-1 levels also can be used to monitor
response to therapy.
● Plasma GH levels are typically elevated. Blood should be taken before the
patient eats breakfast (basal state); in normal people, basal GH levels are low
or undetectable. Transient elevations of GH are normal, due to the pulsatile
secretion of GH, and must be distinguished from pathologic hypersecretion.
The degree of GH suppression after a glucose load remains the standard and
thus should be measured in patients with elevated plasma GH; however, the
results are assay-dependent, and the cutoff for normal suppression is
controversial. Secretion in normal people is suppressed to < 1 ng/mL ([< 1
mcg/L] a cutoff of < 0.4 ng/mL [< 0.4 mcg/L] is often used) within 120 minutes
of oral administration of 75 g of glucose. Most patients with acromegaly have
substantially higher values. In some cases, basal plasma GH levels are also
used in monitoring response to therapy.
● CT or MRI of the sella should be done to look for a tumor. If a tumor is not
visible, excessive secretion of pituitary GH may be due to a non-central
nervous system tumor producing excessive amounts of ectopic GHRH.
Demonstration of elevated levels of plasma GHRH can confirm the diagnosis.
Lungs and pancreas may be first evaluated in searching for the sites of
ectopic production.
● Fasting plasma glucose levels, glycosylated Hb (HbA1C), or an oral glucose
tolerance test can be done to test for diabetes. Electrocardiography and,
preferably, echocardiography are done to detect heart disease. Colonoscopy
 is done to detect colon cancer. Follow-up screening depends on the results of
the initial testing and the patient's response to treatment.

Medical Intervention

The goals of medical therapy for GH excess are as follows:

● Remove or shrink the pituitary mass
● Restore GH secretory patterns to normal
● Restore serum total IGF-I and IGF binding protein 3 (IGFBP-3) levels
to normal
● Retain normal pituitary secretion of other hormones
● Prevent recurrence of disease

Surgery

Removing the tumor is the preferred treatment for gigantism if it’s the
underlying cause.

The surgeon will reach the tumor by making an incision in your child’s nose.
Microscopes or small cameras may be used to help the surgeon see the tumor in the
gland.

Medication

In some cases, surgery may not be an option. For example, if there’s a high
risk of injury to a critical blood vessel or nerve.

Your child’s doctor may recommend medication if surgery is not an option.

This treatment is meant to either shrink the tumor or stop the production of excess
growth hormone.

Your doctor may use the drugs octreotide or lanreotide to prevent the growth
hormone’s release. These drugs mimic another hormone that stops growth hormone
production. They’re usually given as an injection about once a month.
 Bromocriptine and cabergoline are drugs that can be used to lower growth
hormone levels. These are typically given in pill form. They may be used with
octreotide. Octreotide is a synthetic hormone that, when injected, can also lower the
levels of growth hormones and IGF-1.

In situations where these drugs are not helpful, daily shots of pegvisomant
might be used as well. Pegvisomant is a drug that blocks the effects of growth
hormones. This lowers the levels of IGF-1 in your child’s body.

Radiation Therapy

In general, radiation therapy is recommended if GH hypersecretion is not

normalized with surgery. Radiation prevents further growth of the tumor in more than
97% of patients after surgical resection. However, radiation treatment takes years to
reduce/normalize GH/IGF-I levels. About 60% of patients have a GH concentration of
less than 5 ng/mL 10 years after radiotherapy.

Medications

Somatostatin analogues

The most extensively studied and used somatostatin analogue, octreotide, binds
to the somatostatin receptor subtypes II and V, inhibiting GH secretion. They
decrease GH secretion from the pituitary tumor mediated through interactions
predominately with the somatostatin subtype receptor-2 (SSTR-2).

Dopamine-receptor agonists

Dopamine-receptor agonists (eg, bromocriptine, cabergoline) bind to pituitary

dopamine type 2 (D2) receptors and suppress GH secretion, although their precise
mechanism of action remains unclear. Dopamine-receptor agonists are generally
used as adjuvant medical treatments for GH excess, and their effectiveness may be
added to that of octreotide.
 · Bromocriptine

Bromocriptine has an adjunctive role in the treatment of patients with GH excess

who fail to achieve a cure by surgical treatment or who are to be treated with
radiation. Shrinkage in tumor size also occurs, albeit in fewer than 20% of patients.
Patients in whom prolactin is elevated are more likely to have a favorable response
to bromocriptine.

· Cabergoline

Cabergoline, another dopamine-receptor agonist, is somewhat more effective than

bromocriptine in reducing GH levels, with response rates of 46%. In those cases in
which a somatostatin analogue has failed to control acromegaly, cabergoline
adjunction normalized IGF-I levels in about 50% of cases.

GH-receptor antagonists

Tests of pegvisomant (Somavert), a novel hepatic GH-receptor antagonist,

demonstrated effective suppression of GH and IGF-I levels in patients with
acromegaly due to pituitary tumors or ectopic GHRH hypersecretion. However,
pegvisomant does not have direct antiproliferative effects on the underlying pituitary
adenoma.

Combination therapy with pegvisomant and cabergoline or somatostatin

analogues is also being investigated for efficacy.
 DWARFISM

Dwarfism is short stature that results from a genetic or medical condition.

Dwarfism is generally defined as an adult height of 4 feet 10 inches (147
centimeters) or less. The average adult height among people with dwarfism is 4 feet
(122 cm).

Many different medical conditions cause dwarfism. In general, the disorders

are divided into two broad categories:

● Disproportionate dwarfism. If body size is disproportionate, some parts

of the body are small, and others are of average size or above-average
size. Disorders causing disproportionate dwarfism inhibit the
development of bones.
● Proportionate dwarfism. A body is proportionately small if all parts of
the body are small to the same degree and appear to be proportioned
like a body of average stature. Medical conditions present at birth or
appearing in early childhood limit overall growth and development.

Some people prefer the term "short stature" or "little people" rather than
"dwarf" or "dwarfism." So it's important to be sensitive to the preference of someone
who has this disorder. Short stature disorders do not include familial short stature —
short height that's considered a normal variation with normal bone development.

Signs and Symptoms

Disproportionate Dwarfism

The most common cause of dwarfism is a disorder called achondroplasia,

which causes disproportionately short stature. This disorder usually results in the
following:

● An average-size trunk
● Short arms and legs, with particularly short upper arms and upper legs
 ● Short fingers, often with a wide separation between the middle and ring
fingers
● Limited mobility at the elbows
● A disproportionately large head, with a prominent forehead and a
flattened bridge of the nose
● Progressive development of bowed legs
● Progressive development of swayed lower back
● An adult height around 4 feet (122 cm)

Another cause of disproportionate dwarfism is a rare disorder called

spondyloepiphyseal dysplasia congenita (SEDC). Signs may include:

● A very short trunk

● A short neck
● Shortened arms and legs
● Average-size hands and feet
● Broad, rounded chest
● Slightly flattened cheekbones
● Opening in the roof of the mouth (cleft palate)
● Hip deformities that result in thighbones turning inward
● A foot that's twisted or out of shape
● Instability of the neck bones
● Progressive hunching curvature of the upper spine
● Progressive development of swayed lower back
● Vision and hearing problems
● Arthritis and problems with joint movement
● Adult height ranging from 3 feet (91 cm) to just over 4 feet (122 cm)

Proportionate dwarfism

Proportionate dwarfism results from medical conditions present at birth or

appearing in early childhood that limit overall growth and development. So the head,
trunk and limbs are all small, but they're proportionate to each other. Because these
disorders affect overall growth, many of them result in poor development of one or
more body systems.

Growth hormone deficiency is a relatively common cause of proportionate

dwarfism. It occurs when the pituitary gland fails to produce an adequate supply of
growth hormone, which is essential for normal childhood growth. Signs include:

● Height below the third percentile on standard pediatric growth charts

● Growth rate slower than expected for age
● Delayed or no sexual development during the teen years

Pathophysiology
Diagnostic Examination

· Measurements. A regular part of a well-baby medical exam is the

measurement of height, weight and head circumference. At each
visit, your pediatrician will plot these measurements on a chart to
show your child's current percentile ranking for each one. This is
important for identifying abnormal growth, such as delayed growth or
a disproportionately large head. If any trends in these charts are a
concern, your pediatrician may make more-frequent measurements.

· Appearance. Many distinct facial and skeletal features are associated

with each of several dwarfism disorders. Your child's appearance
also may help your pediatrician to make a diagnosis.

· Imaging technology. Your doctor may order imaging studies, such as

X-rays, because certain abnormalities of the skull and skeleton can
indicate which disorder your child may have. Various imaging devices
may also reveal delayed maturation of bones, as is the case in
growth hormone deficiency. A magnetic resonance imaging (MRI)
scan may reveal abnormalities of the pituitary gland or hypothalamus,
both of which play a role in hormone function.

· Genetic tests. Genetic tests are available for many of the known
causal genes of dwarfism-related disorders, but these tests often
aren't necessary to make an accurate diagnosis. Your doctor is likely
to suggest a test only to distinguish among possible diagnoses when
other evidence is unclear or as a part of further family planning. If
your pediatrician believes your daughter may have Turner syndrome,
then a special lab test may be done that assesses the X
chromosomes extracted from blood cells.

· Family history. Your pediatrician may take a history of stature in

siblings, parents, grandparents or other relatives to help determine
 whether the average range of height in your family includes short
stature.

· Hormone tests. Your doctor may order tests that assess levels of
growth hormone or other hormones that are critical for childhood
growth and development.

Medical Treatment

Hormone therapy

For people with growth hormone deficiency, injections of synthetic human growth
hormone may be helpful. Children receiving this treatment don’t always reach an
average height, but they can get close.

The treatment includes daily injections when a child is young, though injections may
continue into a person’s 20s. This may be done if there are concerns about full adult
maturation and sufficient muscle and fat.

Girls with Turner’s syndrome need estrogen therapy and other hormones to help
trigger puberty and appropriate female development. Estrogen therapy may be
necessary until a woman reaches the age of menopause.

Surgical options

For others with dwarfism, surgical treatments may be necessary and helpful to living
a longer, healthier life.

Surgical treatments include those that can help:

· correct the direction of bone growth

· stabilize the spine

 · increase the channel in the vertebrae surrounding the spinal cord to relieve
pressure on the spinal cord

Another surgical procedure for people with excess fluid around the brain is to place a
type of tube, called a shunt, in the brain. This can relieve some of that fluid and
reduce pressure on the brain.

Physical therapy and orthotics

Physical therapy and orthotics are noninvasive solutions to some

complications of dwarfism. Physical therapy is often prescribed after limb or back
surgery to help you regain or improve your range of motion and strength. Physical
therapy may also be advised if dwarfism is affecting the way you walk or is causing
you pain that doesn’t require surgery.

Orthotics are custom-made devices that fit into your shoes to help improve your foot
health and function. If dwarfism is affecting your balance, how you walk, or other
aspects of foot function, talk with a podiatrist about how orthotics may help you.

Medications

Growth hormone replacement therapy can be administered if the child is

lacking growth hormone. A pediatric endocrinologist, a doctor specializing in the
hormones of children, administers this type of therapy before a child's bone growth
plates have fused or joined. Once the growth plates have fused, GH replacement
therapy is rarely effective.
 DIABETES INSIPIDUS

Diabetes insipidus is a rare condition that causes your body to make a lot of
urine that is "insipid," or colorless and odorless. Most people pee out 1 to 2 quarts a
day. People with diabetes insipidus can pass between 3 and 20 quarts a day. It's
also called central DI, pituitary DI, hypothalamic DI, neurohypophyseal DI, or
neurogenic DI.

Diabetes insipidus (DI) is defined as the passage of large volumes (>3 L/24
hr) of dilute urine (< 300 mOsm/kg). It has the following 2 major forms:
● Central (neurogenic, pituitary, or neurohypophyseal) DI, characterized by
decreased secretion of antidiuretic hormone (ADH; also referred to as
arginine vasopressin [AVP])
● Nephrogenic DI, characterized by decreased ability to concentrate urine
because of resistance to ADH action in the kidney.

Signs and Symptoms

The predominant manifestations of DI are as follows:
● Polyuria - The daily urine volume is relatively constant for each patient
but is highly variable between patients (3-20 L)
● Polydipsia
● Nocturia
The most common form is central DI after trauma or surgery to the region of the
pituitary and hypothalamus, which may exhibit 1 of the following 3 patterns:
● Transient
● Permanent
● Triphasic (observed more often clinically)
In infants with DI, the most apparent signs may be the following:
● Crying
● Irritability
● Growth retardation
 ● Hyperthermia
● Weight loss
In children, the following manifestations typically predominate:
● Enuresis
● Anorexia
● Linear growth defects
● Fatigability

Pathophysiology

Diagnostic Examination

The will do a physical exam. A checkup may not show any signs of central DI, except
maybe an enlarged bladder or symptoms of dehydration.

They’ll ask questions about health history, including family’s health and a series of
tests that include:
 · Urinalysis. sample of your urine, and the doctor will send it to a lab to see
whether it’s dilute or concentrated. They can also check for glucose, which
can help them decide if you have diabetes insipidus or diabetes mellitus.
You might need to collect your pee over a 24-hour period to see how much
you’re putting out.

· Blood test. This will measure the electrolytes and glucose in the blood. This
lets the doctor know if you have diabetes mellitus or diabetes insipidus. It
may help them figure out which type.

· Fluid deprivation test. This measures the changes in your body weight,
blood sodium, and urine concentration after you don’t drink anything for a
while. There are two types:

o Short-form fluid deprivation test. You stop drinking for a short time.
You collect a sample and take it back to your doctor, who sends it
to a lab.

o Formal fluid deprivation test. You’ll have this done in a hospital so

doctors can make sure you don’t get dehydrated. You’ll be weighed
and give a sample every hour or two until:

§ Your blood pressure drops too low or you have a rapid

heartbeat when you stand

§ You lose 5% or more of your starting body weight

§ Your urine concentration goes up a little bit over two or three

measurements

· MRI. This test takes detailed pictures of your internal organs and soft
tissues. The doctor uses it to see if there’s a problem with your
hypothalamus or pituitary gland.

· Genetic screening. Your doctor may suggest this test if your family
members have had problems with making too much urine.

Medical Treatment

● Central diabetes insipidus. If you have mild diabetes insipidus, you may
need only to increase your water intake. If the condition is caused by an
 abnormality in the pituitary gland or hypothalamus (such as a tumor), your
doctor will first treat the abnormality.

Typically, this form is treated with a synthetic hormone called desmopressin

(DDAVP, Nocdurna). This medication replaces the missing anti-diuretic
hormone (ADH) and decreases urination. You can take desmopressin in a
tablet, as a nasal spray or by injection.

Most people still make some ADH, though the amount can vary day to day. So,
the amount of desmopressin you need also may vary. Taking more
desmopressin than you need can cause water retention and potentially serious
low-sodium levels in the blood.

Other medications might also be prescribed, such as chlorpropamide. This can

make ADH more available in the body.

● Nephrogenic diabetes insipidus. Since the kidneys don't properly respond

to ADH in this form of diabetes insipidus, desmopressin won't help. Instead,
your doctor may prescribe a low-salt diet to reduce the amount of urine your
kidneys make. You'll also need to drink enough water to avoid dehydration.

Treatment with the drug hydrochlorothiazide (Microzide) may improve your

symptoms. Although hydrochlorothiazide is a type of drug that usually increases
urine output (diuretic), it can reduce urine output for some people with
nephrogenic diabetes insipidus.

If your symptoms are due to medications you're taking, stopping these

medicines may help. However, don't stop taking any medication without first
talking to your doctor.

● Gestational diabetes insipidus. Treatment for most people with gestational

diabetes insipidus is with the synthetic hormone desmopressin.
● Primary polydipsia. There is no specific treatment for this form of diabetes
insipidus, other than decreasing fluid intake. If the condition is related to a
mental illness, treating the mental illness may relieve the diabetes insipidus
symptoms.
Medications
· Desmopressin (drug of choice for central DI)
· Synthetic vasopressin
· Chlorpropamide
· Carbamazepine (rarely used; employed only when all other measures
prove unsatisfactory)
· Clofibrate (no longer on the US market)
· Thiazides
· Nonsteroidal anti-inflammatory drugs (NSAIDs), such as indomethacin
(may be used in nephrogenic DI, but only when no better options
exist)
 ENDEMIC (IODINE-DEFICIENT) GOITER

The most common type of goiter, once encountered chiefly in geographic

regions where the natural supply of iodine is deficient is the so-called simple or
colloid goiter. In addition to being caused by an iodine deficiency, simple goiter may
be caused by an intake of large quantities of goitrogenic substances in patients with
unusually susceptible glands. These substances include excessive amounts of
iodine or lithium, which is used in treating bipolar disorders.

Simple goiter represents a compensatory hypertrophy of the thyroid gland,

caused by stimulation by the pituitary gland. The pituitary gland produces thyrotropin
or TSH, a hormone that controls the release of thyroid hormone from the thyroid
gland. Its production increases if there is subnormal thyroid activity, as when
insufficient iodine is available for production of the thyroid hormone. Such goiters
usually cause no symptoms, except for the swelling in the neck, which may result in
tracheal compression when excessive.

Many goiters of this type recede after the iodine imbalance is corrected.
Supplementary iodine, such as SSKI, is prescribed to suppress the pituitary’s
thyroid-stimulating activity. When surgery is recommended, the risk of postoperative
complications is minimized by ensuring a preoperative euthyroid state through
treatment with antithyroid medications and iodide to reduce the size and vascularity
of the goiter.

Providing children in iodine-poor regions with iodine compounds can prevent

simple or endemic goiter. Although the introduction of iodized salt has been the
single most effective means of preventing goiter in at-risk populations, the World
Health Organization (2007) is exploring alternative strategies to ensure iodine intake
because of the health risks associated with excessive salt intake.

Nodular Goiter
 Some thyroid glands are nodular because of areas of hyperplasia
(overgrowth). No symptoms may arise as a result of this condition, but not
uncommonly these nodules slowly increase in size, with some descending into the
thorax, where they cause local pressure symptoms. Some nodules become
malignant, and some are associated with a hyperthyroid state. Therefore, the patient
with many thyroid nodules may eventually require surgery.

Thyroid Cancer

Cancer of the thyroid is much less prevalent than other forms of cancer;
however, it accounts for 90% of endocrine malignancies. There are several types of
cancer of the thyroid gland; the type determines the course and prognosis. External
radiation of the head, neck, or chest in infancy and childhood increases the risk of
thyroid carcinoma. The incidence of thyroid cancer appears to increase 5 to 40 years
after irradiation. Consequently, people who underwent radiation treatment or were
otherwise exposed to radiation as children should consult a physician, request an
isotope thyroid scan as part of the evaluation, follow recommended treatment of
abnormalities of the gland, and continue with annual checkups.

Symptoms

Not all goiters cause signs and symptoms. When signs and symptoms do
occur they may include:

● A swelling at the base of your neck that may be particularly obvious

when you shave or put on makeup
● A tight feeling in your throat
● Coughing
● Hoarseness
● Difficulty swallowing
● Difficulty breathing

Assessment and Diagnostic Findings

Lesions that are single, hard, and fixed on palpation or associated with
cervical lymphadenopathy suggest malignancy. Thyroid function tests may be helpful
in evaluating thyroid nodules and masses; however, results are rarely conclusive.
Needle biopsy of the thyroid gland is used as an outpatient procedure to make a
diagnosis of thyroid cancer, to differentiate cancerous thyroid nodules from
noncancerous nodules, and to stage the cancer if detected. The procedure is safe
and usually requires only a local anesthetic agent. However, patients who undergo
the procedure are monitored closely, because cancerous tissues may be missed
during the procedure. A second type of aspiration or biopsy uses a large-bore needle
rather than the fine needle used in standard biopsy; it may be used when the results
of the standard biopsy are inconclusive or with rapidly growing tumors. Additional
diagnostic studies include ultrasound, MRI, CT, thyroid scans, radioactive iodine
uptake studies, and thyroid suppression tests.

Pathophysiology

Medical Management

The treatment of choice for thyroid carcinoma is surgical removal. Total or

near-total thyroidectomy is performed if possible. Modified neck dissection or more
extensive radical neck dissection is performed if there is lymph node involvement.
Efforts are made to spare parathyroid tissue to reduce the risk of postoperative
hypocalcemia and tetany. After surgery, ablation procedures are carried out with
radioactive iodine to eradicate residual thyroid tissue if the tumor is radiosensitive.
Radioactive iodine also maximizes the chance of discovering thyroid metastasis at a
later date if total-body scans are carried out. After surgery, thyroid hormone is
administered in suppressive doses to lower the levels of TSH to a euthyroid state
(Cooper, et al., 2006).

If the remaining thyroid tissue is inadequate to produce sufficient thyroid

hormone, thyroxine is required permanently Several routes are available for
administering radiation to the thyroid or tissues of the neck, including oral
administration of radioactive iodine and external administration of radiation therapy.
The patient who receives external sources of radiation therapy is at risk for
mucositis, dryness of the mouth, dysphagia, redness of the skin, anorexia, and
fatigue.

Chemotherapy is infrequently used to treat thyroid cancer. Patients whose

thyroid cancer is detected early and who are appropriately treated usually do very
well. Patients who have had papillary cancer, the most common and least
aggressive tumor, have a 10-year survival rate greater than 90%. Long-term survival
is also common in follicular cancer, a more aggressive form of thyroid cancer
(Tierney, et al., 2005). However, continued thyroid hormone therapy and periodic
follow-up and diagnostic testing are important to ensure the patient’s well-being
(Cooper, et al., 2006).

Postoperatively, the patient is instructed to take exogenous thyroid hormone

to prevent hypothyroidism. Later follow-up includes clinical assessment for
recurrence of nodules or masses in the neck and signs of hoarseness, dysphagia, or
dyspnea. Total-body scans are performed 2 to 4 months after surgery to detect
residual thyroid tissue or metastatic disease. Thyroid hormones are stopped for
about 6 weeks before the tests. Care must be taken to avoid iodine-containing foods
and contrast agents. A repeat scan is performed 1 year after the initial surgery. If
measurements are stable, a final scan is obtained in 3 to 5 years. Free T4, TSH, and
serum calcium and phosphorus levels are monitored to determine whether the
thyroid hormone supplementation is adequate and to note whether calcium balance
is maintained.

Although local and systemic reactions to radiation may occur and may include
neutropenia or thrombocytopenia, these complications are rare when radioactive
iodine is used. Patients who undergo surgery that is combined with radioactive
iodine have a higher survival rate than those who undergo surgery alone. Patient
teaching emphasizes the importance of taking prescribed medications and following
recommendations for follow-up monitoring. The patient who is undergoing radiation
therapy is also instructed in how to assess and manage side effects of treatment.

Nursing Management

Important preoperative goals are to gain the patient’s confidence and reduce
anxiety. Often, the patient’s home life has become tense because of his or her
restlessness, irritability, and nervousness secondary to hyperthyroidism. Efforts are
necessary to protect the patient from such tension and stress to avoid precipitating
thyroid storm. If the patient reports increased stress when with family or friends,
suggestions are made to limit contact with them. Quiet and relaxing forms of
recreation or occupational therapy may be helpful.

Providing Preoperative Care

The nurse instructs the patient about the importance of eating a diet high in
carbohydrates and proteins. A high daily caloric intake is necessary because of the
increased metabolic activity and rapid depletion of glycogen reserves.
Supplementary vitamins, particularly thiamine and ascorbic acid, may be prescribed.
The patient is reminded to avoid tea, coffee, cola, and other stimulants. The nurse
also informs the patient about the purpose of preoperative tests, if they are to be
performed, and explains what preoperative preparations to expect. This information
should help to reduce the patient’s anxiety about the surgery. In addition, special
efforts are made to ensure a good night’s rest before surgery, although many
patients are admitted to the hospital on the day of surgery. Preoperative teaching
includes demonstrating to the patient how to support the neck with the hands after
surgery to prevent stress on the incision. This involves raising the elbows and
placing the hands behind the neck to provide support and reduce strain and tension
on the neck muscles and the surgical incision.

Providing Postoperative Care

 The nurse periodically assesses the surgical dressings and reinforces them if
necessary. When the patient is in a recumbent position, the nurse observes the
sides and the back of the neck as well as the anterior dressing for bleeding. In
addition to monitoring the pulse and blood pressure for any indication of internal
bleeding, it is important to be alert for complaints of a sensation of pressure or
fullness at the incision site. Such symptoms may indicate subcutaneous hemorrhage
and hematoma formation and should be reported. Difficulty in respiration can occur
as a result of edema of the glottis, hematoma formation, or injury to the recurrent
laryngeal nerve. This complication requires that an airway be inserted.

Therefore, a tracheostomy set is kept at the bedside at all times, and the
surgeon is summoned at the first indication of respiratory distress. If the respiratory
distress is caused by hematoma, surgical evacuation is required. The intensity of
pain is assessed, and analgesic agents are administered as prescribed for pain. The
nurse should anticipate apprehension in the patient and should inform the patient
that oxygen will assist breathing. When moving and turning the patient, the nurse
carefully supports the patient’s head and avoids tension on the sutures.

The most comfortable position is the semi-Fowler’s position, with the head
elevated and supported by pillows. IV fluids are administered during the immediate
postoperative period. Water may be given by mouth as soon as nausea subsides.
Usually, there is a little difficulty in swallowing; initially, cold fluids and ice may be
taken better than other fluids. Often, patients prefer a soft diet to a liquid diet in the
immediate postoperative period. The patient is advised to talk as little as possible to
reduce edema to the vocal cords; however, when the patient does speak, any voice
changes are noted, which might indicate injury to the recurrent laryngeal nerve,
which lies just behind the thyroid next to the trachea.

An overbed table is provided for access to frequently used items so the

patient avoids turning his or her head. The table can also be used to support a
humidifier when vapor-mist inhalations are prescribed for the relief of excessive
mucus accumulation.

The patient is usually permitted out of bed as soon as possible and is

encouraged to eat foods that are easily swallowed. A high-calorie diet may be
prescribed to promote weight gain. Sutures or skin clips are usually removed on the
second day. The patient is usually discharged from the hospital on the day of surgery
or soon afterward if the postoperative course is uncomplicated.

RICKETS

Rickets is the softening and weakening of bones in children, usually because

of an extreme and prolonged vitamin D deficiency. Rare inherited problems also can
cause rickets.

Vitamin D helps a child's body absorb calcium and phosphorus from food. Not
enough vitamin D makes it difficult to maintain proper calcium and phosphorus levels
in bones, which can cause rickets.

Adding vitamin D or calcium to the diet generally corrects the bone problems
associated with rickets. When rickets is due to another underlying medical problem,
children may need additional medications or other treatment. Some skeletal
deformities caused by rickets may require corrective surgery.

Rare inherited disorders related to low levels of phosphorus, the other mineral
component in bone, may require other medications.

Pathophysiology
● The primary defect in osteomalacia is a deficiency of activated vitamin D
(calcitriol), which promotes calcium absorption from the gastrointestinal tract
and facilitates mineralization of bone.
● Gastrointestinal disorders (eg, celiac disease, chronic biliary tract obstruction,
chronic pancreatitis, small bowel resection), fats are inadequately absorbed
and produce osteomalacia through loss of vitamin D (along with other fat-
soluble vitamins) and calcium, the latter being excreted in the feces with fatty
acids.
● Liver and kidney diseases also can result to a lack of vitamin D as these are
the organs that convert vitamin D to its active form.
● Hyperparathyroidism leads to skeletal decalcification and thus to
osteomalacia by increasing phosphate excretion in the urine.
● Prolonged use also of antiseizure medication (eg, phenytoin [Dilantin],
phenobarbital) poses a risk of osteomalacia, as well as insufficient vitamin D
(dietary, sunlight).
● In addition, malnutrition (deficiency in vitamin D often associated with poor
intake of calcium) is a result of poverty, poor dietary habits, and lack of
knowledge about nutrition.
 ● Without adequate vitamin D, calcium and phosphate are not moved to
calcification sites in bones.
● As a result of calcium deficiency, muscle weakness, and unsteadiness,
increased risk for falls and fractures, particularly pathologic fractures of the
distal radius and the proximal femur.
● Moreover, with faulty mineralization there is softening and weakening of the
skeleton, causing pain, tenderness to touch, bowing of the bones, and
pathologic fractures.

Symptoms

Signs and symptoms of rickets can include:

● Delayed growth
● Delayed motor skills
● Pain in the spine, pelvis and legs
● Muscle weakness

Because rickets softens the areas of growing tissue at the ends of a child's bones
(growth plates), it can cause skeletal deformities such as:

● Bowed legs or knock knees

● Thickened wrists and ankles
● Breastbone projection

Causes

Patient’s or a child's body needs vitamin D to absorb calcium and phosphorus

from food. Rickets can occur if the child's body doesn't get enough vitamin D or if his
or her body has problems using vitamin D properly. Occasionally, not getting enough
calcium or lack of calcium and vitamin D can cause rickets.

● Lack of vitamin D

Children who don't get enough vitamin D from these two sources can develop a
deficiency:

● Sunlight
A child's skin produces vitamin D when it's exposed to sunlight. But children in
developed countries tend to spend less time outdoors. They're also more likely to
use sunscreen, which blocks the sun's rays that trigger the skin's production of
vitamin D.

● Food

Fish oil, egg yolks and fatty fish such as salmon and mackerel contain vitamin D.
Vitamin D has also been added to some foods and beverages, such as milk, cereal
and some fruit juices.

● Problems with absorption

Some children are born with or develop medical conditions that affect the way their
bodies absorb vitamin D. Some examples include:

● Celiac disease
● Inflammatory bowel disease
● Cystic fibrosis
● Kidney problems
● Risk factors

Factors that can increase a child's risk of rickets include:

● Dark skin. Dark skin has more of the pigment melanin, which lowers the skin's
ability to produce vitamin D from sunlight.
● Mother's vitamin D deficiency during pregnancy. A baby born to a mother with
severe vitamin D deficiency can be born with signs of rickets or develop them
within a few months after birth.
● Northern latitudes. Children who live in geographical locations where there is
less sunshine are at higher risk of rickets.
● Premature birth. Babies born before their due dates tend have lower levels of
vitamin D because they had less time to receive the vitamin from their
mothers in the womb.
 ● Medications. Certain types of anti-seizure medications and antiretroviral
medications, used to treat HIV infections, appear to interfere with the body's
ability to use vitamin D.
● Exclusive breast-feeding. Breast milk doesn't contain enough vitamin D to
prevent rickets. Babies who are exclusively breast-fed should receive vitamin
D drops.

Complications

● Left untreated, rickets can lead to:

● Failure to grow
● An abnormally curved spine
● Bone deformities
● Dental defects
● Seizures

Prevention

Exposure to sunlight provides the best source of vitamin D. During most

seasons, 10 to 15 minutes of exposure to the sun near midday is enough. However,
if you're dark-skinned, if it's winter or if you live in northern latitudes, you might not be
able to get enough vitamin D from sun exposure.

In addition, because of skin cancer concerns, infants and young children, especially,
are warned to avoid direct sun or to always wear sunscreen and protective clothing.

To prevent rickets, make sure the child eats foods that contain vitamin D naturally —
fatty fish such as salmon and tuna, fish oil and egg yolks — or that have been
fortified with vitamin D, such as:

● Infant formula
● Cereal
● Bread
● Milk, but not foods made from milk, such as some yogurts and cheese
● Orange juice

Diagnostic Examinations
 The doctor may be able to diagnose rickets by performing a physical
examination. They will check for tenderness or pain in the bones by lightly pressing
on them. Your doctor may also order certain tests to help make a rickets diagnosis,
including:

● blood tests to measure the levels of calcium and phosphate in the

blood
● bone X-rays to check for bone deformities
● In rare cases, a bone biopsy will be performed. This involves the
removal of a very small section of bone, which will be sent to a
laboratory for analysis.

Treatment

Treatment for rickets focuses on replacing the missing vitamin or mineral in

the body. This will eliminate most of the symptoms associated with rickets. If your
child has a vitamin D deficiency, your doctor will likely want them to increase their
exposure to sunlight, if possible. They will also encourage them to consume food
products high in vitamin D, such as fish, liver, milk, and eggs.

Calcium and vitamin D supplements can also be used to treat rickets. Ask the doctor
about the correct dosage, as it can vary based on the size of the child. Too much
vitamin D or calcium can be unsafe.

If skeletal deformities are present, a child may need braces to position their bones
correctly as they grow. In severe cases, the child may need corrective surgery.

For hereditary rickets, a combination of phosphate supplements and high levels of a

special form of vitamin D are required to treat the disease.
 GYNECOMASTIA

Gynecomastia is a condition that makes breast tissue swell in boys and men.
It can happen when the balance of two hormones in the body is thrown off. If breasts
enlarge because of fat deposits, this is a different condition called
"pseudogynecomastia."

Although breasts don't develop in men the way they do in women, all boys are
born with a small amount of breast tissue. Boys' bodies mostly make a hormone
called testosterone, which guides their sexual growth during puberty. But males also
make some estrogen--the hormone that steers sexual growth in girls.
 When a boy is going through puberty, or when an older man's body makes
less testosterone, the balance of the two hormones changes. Sometimes when that
happens, a higher percentage of estrogen causes male breast tissue to swell. About
half of adolescent boys and as many as two-thirds of men older than 50 will have this
to some degree.

Pathophysiology

● Gynecomastia results from an altered estrogen-androgen balance, in favor of

estrogen, or from increased breast sensitivity to a normal circulating estrogen
level.
● The imbalance is between the stimulatory effect of estrogen and the inhibitory
effect of androgen.
● Estrogens are known to stimulate the growth of breast tissue, whereas
androgens inhibit it; most cases of gynaecomastia result from deficient
androgen action or excessive estrogen action in the breast tissue.
● Estrogens induce ductal epithelial hyperplasia, ductal elongation and
branching, proliferation of the periductal fibroblasts, and an increase in
vascularity.
● Estrogen production in males results mainly from the peripheral conversion of
androgens (testosterone and androstenedione) to estradiol and estrone,
which occurs through the action of the enzyme aromatase (mainly in muscle,
skin, and adipose tissue).
● The testes secrete only 6-10 mg of estradiol and 2.5 mg of estrone per day.
Since this only comprises a small fraction of estrogens in circulation (ie, 15%
of estradiol and 5% of estrone), the remainder of estrogen in males is derived
from the extraglandular aromatization of testosterone and androstenedione to
estradiol and estrone.
● Thus, any cause of estrogen excess from overproduction to peripheral
aromatization of androgens can initiate the cascade to breast development.
Symptoms

● The first sign of gynecomastia may be a lump of fatty tissue under the nipple.
Sometimes this lump is tender or sore.
● This might make patients worry that they have breast cancer, which does
occur in a small number of men. Gynecomastia is not necessarily a sign of
cancer, but doctors may run some tests first to rule it out.
 ● Swelling of the breasts may happen unevenly, with one becoming larger than
the other. One may also have breast tenderness.
● Patient should see a doctor if they notice that their breasts have swelling, are
painful or tender, or there is a discharge from the nipple of one or both
breasts.

Causes

A lot of things can trigger the hormone imbalance that causes male breast
growth, and many times the exact cause isn't known.

In addition to body changes such as puberty and aging, some things that can cause
gynecomastia are:

● Injury or diseases that affect the testicles, which make testosterone

● Thyroid problems, since hormones from that gland control growth and
sexual development
● Some cancers, including tumors of the lungs, pituitary gland, or adrenal
glands
● Obesity, which can result in more estrogen
● Illegal drugs, including anabolic steroids, marijuana, and heroin
● Kidney failure (when they can no longer clean and filter your blood)
● Liver disease

Diagnostic Examinations

If doctors suspect gynecomastia, they will examine patients to make sure

there are no hard lumps, oozing fluid, or skin problems that could be signs of cancer.

They will also likely ask patients questions about their medical history that might
include:

● Have you had illnesses such as mumps, kidney ailments, or liver

disease?
● What drugs have you taken -- legal or illegal?
● You might also be given tests. They could include:
● Blood tests or urine samples
 ● Mammogram
● Biopsy
● CT scans
● MRI scans
● Testicular ultrasounds
● Gynecomastia Treatment

Most cases slowly get better on their own without treatment. When someone
has gynecomastia, doctors might refer the patient to a specialist known as an
endocrinologist, who treats problems related to hormones and how they affect the
body.

Treatment depends on the age, health, how long the condition may last, and
how well the body responds to certain drugs. If gynecomastia happens during
puberty, it usually goes away on its own. This might take anywhere from 6 months to
3 years. If it turns out that the patient’s hormones are out of balance because of
another health problem, the priority is to treat that underlying condition. Patients will
be given medication to address the hormone imbalance that's causing breast growth.

In some cases, patient might need surgery, and doctors may recommend techniques
such as:

● Liposuction (removal of extra breast fat)

● Mastectomy (removal of breast gland tissue)

Prevention

There are steps that patients can take to lower their chances of having
gynecomastia. They include things such as:

● Avoiding the use of illicit or recreational drugs, such as anabolic

steroids, androgens, amphetamines, marijuana, or heroin.
● Avoid drinking alcohol, or drinking moderately.
● Go over their medicine list with doctors. If any of the medications can
cause gynecomastia, doctors will provide alternatives.
 HYPOTHYROIDISM

Hypothyroidism is a condition that results from suboptimal levels of thyroid

hormone. The thyroid gland is not able to produce thyroid hormone. Thyroid
hormones control the way the body uses energy, thus affecting nearly every organ in
your body, even the way your heart beats. This results in many body functions
slowing down.
Signs and Symptoms

Early signs are nonspecific. It includes the following:

● Fatigue, which may hinder individual to complete daily task

● Hair loss
● Brittle nails
● Dry skin
● Numbness and tingling of finger
● Husky and hoarseness of voice
● Menstrual disturbance, such as menorrhea or amenorrhea
● Loss of libido

Severe hypothyroidism results to the following signs and symptoms:

● Subnormal temperature and pulse rate

● Weight gain without increase in food intake
● Skin becomes thickened (myxedema)
● Hair loss
● Emotionless and masklike expression
● Complaints of being cold in warm environment
● Complaints of constipation
● Deafness
● Slow speech, enlarge tongue, and hands and feet increase in
size

Associated with the following:

o Elevated serum cholesterol level

o Atherosclerosis

o Coronary artery disease

o Poor left ventricular function

Advanced hypothyroidism may produce the following:

 ● Personality and cognitive changes characteristic of dementia
● Hypothermic
● Abnormal sensitivity to sedatives, opioids, and anesthetic agents.
Administer with extreme caution

Myxedema coma- most extreme, severe stage of hypothyroidism in which patient is

hypothermic and unconscious

Pathophysiology

● Hypothyroidism can be classified as primary or secondary

● Primary hypothyroidism is caused by destruction of thyroid tissue or
defective hormone synthesis.
● Secondary hypothyroidism is caused by pituitary disease with
decreased TSH secretion of hypothalamic dysfunction with decreased
thyrotropin releasing hormone (TRH) secretion.
● Hypothyroidism may also be transient and related to thyroiditis or
discontinuance of thyroid hormone therapy.
● Iodine deficiency is the most common cause of hypothyroidism
worldwide.
● The manifestations of hypothyroidism are the result of decreased
metabolism from low levels of thyroid hormones.
● This lowered metabolism causes the hypothalamus and anterior
pituitary gland to make stimulatory hormones, especially thyroid-
stimulating hormone (TSH), in an attempt to trigger hormone release
from the poorly responsive thyroid gland.
● The TSH binds to thyroid cells and causes the thyroid gland to enlarge,
forming a goiter, although thyroid hormone production does not
increase.
● Cellular energy is decreased, and metabolites that are compounds of
proteins and sugars called glycosaminoglycans build up inside cells;
this buildup increases the mucus and water, forms cellular edema, and
changes organ texture. The edema is mucinous (called myxedema),
 rather than edema caused by water alone, and changes the patient’s
appearance.
● Non pitting edema forms everywhere, especially around the eyes, in
the hands and feet, and between the shoulder blades.
● The tongue thickens, and edema forms in the larynx, making the voice
husky.
● All general physiologic function is decreased.
● The decreased metabolism causes the heart muscle to become flabby
and the chamber size to increase.
● The result is decreased cardiac output and decreased perfusion to the
brain and other vital organs.
● The decreased perfusion makes the already slowed cellular
metabolism worse, resulting eventually in tissue and organ failure.

Diagnostic Examination
 In addition to physical examination, laboratory and diagnostic studies are
performed to detect thyroid disorders. These includes the following:

Thyroid Test

● Serum thyroid-stimulating hormone

- measures how much of the thyroid hormone thyroxine (T4) the

thyroid gland is being asked to make

- measurement of the serum TSH concentration is single best

screening test of thyroid function in outpatients because
of its high sensitivity

- it detects minute changes in serum TSH that makes it possible to

distinguish subclinical thyroid disease from euthyroid
disease in patient with low or high normal values

- greater than the normal value indicates hypothyroidism

Normal value: 0.4-6.15 µU/mL

● Serum Free T4

- Test commonly used to confirm abnormal TSH

- It is a direct measurement of free (unbound) thyroxine, the only

metabolically active fraction of T4

Normal value: 0.9-1.7 ng/dL (11.5-21.8 pmol/L)

Medical Intervention

The primary objective in the management of hypothyroidism is to restore a

normal metabolic state by replacing the missing hormone.

Medications
 ● Synthetic levothyroxine (Synthroid or Levothroid)

- a thyroid hormone medicine identical to a hormone a healthy

thyroid makes

- Usually prescribed in pill form, but also available as a liquid and

as a soft gel capsule

- Recommended taking in the morning before eating

● If angina or dysrhythmias occur, immediately discontinue thyroid

hormone
● Use cautiously with the following medications

- Insulin or antidiabetic agent, increases blood glucose level

- Phenytoin and tricyclic antidepressants, increases effects of

thyroid hormone

- Digitalis glycosides, anticoagulant agents, and

indomethacin, increases pharmacologic effects of these
drugs

- Sedative agents

Supportive Therapy

In severe hypothyroidism and myxedema coma, management includes

maintaining vital function.

● Monitor arterial blood gases to determine carbon dioxide retention and

to guide the use of assisted ventilation to combat hypoventilation
● Pulse oximetry to monitor oxygen saturation
● Administer fluid cautiously to avoid water intoxication
● Avoid application of external heat, increases oxygen requirement and
may lead to vascular collapse.
 ● If myxedema progresses, administer Levothyroxine intravenously until
consciousness is restored.

HYPERTHYROIDISM

Hyperthyroidism is a condition in which there is an excessive production of

thyroid hormones (thyroxine) of the thyroid glands. Hyperthyroidism can accelerate
your body's metabolism, causing unintentional weight loss and a rapid or irregular
heartbeat. Grave’s disease is the most common type of hyperthyroidism which
causes excessive output of thyroid hormones caused by abnormal stimulation of the
thyroid gland by circulating immunoglobulin.

Signs and Symptoms

Patients with well-developed hyperthyroidism exhibit a characteristic group of

signs and symptoms sometimes referred to as thyrotoxicosis. These includes the
following:

● Nervousness
● Hyper excitability, irritability, apprehensive
● Palpitations
● Rapid pulse, even at rest as well on exertion, ranging between 90 and
160 bpm
● Increase sensitivity to heat, perspire unusually freely
● Skin is flushed, characterize by salmon color, warm, soft, and moist
 ● Dry skin and diffuse pruritus in elderly
● Fine hand tremor
● Exophthalmos (bulging of eyes)
● Increase appetite
● Progressive weight loss
● Abnormal muscular fatigability and weakness
● Amenorrhea
● Changes in bowel function, especially more frequent bowel movements
● An enlarged thyroid gland (goiter), which may appear as a swelling at
the base of your neck
● Sinus tachycardia or dysrhythmias

Complications

● Osteoporosis
● Myocardial hypertrophy
● Heart failure

Pathophysiology

● Graves’ disease is an autoimmune disease of unknown etiology

characterized by diffuse thyroid enlargement and excessive thyroid
hormone secretion.
● In Graves’ disease the patient develops antibodies to the TSH
receptor.
● These antibodies attach to the receptors and stimulate the thyroid
gland to release T3, T4, or both.
● The excessive release of thyroid hormones leads to the clinical
manifestations associated with thyrotoxicosis.
● Excessive thyroid hormones stimulate most body systems, causing
hypermetabolism and increased sympathetic nervous system activity.
● Thyroid hormones stimulate the heart, increasing both heart rate and
stroke volume resulting in an increased cardiac output, systolic blood
pressure, and blood flow.
 ● Elevated thyroid hormone levels affect protein, lipid, and carbohydrate
metabolism.
● Protein synthesis (buildup) and degradation (breakdown) are
increased, but breakdown exceeds buildup, causing a net loss of body
protein known as a negative nitrogen balance.
● Glucose tolerance is decreased, and the patient has hyperglycemia
(elevated blood glucose levels).
● Fat metabolism is increased, and body fat decreases.
● This leads to weight loss and nutritional deficiency even if appetite is
increased due to hypermetabolism.

Diagnostic Examination

● History and physical examination

● Ophthalmic examination
● ECG
● Laboratory Test
 ❖ TSH levels, serum free T4
❖ Thyroid antibodies (e.g. Thyroid peroxidase antibody)
❖ Total serum T3 and T4
● Radioactive iodine uptake (RAIU)

Medical Intervention

The goal of management of hyperthyroidism is to block the adverse effects of

excessive thyroid hormone, suppress oversecretion of thyroid hormone, and prevent
complications. These include radioactive iodine therapy, surgery, antithyroid
medications, and beta adrenergic blockers.

Radioactive iodine

- The goal of radioactive iodine therapy ( 131I) is to destroy the

overactive thyroid cells.

- Radioactive isotope of iodine is concentrated in the thyroid

gland where it destroys thyroid cells without jeopardizing
other radiosensitive tissues.

Surgery

Thyroidectomy is indicated for individuals who have (1) a large goiter

causing tracheal compression, (2) been unresponsive to antithyroid therapy,
or (3) thyroid cancer. Surgery for treatment of hyperthyroidism is performed
soon after the thyroid function has returned to normal, about 4 to 6 weeks.

● Subtotal thyroidectomy is often the preferred surgical procedure

and involves the removal of a significant portion (90%) of the
thyroid gland.
● Endoscopic thyroidectomy is a minimally invasive procedure.
Several small incisions are made, and a scope is inserted.
Instruments are passed through the scope to remove thyroid
 tissue or nodules. It is an appropriate procedure for patients with
small nodules (less than 3 cm) and no evidence of malignancy.

Nutritional Therapy

With the increased metabolic rate in hyperthyroid patients, there is a

high potential for the patient to have a nutritional deficit.

● High-calorie diets (4000 to 5000 cal/day) may be ordered to

satisfy hunger, prevent tissue breakdown, and decrease weight
loss.

- Six full meals a day and snacks high in protein,

carbohydrates, minerals, and vitamins.

- Increase carbohydrate intake to compensate for increased

metabolism.

● Avoid highly seasoned and high-fiber foods because these

foods can further stimulate the already hyperactive GI tract.

Medications

● Propylthiouracil (PTU)
● Methimazole (Tapazole)

- These drugs inhibits the synthesis of thyroid hormones

- Indicated in Grave’s disease in young patient,

hyperthyroidism during pregnancy, and to achieve
euthyroid state before surgery or radiation therapy

- Effects of drug begins usually at 1 to 2 weeks, good results

at 4 to 8 weeks

● Iodine or Iodine compounds

- Potassium Iodide (KI)
- Lugol’s solution
- Saturated solution of potassium iodide (SSKI)
 - Used with other antithyroid drugs for the treatment of
thyrotoxicosis and preparing patients for thyroidectomy.

- Large doses rapidly inhibit synthesis of T 3 and T4 and block

the release into the circulation, but action does not last
long.

- Decreases vascularity of the thyroid gland, making surgery

safer and easier.

- Maximal effect is usually seen within 1 to 2 weeks.

● Beta adrenergic blockers

❖ Propanolol (Inderal)
❖ Atenolol (Tenormin) or metoprolol (Toprol)

- These drugs block the effects of the sympathetic nervous

system stimulation, thereby decreasing tachycardia,
nervousness, irritability, and tremors.

- Propranolol is usually administered with other antithyroid

agents.

- Atenolol is preferred to patient with asthma or heart

disease.
 CRETINISM

Cretinism refers to the congenital hypothyroidism or underactivity of thyroid

glands during early childhood leading to stunted growth and mental retardation. The
term cretin was derived from the French word chrétien, literally meaning “Christian”
or “Christ-like” as the diseased were mentally retarded and incapable of doing sin. It
is the Iodine deficiency disorder associated with insufficient thyroid hormone activity
occurring during fetal, infant or childhood phases.

Types of Cretinism

● Congenital Cretinism

· Incidence is 1:3000 to 1:4000 in an iodine-deficient endemic area.

· It can be caused due to a defect in the genes encoding various

enzymes involved in thyroid hormone synthesis such as
thyroglobulin, iodotyrosine deiodinase and also thyroid-stimulating
hormone (TSH). This type of hypothyroidism is also called
congenital hypothyroidism, non-goitrous (CHNG).

· There are at least 5 types of CHNG due to mutation of five different

genes namely CHNG1 to CHNG5.
 · Non Goitrous congenital hypothyroidism is considered as the most
prevalent inborn endocrine disorder.

● Endemic Cretinism

· For adults, the normal recommended dietary intake of iodine is 150

μg / day.

· This type of cretinism often occurs in children who live in the

geographical settings where iodine is deficient and it is not
corrected by either supplementing iodine or thyroid hormone to
regain normal thyroid hormone levels during early life.

· Mostly, the mother of endemic cretinism children had been affected

with hypothyroidism during pregnancy (Maternal hypothyroidism).

· Exposure to radioactive Iodine during pregnancy may also be the

cause in some cases.

· Use of antithyroid drugs or sulfonamides during pregnancy.

· Iodine intake as low as 25 mcg/day during pregnancy would be a

potential risk factor for giving birth to cretinism neonates.

Neurological cretinism – It is characterized by the following conditions:

● Retarded growth
● Deaf-mutism
● Motor spasticity
● Severe mental retardation with a squint

Myxedematous cretinism – It is characterized by the following conditions:

● Retarded growth.
● Incomplete maturation of facial expression.
● Thickened and dry skin.
● Small and dry hair, eyelashes and eyebrows.
 ● Mental retardation of comparatively lesser intensity to neurological
cretinism.
● Delayed sexual maturation.
● Other clinical manifestations of hypothyroidism

Signs and Symptoms

The main symptoms of cretinism are the following:

● Stunted growth and mental retardation.

● Short stature (dwarfism).
● Mild neurological impairment with reduced muscle tone and
coordination.
● Hearing and speech defects.
● Unable to maintain posture and balance with characteristic
walking style.
● Myxoedema.
● Enlargement of the thyroid gland (goitre)

Other symptoms are the following:

● lack of weight gain

● fatigue, lethargy
● poor feeding
● thickened facial features
● abnormal bone growth
● ·very little crying
● excessive sleep
● constipation
● yellowing of the skin and whites of the eyes (jaundice)
● hoarse voice
● unusually large tongue
● swelling near the navel (umbilical hernia)
● cool, dry skin
● pale skin
Pathophysiology

The main causes of cretinism are the following:

- a missing, poorly formed, or abnormally small thyroid gland

- a genetic defect that affects thyroid hormone production
- too little iodine in the mother’s diet during pregnancy
- radioactive iodine or antithyroid treatment for thyroid cancer during
pregnancy
- use of medicines that disrupt thyroid hormone production — such as
antithyroid drugs, sulfonamides, or lithium — during pregnancy

Disease Process

● An optimal level of maternal thyroid status is essential for the normal

growth of the fetus. It is the maternal thyroid hormone, the only source
for the fetus that crosses placenta for fetal brain development.
● Thyroid hormone is essential for growth, branching and myelination of
neuronal cells of CNS at fetal and neonatal stage. So, the absence of
thyroid hormone at these stages would severely affect the generalized
nervous system development.
● Thyroid hormone also plays a critical role in skeletal muscle
development than soft tissue development. During cretinism, this
disproportionate rate of growth leads to excessive growth of soft tissue
compared to skeletal tissues.
Diagnostic Examination

Routine screening of the newborn using a blood-spot, as in the Guthrie test, to

detect a high TSH level as an indicator of primary hypothyroidism, usually done at 5-
7 days; cretinism is prevented if T4 is started within the first few months of life.

Medical Intervention

The goal of treatment in congenital hypothyroidism is to correct

hypothyroidism and ensure normal growth and neuropsychological development.
The mainstay in the treatment of congenital hypothyroidism is early diagnosis and
thyroid hormone replacement. Optimal care includes diagnosis before age 10-13
days and normalization of thyroid hormone blood levels by age 3 weeks.
 HYPOPARATHYROIDISM

The most common cause of hypoparathyroidism is inadequate secretion of

parathyroid hormone after interruption of the blood supply or surgical removal of
parathyroid gland tissue during thyroidectomy, parathyroidectomy, or radical neck
dissection. Atrophy of the parathyroid glands of unknown cause is a less common
cause of hypoparathyroidism.

Hypoparathyroidism occurs when your parathyroid glands don't secrete enough

parathyroid hormone. You have four small parathyroid glands in your neck behind
your thyroid gland. The major function of PTH is to regulate the level of calcium in
your body. It also controls the level of phosphorus and has a role in the production of
the active form of vitamin D. All of these activities are required to maintain calcium
balance.
Having too little PTH causes low levels of calcium and high levels of phosphorus in
the body. This condition may not cause any serious medical problems when it’s
caught early, but it does require lifelong monitoring and treatment.

Types of Hypoparathyroidism

Acquired hypoparathyroidism (Acquired hypothyroidism is a condition that

develops when your child's thyroid gland makes little or no thyroid hormone. Thyroid
hormones help control body temperature, heart rate, and how your child gains or
loses weight. Thyroid hormones play an important role in normal growth and
development of children.)

Transient hypoparathyroidism (occurs most commonly in babies who are born too
soon (prematurely)

Congenital hypoparathyroidism or DiGeorge's syndrome (The parathyroid glands

do not develop properly while the baby is growing in the womb)

Inherited hypoparathyroidism (caused by an inherited problem caused by

chemicals called antibodies attacking the parathyroid gland. This is called an
autoimmune illness)

Factors that can cause hypoparathyroidism include:

· Neck surgery. This most common cause of hypoparathyroidism develops

after accidental damage to or removal of the parathyroid glands during
surgery. Neck surgery may be done to treat conditions of the thyroid gland,
or to treat throat or neck cancer.

· Autoimmune disease. In some cases, your immune system attacks

parathyroid tissues as if they were foreign bodies. In the process, the
parathyroid glands stop producing their hormone.

· Hereditary hypoparathyroidism. In this form, either you're born without

parathyroid glands or they don't work properly. Some types of hereditary
 hypoparathyroidism are associated with deficiencies of other hormone-
producing glands.

· Low levels of magnesium in your blood. Low magnesium levels can

affect the function of your parathyroid glands. Normal magnesium levels
are required for normal production of parathyroid hormone.

· Extensive cancer radiation treatment of your face or neck. Radiation can

result in destruction of your parathyroid glands. In rare cases, radioactive
iodine treatment for hyperthyroidism may lead to hypoparathyroidism.

SIGNS AND SYMPTOMS

Onset of the disease is very gradual and symptoms can be mild. Many people
diagnosed with hypoparathyroidism have had symptoms for years before they are
diagnosed. Symptoms may be so mild that the diagnosis is made after a screening
blood test that shows low calcium.

Hypocalcemia causes irritability of the neuromuscular system and contributes

to the chief symptom of hypoparathyroidism—tetany. Tetany is a general muscle
hypertonia, with tremor and spasmodic or uncoordinated contractions occurring with
or without efforts to make voluntary movements. Symptoms of latent tetany are
numbness, tingling, and cramps in the extremities, and the patient complains of
stiffness in the hands and feet. In overt tetany, the signs include bronchospasm,
laryngeal spasm, carpopedal spasm (flexion of the elbows and wrists and extension
of the carpophalangeal joints), dysphagia, photophobia, cardiac dysrhythmias, and
seizures. Other symptoms include anxiety, irritability, depression, and even delirium.
ECG changes and hypotension also may occur.

Symptoms may include any of the following:

● Tingling lips, fingers, and toes (most common)

● Muscle cramps (most common)
 ● Muscle spasms called tetany (can affect the larynx, causing breathing
difficulties)
● Abdominal pain
● Abnormal heart rhythm
● Brittle nails
● Cataracts
● Calcium deposits in some tissues
● Decreased consciousness
● Dry hair
● Dry, scaly skin
● Pain in the face, legs, and feet
● Painful menstruation
● Seizures
● Teeth that do not grow in on time, or at all
● Weakened tooth enamel (in children)
● Positive Trousseau's sign (When we inflate the BP cuff on arm (Inflate
above systolic) then there is spasm/contraction of finger of that arm.
● Positive Chevostek sign:-Contraction of facial muscle when light tapping
of facial nerve in front of the ear.

DIAGNOSTIC EXAM

The health care provider will do a physical exam and ask about symptoms.

Tests that will be done include:

● PTH blood test

● Calcium blood test
● Magnesium
● 24-hour urine test

Other tests that may be ordered include:

● ECG to check for an abnormal heart rhythm

● CT scan to check for calcium deposits in the brain
MEDICAL MANAGEMENT

The goal of therapy is to raise the serum calcium level to 9 to 10 mg/dL (2.2 to
2.5 mmol/L) and to eliminate the symptoms of hypoparathyroidism and
hypocalcemia. When hypocalcemia and tetany occur after a thyroidectomy, the
immediate treatment is to administer calcium gluconate intravenously. If this does
not decrease neuromuscular irritability and seizure activity immediately, sedative
agents such as pentobarbital may be administered.

Parenteral parathormone can be administered to treat acute

hypoparathyroidism with tetany. The high incidence of allergic reactions to injections
of parathormone, however, limits its use to acute episodes of hypocalcemia. The
patient receiving parathormone is monitored closely for allergic reactions and
changes in serum calcium levels.

Because of neuromuscular irritability, the patient with hypocalcemia and

tetany requires an environment that is free of noise, drafts, bright lights, or sudden
movement. Tracheostomy or mechanical ventilation may become necessary, along
with bronchodilating medications, if the patient develops respiratory distress.

Therapy for the patient with chronic hypoparathyroidism is determined after

serum calcium levels are obtained. A diet high in calcium and low in phosphorus is
prescribed. Although milk, milk products, and egg yolk are high in calcium, they are
restricted because they also contain high levels of phosphorus. Spinach also is
avoided because it contains oxalate, which would form insoluble calcium
substances. Oral tablets of calcium salts, such as calcium gluconate, may be used to
supplement the diet. Aluminum hydroxide gel or aluminum carbonate (Gelusil,
Amphojel) also is administered after meals to bind phosphate and promote its
excretion through the gastrointestinal tract.

Variable dosages of a vitamin D preparation—dihydrotachysterol (AT 10 or

Hytakerol), ergocalciferol (vitamin D), cholecalciferol (vitamin D)—are usually
required and enhance calcium absorption from the gastrointestinal tract.

TREATMENT
 The goal of treatment is to relieve symptoms and to normalize levels of
calcium and phosphorus in your body. A treatment regimen usually includes:

● Oral calcium carbonate tablets. Oral calcium supplements can increase

calcium levels in your blood. However, at high doses, calcium supplements
can cause gastrointestinal side effects, such as constipation, in some people.
● Vitamin D. High doses of vitamin D, generally in the form of calcitriol, can
help your body absorb calcium and eliminate phosphorus.
● Magnesium. If your magnesium level is low and you're experiencing
symptoms of hypoparathyroidism, your doctor may recommend that you take
a magnesium supplement.
● Thiazide diuretics. If your calcium levels remain low even with treatment,
thiazide diuretics can help decrease the amount of calcium lost through your
urine. However, some people with hypoparathyroidism, including people who
inherited the condition, shouldn't take thiazide diuretics.
● Parathyroid hormone (Natpara). The U.S. Food and Drug Administration
has approved this once-daily injection for treatment of low blood calcium due
to hypoparathyroidism. Because of the potential risk of bone cancer
(osteosarcoma), at least in animal studies, this drug is available only through
a restricted program to people whose calcium levels can't be controlled with
calcium and vitamin D supplements and who understand the risks.

Diet

Your doctor might recommend that you consult a dietitian, who is likely to
advise a diet that's:

● Rich in calcium. This includes dairy products, green leafy vegetables,

broccoli and foods with added calcium, such as some orange juice and
breakfast cereals.
● Low in phosphorus. This means avoiding carbonated soft drinks,
which contain phosphorus in the form of phosphoric acid, and limiting
meats, hard cheeses and whole grains.

Intravenous infusion
 If you need immediate symptom relief, your doctor might recommend
hospitalization so that you can receive calcium by intravenous (IV) infusion, as well
as oral calcium tablets. After hospital discharge, you'll continue to take calcium and
vitamin D orally.

Monitoring

Your doctor will regularly check your blood to monitor levels of calcium and
phosphorus. Initially, these tests will probably be weekly to monthly. Eventually, you'll
need blood tests just twice a year.

Because hypoparathyroidism is usually a long-lasting disorder, treatment

generally is lifelong, as are regular blood tests to determine whether calcium is at
normal levels. Your doctor will adjust your dose of supplemental calcium if your
blood-calcium levels rise or fall

HYPERPARATHYROIDISM

Hyperparathyroidism is a condition in which one or more of your parathyroid

glands become overactive and release (secrete) too much parathyroid hormone
(PTH). This causes the levels of calcium in your blood to rise, a condition known as
hypercalcemia.

Your parathyroid glands secrete PTH to help control the levels of calcium and
phosphorus in your body. You have four parathyroid glands, located on the outside
borders on the backside of your thyroid gland. Your thyroid gland is located on the
front of your neck.

If you have an overactive parathyroid, one or more of your parathyroid glands

makes too much parathyroid hormone (PTH). Too much PTH signals your body to
make more calcium available. Your body responds by:

● Releasing more calcium into your blood from your bones (where most
of your calcium is stored). Loss of calcium from your bones weakens
them and increases your risk of a fracture.
● Having your digestive tract absorb more calcium from the foods you
eat.
 ● Having your kidneys retain calcium and return it to your blood instead
of flushing it out in your urine. Too much calcium in your kidneys can
cause kidney stones to form.

Approximately 100,000 people develop hyperparathyroidism in the United

States every year. Older women who are postmenopausal are at the highest risk for
the condition.

There are two types of hyperparathyroidism, primary and secondary:

● In primary hyperparathyroidism, your parathyroid glands make too much

PTH, which causes the level of calcium in your blood to rise.
● In secondary hyperparathyroidism, the overactivity of the parathyroid
glands occurs in response to another condition that’s causing calcium loss.
Parathyroid overactivity is an attempt on your body’s part to keep the calcium
levels normal. Examples of conditions that lower calcium levels include kidney
failure, severe vitamin D deficiency and severe calcium deficiency.

Causes of primary hyperparathyroidism include:

● A noncancerous (benign) growth, called an adenoma, forms on a

single parathyroid gland. The adenoma causes the gland to overact
and make more PTH. This is the most common cause.
● Two or more of your parathyroid glands become enlarged, a
condition called hyperplasia, and produce too much hormone.
● Radiation treatment to the neck area.
● Inherited conditions, such as multiple endocrine neoplasia type 1.
This is a rare cause.
● Cancer of a parathyroid gland (rare).

SIGNS AND SYMPTOMS

If you have early hyperparathyroidism, you may not have any symptoms. If you have
mild hyperparathyroidism, you may have some of the following symptoms:
 ● Joint pain.
● Muscle weakness.
● Feeling tired.
● Depression.
● Trouble concentrating.
● Loss of appetite.

If your hyperparathyroidism is more severe, you may have these symptoms:

● Nausea and vomiting.

● Confusion, forgetfulness.
● Increased thirst and need to urinate.
● Constipation.
● Bone pain.

Other problems associated with severe hyperparathyroidism include:

● Reduced kidney function, which affects your kidney’s ability to filter

blood.
● Kidney stones.
● Thinning bones (osteoporosis).
● High blood pressure. High blood calcium levels may play a role in the
development of high blood pressure.
DIAGNOSTIC EXAM

Blood tests

If blood test results show you have high calcium levels in your blood, your
doctor will likely repeat the test to confirm the results after you haven't eaten for a
period of time. Many conditions can raise calcium levels. But your doctor can
diagnose hyperparathyroidism if blood tests show you also have high levels of
parathyroid hormone.

Additional diagnostic tests

After diagnosing hyperparathyroidism, your doctor will likely order more tests
to rule out possible secondary causes, to identify possible complications and to
judge the severity of the condition. These tests include:

● Bone mineral density test. This test is done to see if you have
developed osteoporosis. The most common test to measure bone
mineral density is dual energy X-ray absorptiometry (DEXA). This test
 uses special X-ray devices to measure how many grams of calcium
and other bone minerals are packed into a bone segment.
● Urine test. A 24-hour collection of urine can provide information on
how well your kidneys work and how much calcium is excreted in your
urine.This test may help in judging the severity of hyperparathyroidism
or diagnosing a kidney disorder causing hyperparathyroidism. If a very
low calcium level is found in the urine, this may mean it's a condition
that doesn't need treatment.
● Imaging tests of kidneys. Your doctor may order an X-ray or other
imaging tests of your abdomen to determine if you have kidney stones
or other kidney abnormalities.

Imaging tests before surgery

If your doctor recommends surgery, he or she will likely use one of these imaging
tests to locate the parathyroid gland or glands that are causing problems:

○ Sestamibi parathyroid scan. Sestamibi is a radioactive compound

that is absorbed by overactive parathyroid glands and can be detected
by a scanner that detects radioactivity.
■ The normal thyroid gland also absorbs sestamibi. To eliminate
uptake in the thyroid obscuring the uptake in a parathyroid
adenoma, radioactive iodine, which is only taken up by the
thyroid, also is given and the thyroid image is digitally
subtracted.
■ Computerized tomography (CT) scanning may be combined with
the sestamibi scan to improve detection of an abnormality.
○ Ultrasound. Ultrasound uses sound waves to create images of your
parathyroid glands and surrounding tissue.
■ A small device held against your skin (transducer) emits high-
pitched sound waves and records the sound wave echoes as
they reflect off internal structures. A computer converts the
echoes into images on a monitor.
MEDICAL INTERVENTION

If you have mild hyperparathyroidism (no symptoms, blood calcium levels only
slightly elevated), your healthcare provider may not choose to treat it right away.
Instead, your provider will monitor your blood calcium levels (every six months),
blood pressure (every six months), kidney function (every year), and bone density
(every one to three years).

If your healthcare provider believes your hyperparathyroidism doesn’t need

immediate treatment, be sure to:

● Drink more water.

● Keep active and get more exercise to keep your bones strong.
● Don’t take thiazide diuretics or lithium because these drugs can
increase the level of calcium in your blood.
● Ask your provider if you need to take a vitamin D supplement if your
vitamin D level is low.

If you have more severe hyperparathyroidism symptoms or have an enlarged

parathyroid gland (or glands) or a growth on your parathyroid gland, your provider
may recommend surgery to remove the overactive gland(s). Surgery by an
experienced surgeon can cure hyperparathyroidism in about 95% of cases.

MEDICATION

Medications to treat hyperparathyroidism include the following:

● Calcimimetics. A calcimimetic is a drug that mimics calcium circulating in the

blood. The drug may trick the parathyroid glands into releasing less
parathyroid hormone. This drug is sold as cinacalcet (Sensipar).
○ Some doctors may prescribe cinacalcet to treat primary
hyperparathyroidism, particularly if surgery hasn't successfully cured
the disorder or a person isn't a good surgery candidate.
 ○ The most commonly reported side effects of cinacalcet are joint and
muscle pain, diarrhea, nausea, and respiratory infection.
● Hormone replacement therapy. For women who have gone through
menopause and have signs of osteoporosis, hormone replacement therapy
may help bones retain calcium. This treatment doesn't address the underlying
problems with the parathyroid glands.
○ Prolonged use of hormone replacement therapy can increase the risk
of blood clots and breast cancer. Work with your doctor to evaluate the
risks and benefits to help you decide what's best for you.
○ Some common side effects of hormone replacement therapy include
breast pain and tenderness, dizziness, and headaches.
● Bisphosphonates. Bisphosphonates also prevent the loss of calcium from
bones and may lessen osteoporosis caused by hyperparathyroidism. Some
side effects associated with bisphosphonates include low blood pressure, a
fever and vomiting. This treatment doesn't address the underlying problems
with the parathyroid glands.

● Cinacalcet (Sensipar®) has been approved by the Food and Drug

Administration for the treatment of secondary hyperparathyroidism. The drug
works by signaling the parathyroid glands to produce less PTH. Although
cinacalcet is intended for secondary hyperparathyroidism, some healthcare
providers prescribe it for primary hyperparathyroidism.

Another medication type that is sometimes prescribed is

bisphosphonates. These drugs help prevent loss of calcium from bones,
which reduces the risk of fracture and osteoporosis. Examples of
bisphosphonates include etidronate (Didronel®), alendronate (Fosamax®),
zoledronic acid (Zometa®) and ibandronate (Boniva®).

If you're a woman and you’ve already gone through menopause and

have signs of osteoporosis, your provider may prescribe hormone
replacement therapy (HRT). HRT may help your bones retain calcium.
DIABETES MELLITUS

Diabetes mellitus (DM) is a chronic disorder of carbohydrate, protein, and fat

metabolism in which there is a discrepancy between the amount of insulin required
by the body and the amount of insulin available. The Centers for Disease Control
and Prevention (CDC) state that more than 100 million people in the United States
are living with DM or prediabetes. Almost 10% of the U.S. population has DM. The
84.1 million people who are prediabetic will likely have DM within 5 years if they are
not treated, and more than half of the people with that condition are unaware that
they are prediabetic. The health-related problems of DM are extensive in lives lost
and money spent. It is the seventh leading cause of death in the United States. DM
is classified into several categories.

TYPE DESCRIPTION

1 ● Patients are dependent on insulin for prevention

of hyperglycemia or ketosis
● Referred to as insulin-dependent DM
Approximately 10%–20% of patients with DM
have this type; estimates are that 1 million people
in the United States have type 1 DM
● The most serious life-threatening problem is
diabetic ketoacidosis
● Time of onset is usually under age 20 but may
occur in adults 30 to 40
● Beta cells of pancreas have insulitis (pancreatic
inflammatory response) with beta cell destruction
 2 ● Patients are not dependent on insulin
● Patients have insulin resistance, impaired insulin
secretion, and/or inappropriate glucagon
secretion
● Referred to as non-insulin-dependent DM
● Most common type of DM: Approximately 80%–
90% of DM patients have this type
● Most serious problem is the development of
hyperosmolar hyperglycemic non-ketotic
syndrome
● Time of onset is usually over age 40
● Beta cells have no insulitis; resistance to insulin
occurs at the target cell receptor

Gestational DM ● Patients develop glucose intolerance during

(GDM) pregnancy

Other types of ● Diabetes develops secondary to other conditions,

diabetes including pancreatic, hormonal, or endocrine
disease and insulin resistance, or it is drug
induced

Malnutrition-related ● Occurs in underdeveloped countries to individuals

DM with a history of malnutrition

OVERVIEW

The beta cells of the pancreas produce insulin and a protein called C-peptide,
which are stored in the secretory granules of the beta cells and are released into the
bloodstream as blood glucose levels increase. Insulin transports glucose and amino
acids across the membranes of many body cells, particularly muscle and fat cells. It
also increases the liver storage of glycogen, the chief carbohydrate storage material,
and aids in the metabolism of triglycerides, nucleic acids, and proteins. In type 1 DM,
beta cells of the pancreas have been destroyed by autoimmune processes, whereas
in type 2 DM, relative insulin deficiency occurs accompanied by resistance to the
actions of insulin in muscle, fat, and liver cells. Insulin resistance is associated with
increased levels of free fatty acids in the blood, reduced glucose transport in muscle
cells, elevated hepatic glucose production, and increased breakdown of fat. For type
2 DM to occur, both insulin resistance and inadequate insulin secretion must occur.

Long-term complications, such as disease of the large and small blood

vessels, lead to cardiovascular disease (coronary artery disease, peripheral vascular
disease, hypertension), retinopathy, renal failure, and premature death. Diabetic
patients also have nerve damage (neuropathy) that can affect vision and the
peripheral nerves, resulting in numbness and pain of the hands or feet.

Because diabetic patients are hyperglycemic, they are at higher risk for
infection because elevated glucose encourages bacterial growth. The combination of
peripheral neuropathies with numbness of the extremities, peripheral vascular
disease leading to poor tissue perfusion, and the risk for infection makes the diabetic
patient prone to feet and leg ulcers.

SIGNS AND SYMPTOMS

Signs and symptoms depend on the patient’s level of hyperglycemia. Classic

clinical manifestations of diabetes include the “three Ps”: polyuria, polydipsia, and
polyphagia. Polyuria (increased urination) and polydipsia (increased thirst) occur as
a result of the excess loss of fluid associated with osmotic diuresis. Patients also
experience polyphagia (increased appetite) that results from the catabolic state
induced by insulin deficiency and the breakdown of proteins and fats. Other
symptoms include fatigue and weakness, sudden vision changes, tingling or
numbness in hands or feet, dry skin, skin lesions or wounds that are slow to heal,
and recurrent infections. The onset of type 1 diabetes may also be associated with
sudden weight loss or nausea, vomiting, or abdominal pains, if DKA has developed.
TYPE 1 DIABETES

Type 1 diabetes affects approximately 5% of adults with the disease. It is

characterized by the destruction of the pancreatic beta cells. Combined genetic,
immunologic, and possibly environmental (e.g., viral) factors are thought to
contribute to beta-cell destruction. Although the events that lead to beta-cell
destruction are not fully understood, it is generally accepted that a genetic
susceptibility is a common underlying factor in the development of type 1 diabetes.
People do not inherit type 1 diabetes itself but rather a genetic predisposition, or
tendency, toward the development of type 1 diabetes. This genetic tendency has
been found in people with certain human leukocyte antigen types. There is also
evidence of an autoimmune response in type 1 diabetes. This is an abnormal
response in which antibodies are directed against normal tissues of the body,
responding to these tissues as if they were foreign. Autoantibodies against islet cells
and against endogenous (internal) insulin have been detected in people at the time
of diagnosis and even several years before the development of clinical signs of type
1 diabetes. In addition to genetic and immunologic components, environmental
factors such as viruses or toxins that may initiate destruction of the beta cell continue
to be investigated.

Regardless of the specific cause, the destruction of the beta cells results in
decreased insulin production, increased glucose production by the liver, and fasting
hyperglycemia. In addition, glucose derived from food cannot be stored in the liver
but instead remains in the bloodstream and contributes to postprandial (after meals)
hyperglycemia.

If the concentration of glucose in the blood exceeds the renal threshold for
glucose, usually 180 to 200 mg/dL (9.9 to 11.1 mmol/L), the kidneys may not
reabsorb all of the filtered glucose; the glucose then appears in the urine
(glycosuria). When excess glucose is excreted in the urine, it is accompanied by
excessive loss of fluids and electrolytes. This is called osmotic diuresis.

Because insulin normally inhibits glycogenolysis (breakdown of stored

glucose) and gluconeogenesis (production of new glucose from amino acids and
other substrates), these processes occur in an unrestrained fashion in people with
insulin deficiency and contribute further to hyperglycemia. In addition, fat breakdown
occurs, resulting in an increased production of ketone bodies, a highly acidic
substance formed when the liver breaks down free fatty acids in the absence of
insulin.

Diabetic ketoacidosis (DKA) is a metabolic derangement that occurs most

commonly in persons with type 1 diabetes and results from a deficiency of insulin;
highly acidic ketone bodies are formed, and metabolic acidosis occurs. The three
major metabolic derangements are hyperglycemia, ketosis, and metabolic acidosis
(Grossman & Porth, 2014). DKA is commonly preceded by a day or more of polyuria,
polydipsia, nausea, vomiting, and fatigue with eventual stupor and coma if not
treated. The breath has a characteristic fruity odor due to the presence of ketoacids.

PATHOPHYSIOLOGY OF TYPE I DIABETES MELLITUS

TYPE 2 DIABETES

Type 2 diabetes affects approximately 95% of adults with the disease (CDC,
2014). It occurs more commonly among people who are older than 30 years and
obese, although its incidence is rapidly increasing in younger people because of the
growing epidemic of obesity in children, adolescents, and young adults (CDC, 2014).

The two main problems related to insulin in type 2 diabetes are insulin
resistance and impaired insulin secretion. Insulin resistance refers to a decreased
tissue sensitivity to insulin. Normally, insulin binds to special receptors on cell
surfaces and initiates a series of reactions involved in glucose metabolism. In type 2
diabetes, these intracellular reactions are diminished, making insulin less effective at
stimulating glucose uptake by the tissues and at regulating glucose release by the
liver (see Fig. 51-1). The exact mechanisms that lead to insulin resistance and
impaired insulin secretion in type 2 diabetes are unknown, although genetic factors
are thought to play a role.

To overcome insulin resistance and to prevent the buildup of glucose in the

blood, increased amounts of insulin must be secreted to maintain the glucose level
at a normal or slightly elevated level. If the beta cells cannot keep up with the
increased demand for insulin, the glucose level rises and type 2 diabetes develops.
Insulin resistance may also lead to metabolic syndrome, which is a constellation of
symptoms, including hypertension, hypercholesterolemia, abdominal obesity, and
other abnormities (Grossman & Porth, 2014).

Despite the impaired insulin secretion that is characteristic of type 2 diabetes,

there is enough insulin present to prevent the breakdown of fat and the
accompanying production of ketone bodies. Therefore, DKA does not typically occur
in type 2 diabetes. However, uncontrolled type 2 diabetes may lead to another acute
problem—hyperglycemic hyperosmolar syndrome (HHS).
 Because type 2 diabetes is associated with a slow, progressive glucose
intolerance, its onset may go undetected for many years. If the patient experiences
symptoms, they are frequently mild and may include fatigue, irritability, polyuria,
polydipsia, poorly healing skin wounds, vaginal infections, or blurred vision (if
glucose levels are very high).

For most patients (approximately 75%), type 2 diabetes is detected

incidentally (e.g., when routine laboratory tests or ophthalmoscopic examinations are
performed). One consequence of undetected diabetes is that long-term diabetes
complications (e.g., eye disease, peripheral neuropathy, peripheral vascular disease)
may have developed before the actual diagnosis of diabetes is made (ADA, 2016b),
signifying that the blood glucose has been elevated for a time before diagnosis.

Gestational diabetes is any degree of glucose intolerance with its onset during
pregnancy. Hyperglycemia develops during pregnancy because of the secretion of
placental hormones, which causes insulin resistance. Gestational diabetes occurs in
as many as 18% of pregnant women and increases their risk for hypertensive
disorders during pregnancy (CDC, 2014; Wu, Nien, Kuo, et al., 2016).

Women who are considered to be at high risk for gestational diabetes and
should be screened by blood glucose testing at their first prenatal visit are those with
marked obesity, a personal history of gestational diabetes, glycosuria, or a strong
family history of diabetes. High-risk ethnic groups include Hispanic Americans,
Native Americans, Asian Americans, African Americans, and Pacific Islanders. If
these high-risk women do not have gestational diabetes at initial screening, they
should be retested between 24 and 28 weeks of gestation. All women of average risk
should be tested at 24 to 28 weeks of gestation. Testing is not specifically
recommended for women identified as being at low risk. Low-risk women are those
who meet all of the following criteria: age younger than 25 years, normal weight
before pregnancy, member of an ethnic group with low prevalence of gestational
diabetes, no history of abnormal glucose tolerance, no known history of diabetes in
first-degree relatives, and no history of poor obstetric outcome (ADA, 2016c).
Women considered to be at high risk or average risk should have either an oral
glucose tolerance test (OGTT) or a glucose challenge test (GCT) followed by OGTT
in women who exceed the glucose threshold value of 140 mg/dL (7.8 mmol/L) (ADA,
2016c).

Initial management includes dietary modification and blood glucose

monitoring. If hyperglycemia persists, insulin is prescribed. Goals for blood glucose
levels during pregnancy are 95 mg/dL (5.3 mmol/L) or less before meals and 120
mg/dL (6.72 mmol/L) or less 2 hours after meals (ADA, 2016c).

After delivery, blood glucose levels in women with gestational diabetes usually
return to normal. However, many women who have had gestational diabetes develop
type 2 diabetes later in life. Approximately 35% to 60% of women who have had
gestational diabetes develop diabetes in the next 10 to 20 years.

PATHOPHYSIOLOGY OF TYPE II DIABETES MELLITUS

GESTATIONAL DIABETES

Gestational diabetes is any degree of glucose intolerance with its onset during
pregnancy. Hyperglycemia develops during pregnancy because of the secretion of
placental hormones, which causes insulin resistance. Gestational diabetes occurs in
as many as 18% of pregnant women and increases their risk for hypertensive
disorders during pregnancy,

Women who are considered to be at high risk for gestational diabetes and
should be screened by blood glucose testing at their first prenatal visit are those with
marked obesity, a personal history of gestational diabetes, glycosuria, or a strong
family history of diabetes. High-risk ethnic groups include Hispanic Americans,
Native Americans, Asian Americans, African Americans, and Pacific Islanders. If
these high-risk women do not have gestational diabetes at initial screening, they
should be retested between 24 and 28 weeks of gestation. All women of average risk
should be tested at 24 to 28 weeks of gestation. Testing is not specifically
recommended for women identified as being at low risk. Low-risk women are those
who meet all of the following criteria: age younger than 25 years, normal weight
before pregnancy, member of an ethnic group with low prevalence of gestational
diabetes, no history of abnormal glucose tolerance, no known history of diabetes in
first-degree relatives, and no history of poor obstetric outcome (ADA, 2016c).
Women considered to be at high risk or average risk should have either an oral
glucose tolerance test (OGTT) or a glucose challenge test (GCT) followed by OGTT
in women who exceed the glucose threshold value of 140 mg/dL (7.8 mmol/L).

LATENT AUTOIMMUNE DIABETES OF ADULTS (LADA)

In adults, LADA is a subtype of diabetes in which the progression of

autoimmune beta cell destruction in the pancreas is slower than in types 1 and 2
diabetes. Patients with LADA are not insulin-dependent in the initial 6 months of
disease onset. Clinical manifestation of LADA shares the features of types 1 and 2
diabetes (Deng et al., 2016). The emergence of this subtype has led some to
propose the diabetes classification scheme should be revised to reflect changes in
the beta cells in the pancreas (Schwartz, Epstein, Corkey, et al. 2016).

DIAGNOSTIC EXAMINATION

Diagnostic Highlights

Test Normal Result Abnormality With Explanation

Condition

Fasting (no food 70–100 mg/dL >126 mg/dL Insufficient

for at least 8hr insulin is
before available to
measurement) transport insulin
plasma glucose into body cells
(FPG)

Glucose <140 mg/dL >200 mg/dL; Insufficient

tolerance test levels from 140– insulin is
(2hr after oral 200 mg/dL available to
ingestion of 75 g indicate impaired transport insulin
of glucose; glucose into body cell
glucose is given tolerance
after an overnight
fast)

Hemoglobin A1c 4%–6% > 8% poorly Integrated

controlled measure of blood
diabetics; 7% glucose profile
 wellcontrolled over the
diabetics; initial preceding 2–3
diagnosis is mo; A1c is
made when level formed when
reaches 6.5% glucose in the
blood binds
irreversibly to
hemoglobin;
since normal life
span of red blood
cells is 90–120
days, A1c is
eliminated only
when the red
cells are
replaced.

Other Tests: Urinalysis (glycosuria). Note: The diagnosis of DM is made when FPG
is greater than or equal to 126 mg/dL on two occasions or random glucose is greater
than or equal to 200 mg/dL along with the classic symptoms of DM (polyuria,
polydipsia, polyphagia, weight loss). The goal of treatment is to lower and maintain
blood glucose levels into the following range: pre-prandial blood glucose levels of 90
to 130 mg/ dL and HbA1c levels of less than 7%.

PARAMETERS THAT SHOULD BE REGULARLY ASSESSED ARE

History

Ø Symptoms related to the diagnosis of diabetes:

Ø Symptoms of hyperglycemia

Ø Symptoms of hypoglycemia
 Ø Frequency, timing, severity, and resolution

Ø Results of blood glucose monitoring

Ø Status, symptoms, and management of chronic complications of diabetes:

o Eye; kidney; nerve; genitourinary and sexual, bladder, and

gastrointestinal

o Cardiac; peripheral vascular; foot complications associated with diabetes

Ø Adherence to/ability to follow prescribed dietary management plan

Ø Adherence to prescribed exercise regimen

Ø Adherence to/ability to follow prescribed pharmacologic treatment (insulin or

oral antidiabetic agents)

Ø Use of tobacco, alcohol, and prescribed and over-the-counter

medications/drugs

Ø Lifestyle, cultural, psychosocial, and economic factors that may affect diabetes
treatment

Ø Effects of diabetes or its complications on functional status (e.g., mobility,

vision)

Physical Examination

Ø Blood pressure (sitting and standing to detect orthostatic changes)

Ø Body mass index (height and weight)

Ø Funduscopic examination and visual acuity

Ø Foot examination (lesions, signs of infection, pulses)

Ø Skin examination (lesions and insulin injection sites)

Ø Neurologic examination
 o Vibratory and sensory examination using monofilament

o Deep tendon reflexes

Ø Oral examination

Laboratory Examination

Ø HgbA1C (A1C)

Ø Fasting lipid profile

Ø Test for microalbuminuria

Ø Serum creatinine level

Ø Urinalysis

Ø Electrocardiogram

CRITERIA FOR THE DIAGNOSIS OF DIA

Medical Management

The main goal of diabetes treatment is to normalize insulin activity and blood
glucose levels to reduce the development of complications. The Diabetes Control
and Complications Trial Research Group (DCCT), a 10- year prospective clinical trial
conducted from 1983 to 1993, demonstrated the importance of achieving blood
glucose control in the normal, nondiabetic range. This landmark trial demonstrated
that intensive glucose control dramatically reduced the development and progression
of complications such as retinopathy (damage to small blood vessels that nourish the
retina), nephropathy (damage to kidney cells), and neuropathy (damage to nerve
cells). Intensive treatment is defined as 3 or 4 insulin injections per day or an insulin
pump (i.e., a continuous subcutaneous insulin infusion) plus frequent blood glucose
monitoring and weekly contacts with diabetes educators (DCCT, 1993). The ADA
now recommends that all patients with diabetes strive for glucose control (HgbA1c
less than 7%) to reduce their risk of complications.

Intensive therapy must be initiated with caution and must be accompanied by

thorough education of the patient and family and by responsible behavior of the
patient. Careful screening of patients for capability and responsibility is a key step in
initiating intensive therapy.

The therapeutic goal for diabetes management is to achieve normal blood

glucose levels (euglycemia) without hypoglycemia while maintaining a high quality of
life. Diabetes management has five components: nutritional therapy, exercise,
monitoring, pharmacologic therapy, and education. Diabetes management involves
constant assessment and modification of the treatment plan by health professionals
and daily adjustments in therapy by the patient. Although the health care team
directs the treatment, it is the individual patient who must manage the complex
therapeutic regimen. For this reason, patient and family education is an essential
component of diabetes treatment and is as important as all other components of the
regimen.

Nutritional Therapy
 Nutrition, meal planning, weight control, and increased activity are the
foundation of diabetes management (ADA, 2016d). The most important objectives in
the dietary and nutritional management of diabetes are control of total caloric intake
to attain or maintain a reasonable body weight, control of blood glucose levels, and
normalization of lipids and blood pressure to prevent heart disease. Success in this
area alone is often associated with reversal of hyperglycemia in type 2 diabetes.
However, achieving these goals is not always easy. Because medical nutrition
therapy (MNT)—nutritional therapy prescribed for management of diabetes usually
given by a registered dietician—is complex, a registered dietitian who understands
the therapy has the major responsibility for designing and educating about this
aspect of the therapeutic plan. Nurses and all other members of the health care team
must be knowledgeable about nutritional therapy and supportive of patients who
need to implement nutritional and lifestyle changes.

MEDICATIONS

Insulin is secreted by the beta cells of the islets of Langerhans and lowers the
blood glucose level after meals by facilitating the uptake and utilization of glucose by
muscle, fat, and liver cells. In the absence of adequate insulin, pharmacologic
therapy is essential.

Insulin Regimens
 insulin regimens vary from 1 to 4 injections per day. Usually, there is a
combination of a short-acting insulin and a longer-acting insulin. The normally
functioning pancreas continuously secretes small amounts of insulin during the day
and night.

Conventional Regimen. One approach is to simplify the insulin regimen as much as

possible, with the aim of avoiding the acute complications of diabetes (hypoglycemia
and symptomatic hyperglycemia). With this type of simplified regimen (e.g., one or
more injections of a mixture of shortand intermediate-acting insulins per day), the
patient should not vary meal patterns and activity levels. The simplified regimen
would be appropriate for the terminally ill, the older adult who is frail and has limited
self-care abilities, or patients who are completely unwilling or unable to engage in the
self-management activities that are part of a more complex insulin regimen.

Intensive Regimen. The second approach is to use a more complex insulin regimen
to achieve as much control over blood glucose levels as is safe and practical. A
more complex insulin regimen allows the patient more flexibility to change the insulin
doses from day to day in accordance with changes in eating and activity patterns,
with stress and illness, and as needed for variations in the prevailing glucose level.

While intensive treatment (3 or 4 injections of insulin per day) reduces the risk of
complications, not all people with diabetes are candidates for very tight control of
blood glucose. The risk of severe hypoglycemia increases threefold in patients
receiving intensive treatment (ADA, 2016d). Patients who have received a kidney
transplant because of nephropathy and chronic kidney failure should follow an
intensive insulin regimen to preserve function of the new kidney.

Those who are not candidates include those with:

Ø Nervous system disorders rendering them unaware of hypoglycemic episodes

(e.g., those with autonomic neuropathy)

Ø Recurring severe hypoglycemia

Ø Irreversible diabetic complications, such as blindness or ESKD

Ø Severe cerebrovascular or cardiovascular disease

 Ø Ineffective self-care skills

Complications of Insulin Therapy

Systemic Allergic Reactions. Systemic allergic reactions to insulin are rare.

When they do occur, there is an immediate local skin reaction that gradually spreads
into generalized urticaria (hives). These rare reactions are occasionally associated
with generalized edema or anaphylaxis. The treatment is desensitization, with small
doses of insulin given in gradually increasing amounts using a desensitization kit

Insulin Lipodystrophy. Lipodystrophy refers to a localized reaction, in the form

of either lipoatrophy or lipohypertrophy, occurring at the site of insulin injections.
Lipoatrophy is the loss of subcutaneous fat; it appears as slight dimpling or more
serious pitting of subcutaneous fat. The use of human insulin has almost eliminated
this disfiguring complication.

Lipohypertrophy, the development of fibrofatty masses at the injection site, is

caused by the repeated use of an injection site. If insulin is injected into scarred
areas, absorption may be delayed. This is one reason that rotation of injection sites
is so important. Patients should avoid injecting insulin into these areas until the
hypertrophy disappears.

Resistance to Injected Insulin. Patients may develop insulin resistance and

require large insulin doses to control symptoms of diabetes (Comerford, 2015). In
most patients with diabetes who take insulin, immune antibodies develop and bind
the insulin, thereby decreasing the insulin available for use. All insulins cause some
antibody production in humans.

Morning Hyperglycemia. An elevated blood glucose level on arising in the

morning is caused by an insufficient level of insulin, which may be caused by several
factors: the dawn phenomenon, the Somogyi effect, or insulin waning. The dawn
phenomenon is characterized by a relatively normal blood glucose level until
approximately 3 am, when blood glucose levels begin to rise. The phenomenon is
thought to result from nocturnal surges in growth hormone secretion, which creates a
greater need for insulin in the early morning hours in patients with type 1 diabetes.
 CUSHING SYNDROME

Cushing syndrome results from excessive, rather than deficient,

adrenocortical activity. Cushing syndrome is commonly caused by the use of
corticosteroid medications and is infrequently the result of excessive corticosteroid
production secondary to hyperplasia of the adrenal cortex. However, overproduction
of endogenous corticosteroids may be caused by several mechanisms, including a
tumor of the pituitary gland that produces ACTH and stimulates the adrenal cortex to
increase its hormone secretion despite production of adequate amounts. Primary
hyperplasia of the adrenal glands in the absence of a pituitary tumor is less common.
Another less common cause of Cushing syndrome is the ectopic production of ACTH
by malignancies; bronchogenic carcinoma is the most common type. Regardless of
the cause, the normal feedback mechanisms that control the function of the adrenal
cortex become ineffective, and the usual diurnal pattern of cortisol is lost. The signs
and symptoms of Cushing syndrome are primarily a result of oversecretion of
glucocorticoids and androgens, although mineralocorticoid secretion may be affected
as well.

SIGNS AND SYMPTOMS

When overproduction of the adrenocortical hormone occurs, arrest of growth,

obesity, and musculoskeletal changes occur along with glucose intolerance. The
classic picture of Cushing syndrome in the adult is that of central-type obesity, with a
fatty “buffalo hump” in the neck and supraclavicular areas, a heavy trunk, and
relatively thin extremities. The skin is thin, fragile, and easily traumatized;
ecchymoses (bruises) and striae develop. The patient complains of weakness and
lassitude. Sleep is disturbed because of altered diurnal secretion of cortisol.

Excessive protein catabolism occurs, producing muscle wasting and

osteoporosis. Kyphosis, backache, and compression fractures of the vertebrae may
result. Retention of sodium and water occurs as a result of increased
mineralocorticoid activity, producing hypertension and heart failure.
 The patient develops a “moon-faced” appearance and may experience
increased oiliness of the skin and acne. Hyperglycemia or overt diabetes may
develop. The patient may also report weight gain, slow healing of minor cuts, and
bruises.

Women between the ages of 20 and 40 years are five times more likely than
men to develop Cushing syndrome. In females of all ages, virilization may occur as a
result of excess androgens. Virilization is characterized by the appearance of
masculine traits and the recession of feminine traits. There is an excessive growth of
hair on the face (hirsutism), the breasts atrophy, menses cease, the clitoris enlarges,
and the voice deepens. Libido is lost in men and women. Distress and depression
are common and are increased by the severity of the physical changes that occur
with this syndrome. If Cushing syndrome is a consequence of pituitary tumor, visual
disturbances may occur because of pressure of the growing tumor on the optic
chiasm.

OVERVIEW OF SIGNS AND SYMPTOMS

PATHOPHYSIOLOGY

DIAGNOSTIC EXAMINATIONS

Diagnostic Highlights

Test Normal Result Abnormality Explanation

With Condition

24-hour urine Urinary free Elevated Increased

testing for urinary cortisol: production or
free cortisol ingestion of
>70mg/1.73
glucocorticoid
m2/24 hr
Overnight Plasma cortisol Elevated above 5 cortisol response
dexamethasone level: 5 mcg/dL mcg/dL is diagnostic of
suppression test: CS; abnormal
1 mg given PO at results indicate
11 p.m.; plasma need for low-dose
cortisol levels are dexamathasone
measured at 8 a.m. suppression test
the next morning

Low-dose Urine cortisol: 20 Elevated above Failure to suppress

dexamathasone mcg/dL for 24 hr 20 mcg/dL for 24 normal cortisol
suppression test; hr response is
0.5 mg diagnostic of CS;
dexamethasone testing should not
given PO q 6 hr for be done during
48 hr severe illness or
depression, which
may lead to false-
positive results;
phenytoid therapy
alters
dexamethasone
metabolism and
may lead to false
results

Adrenocorticotropi <80 pg/mL in Results vary; see Elevated with high

c hormone level a.m.; explanation cortisol levels if
ACTH-producing
<50 pg/mL in
tumor; decreased
p.m.
with high cortisol
levels if adrenal
adenoma or
carcinoma is
 present

Other Tests: Complete blood count, computed tomography scan, bone age, bone
mineral density, pituitary magnetic resonance imaging, ultrasound, and angiogram.

The three tests used to diagnose Cushing syndrome are serum cortisol,
urinary cortisol, and low-dose dexamethasone (Decadron) suppression tests. Two of
these three tests need to be unequivocally abnormal to diagnose Cushing syndrome.
If the results of all three tests are normal, the patient likely does not have Cushing
syndrome (but may have a mild case, or the manifestations may be cyclic). For these
patients, further testing is not recommended unless symptoms progress. If test
results are either slightly abnormal or discordant, further testing is recommended.

Serum cortisol levels are usually higher in the early morning (6 to 8 am) and
lower in the evening (4 to 6 pm). This variation is lost in patients with Cushing
syndrome.

A urinary cortisol test requires a 24-hour urine collection. The nurse instructs
the patient how to collect and store the specimen. If the results of the urinary cortisol
test are three times the upper limit of the normal range and one other test is
abnormal, Cushing syndrome can be assumed.

An overnight dexamethasone suppression test is used to diagnosis pituitary

and adrenal causes of Cushing syndrome. It can be performed on an outpatient
basis. Dexamethasone (1 mg or 8 mg) is given orally late in the evening or at
bedtime, and a plasma cortisol level is obtained at 8 am the next morning.
Suppression of cortisol to less than 5 mg/dL indicates that the hypothalamic–
pituitary–adrenal axis is functioning properly (Fischbach & Dunning, 2015). Stress,
obesity, depression, and medications such as anticonvulsant agents, estrogen
(during pregnancy or as oral medications), and rifampin (Rifadin) can falsely elevate
cortisol levels.

Indicators of Cushing syndrome include an increase in serum sodium and

blood glucose levels and a decrease in serum potassium, a reduction in the number
of blood eosinophils, and disappearance of lymphoid tissue. Measurements of
plasma and urinary cortisol levels are obtained. Several blood samples may be
collected to determine whether the normal diurnal variation in plasma levels is
present; this variation is frequently absent in adrenal dysfunction. If several blood
samples are required, they must be collected at the times specified, and the time of
collection must be noted on the requisition slip.

MEDICAL MANAGEMENT

If Cushing syndrome is caused by pituitary tumors rather than tumors of the

adrenal cortex, treatment is directed at the pituitary gland. Surgical removal of the
tumor by transsphenoidal hypophysectomy (see Chapter 66) is the treatment of
choice and has an 80% success rate. Radiation of the pituitary gland also has been
successful, although it may take several months for control of symptoms.
Adrenalectomy is the treatment of choice in patients with unilateral primary adrenal
hypertrophy. Medical management is recommended for bilateral adrenal dysplasia.

Postoperatively, symptoms of adrenal insufficiency may begin to appear 12 to

48 hours after surgery because of reduction of the high levels of circulating adrenal
hormones. Temporary replacement therapy with hydrocortisone may be necessary
for several months, until the adrenal glands begin to respond normally to the body’s
needs.

Adrenal enzyme inhibitors (e.g., metyrapone [Metopirone], aminoglutethimide

[Cytadren], mitotane [Lysodren], and ketoconazole [Nizoral]) may be used to reduce
hyperadrenalism if the syndrome is caused by ectopic ACTH secretion by a tumor
that cannot be eradicated. Close monitoring is necessary, because symptoms of
inadequate adrenal function may result and side effects of the medications may
occur.

If Cushing syndrome is a result of the administration of corticosteroids, an

attempt is made to reduce or taper the medication to the minimum dosage needed to
treat the underlying disease process (e.g., autoimmune or allergic disease, rejection
of a transplanted organ). Frequently, alternate day therapy decreases the symptoms
of Cushing syndrome and allows recovery of the adrenal glands’ responsiveness to
ACTH.

MEDICATIONS

Medications to control excessive production of cortisol at the adrenal gland

include ketoconazole, mitotane (Lysodren) and metyrapone (Metopirone).

Mifepristone (Korlym, Mifeprex) is approved for people with Cushing

syndrome who have type 2 diabetes or glucose intolerance. Mifepristone does not
decrease cortisol production, but it blocks the effect of cortisol on your tissues.

Side effects from these medications may include fatigue, nausea, vomiting,
headaches, muscle aches, high blood pressure, low potassium and swelling. Some
have more-serious side effects, such as neurological side effects and liver toxicity.

Newer me`dications for Cushing syndrome include pasireotide (Signifor), given as a

twice-daily injection, and osilodrostat (Isturisa), a pill. Other medications are being
developed.

CONN’S SYNDROME

Conn's syndrome is a condition associated with the development of high

blood pressure in the presence of low potassium levels in the blood. This is usually
due to the presence of a tumor in the adrenal cortex, the outer part of the adrenal
gland.

The tumor causes excessive amounts of the hormone aldosterone to be

released. This is also called hyperhyperaldosteronism. Aldosterone is a hormone
that helps to regulate the amount of salt in the body. In patients who have
overproduction of this hormone, excessive salt is retained and potassium lost,
leading to high blood pressure and low potassium levels.

Signs and symptoms

Primary aldosteronism generally causes high blood pressure with low potassium.
Blood tests help to tell if high blood pressure is from Conn’s Syndrome or something
else. The usual treatment for high blood pressure doesn’t generally help treat
hyperaldosteronism.

The abnormal electrolyte levels often seen with too much aldosterone lead to signs
such as:

● Lack of muscle strength

● Frequent voiding
● Nighttime voiding
● Headache
● Increased thirst
● Pins and needles feeling
● Eyesight problems
● Paralysis that comes and goes
● Muscle twitching and cramps

The severity may depend on the degree of the electrolyte abnormality.

Diagnostic Examination
 Computed Tomography (CT or CAT Scan) of the adrenal glands can
diagnose all but the smallest tumors that cause Conn's syndrome.

Where diagnosis is suspected, i.e. the patient has both high blood pressure
and low potassium levels, but the tumor is not seen on CT scan, a test called
differential venous sampling for aldosterone may provide the diagnosis. A radiologist
inserts a small catheter into the adrenal vein to measure the amount of aldosterone
in the blood. In patients with a tumor, the side with the tumor will show excessive
amounts of aldosterone.

Medical Intervention
Surgical removal of the tumor is the definitive treatment for Conn's syndrome.
The procedure, called an adrenalectomy, usually cures the high blood pressure and
low potassium levels, which usually return to normal in most patients.Occasionally, in
patients with longstanding tumors, persistent elevation in blood pressure continue
after surgery because of damage to blood vessels.In patients with only adrenal
hyperplasia, surgery is often not recommended.

In most cases, a laparoscopic adrenalectomy can be performed, a minimally

invasive surgery using tiny incisions and a small scope connected to a video camera.
The camera sends a magnified image from inside the body to a monitor, giving the
surgeon a close-up view of the adrenal anatomy. The surgeon then operates
manipulating miniature surgical instruments that were passed through the scope.

Laparoscopic adrenalectomy has key advantages for patients including:

● Less post-operative pain

● Faster recovery from surgery
● Shorter hospital stay
● A more rapid return to work and normal activities

Medications
 If the extra aldosterone is produced by both adrenal glands it is usually
treated with medications like spirinolacone (brand name Aldactone®) or eplerenone
(Inspra®) which block the effects of aldosterone. If it is produced by one adrenal
gland, removing that gland is an alternative to those medications.

The doctor may also recommend lifestyle changes, including:

● Frequent exercise.

● Limiting alcohol intake.

● Reducing sodium in your diet.

● Stopping smoking.

Conn’s Syndrome Pathophysiology

Conn’s
Syndrome

Benign Cortical Bilateral Adrenal

Adenoma Hyperplasia

Excessive aldosterone
production

Excessive salt Potassium lost

retention

Hypertensio Hypokalemia
n
 ADDISON’S DISEASE
The adrenal glands are 2 small glands that sit on top of the kidneys. They
produce 2 essential hormones: cortisol and aldosterone.

The adrenal gland is damaged in Addison's disease, so it does not produce enough
cortisol or aldosterone.It can affect people of any age, although it's most common
between the ages of 30 and 50. It's also more common in women than men.

Signs and symptoms

The symptoms of Addison’s disease can vary from one individual to another.
Symptoms usually develop slowly over time and are usually vague and common to
many conditions (nonspecific). This often leads to delays in the proper diagnosis of
Addison’s disease. In rare cases, the symptoms of Addison’s disease can develop
rapidly causing a condition called acute adrenal failure.

Fatigue is the most common symptom of Addison’s disease. Another common initial
symptom of Addison’s disease is the development of patches of skin that are darker
than the surrounding skin (hyperpigmentation). This discoloration most commonly
occurs near scars, by skin creases such as the knuckles, and on the mucous
membranes such as the gums. Skin abnormalities can precede the development of
other symptoms by months or years, but do not occur in every person.

Some individuals with Addison’s disease may also develop a condition called vitiligo
in which white patches may appear on different areas of the body. This may vary
from one or two small spots on the skin or multiple, larger affected areas. Black
freckles may develop on the forehead, face or shoulders in some cases.

A variety of gastrointestinal symptoms may be present including nausea, vomiting,

and abdominal pain. Diarrhea is less common, but may also occur. Affected
individuals may have a poor appetite and unintentional weight loss and may develop
progressive fatigue and muscle weakness. Muscle pain (myalgia), muscle spasms
and joint pain may also occur. Dehydration can also affect individuals with Addison’s
disease.
An additional symptom that may occur is low blood pressure (hypotension), which
can cause lightheadedness or dizziness upon standing. Temporary loss of
consciousness (syncope) can occur in some cases. Addison’s disease can also lead
to changes in emotion and behavior. The disorder has been associated with
irritability, depression, and poor concentration.

Individuals with Addison’s disease may have cravings for salt or salty foods and low
blood sugar (glucose) levels. Women with Addison’s disease may have irregular
menstrual periods, lose body hair and have a decreased sexual drive.

In some cases, symptoms of Addison’s disease may appear suddenly, a condition

called acute adrenal failure or an addisonian crisis. During an addisonian crisis,
affected individuals may develop a sudden loss of strength; severe pain in the lower
back, abdomen or legs; vomiting and diarrhea potentially causing dehydration; and
low blood pressure and loss of consciousness. An addisonian crisis is a medical
emergency that can cause life-threatening complications such as shock or kidney
failure if not treated. A crisis is usually set off when affected individuals are under
stress such as during an accident, trauma, surgery or severe infection.

Diagnostic Examination

● History and physical: The doctor will review the patient’s symptoms and
perform a physical exam. Dark patches on the skin might be a clue for your
doctor to consider testing for Addison’s disease.

● Blood tests: These will be done to measure the levels of sodium, potassium,
cortisol and ACTH in your blood.

● ACTH stimulation test: This tests the adrenal glands’ response after a patient
is given a shot of artificial ACTH. If the adrenal glands produce low levels of
cortisol after the shot, they may not be functioning properly.

● X-rays: These may be done to look for calcium deposits on the adrenal
glands.

● Computed tomography (CT scan): Computed tomography uses computers to

combine many X-ray images into cross-sectional views. A CT scan might be
done to evaluate the adrenals and/or pituitary gland. For example, it can show
 if the immune system has damaged the adrenal glands or if the glands are
infected.

Medical Intervention
The healthcare provider will figure out the best treatment for the patient based on:

● Age, overall health, and past health

● How sick the patient is
● How well he/she can handle certain medicines, procedures, or therapies
● How long the condition is expected to last
● Patient’s opinion or preference

Addison's disease can be deadly. Treatment often starts with IV (intravenous) fluids
and medicines called corticosteroids. You may take these medicines by mouth or by
IV. You may have to take them for the rest of your life. You may also need to take
other medicines (fludrocortisones). These can help keep your body's sodium and
potassium levels normal.

Medications
All treatment for Addison's disease involves medication. You will be given hormone
replacement therapy to correct the levels of steroid hormones your body isn't
producing. Some options for treatment include oral corticosteroids such as:

● Hydrocortisone (Cortef), prednisone or methylprednisolone to replace

cortisol. These hormones are given on a schedule to mimic the normal 24-
hour fluctuation of cortisol levels.
● Fludrocortisone acetate to replace aldosterone.
Pathophysiology

Destruction of Adrenal Cortex

Low production of Aldosterone

Kidney: sodium & water loss with potassium retention

Decreased blood volume (Hypovolemia)

Increase of urea in blood (Hyperuricemia)

 Hypertension

High blood pressure, or hypertension, occurs when blood pressure increases

to unhealthy levels. The blood pressure measurement takes into account how much
blood is passing through the blood vessels and the amount of resistance the blood
meets while the heart is pumping.

Narrow arteries increase resistance. The narrower the arteries are, the higher the
blood pressure will be. Over the long term, increased pressure can cause health
issues, including heart disease.

There are two types of hypertension. Each type has a different cause.

Primary hypertension

Primary hypertension is also called essential hypertension. This kind of hypertension

develops over time with no identifiable cause. Most people have this type of high
blood pressure.

Researchers are still unclear what mechanisms cause blood pressure to slowly
increase. A combination of factors may play a role. These factors include:

● Genes: Some people are genetically predisposed to hypertension. This may

be from gene mutations or genetic abnormalities inherited from your parents.
● Physical changes: If something in your body changes, you may begin
experiencing issues throughout your body. High blood pressure may be one
of those issues. For example, it’s thought that changes in your kidney function
due to aging may upset the body’s natural balance of salts and fluid. This
change may cause your body’s blood pressure to increase.
● Environment: Over time, unhealthy lifestyle choices like lack of physical
activity and poor diet can take their toll on your body. Lifestyle choices can
 lead to weight problems. Being overweight or obese can increase your risk for
hypertension.

Secondary hypertension

Secondary hypertension often occurs quickly and can become more severe than
primary hypertension. Several conditions that may cause secondary hypertension
include:

● kidney disease
● obstructive sleep apnea
● congenital heart defects
● problems with your thyroid
● side effects of medications
● use of illegal drugs
● alcohol abuse or chronic use
● adrenal gland problems
● certain endocrine tumors

Risk factors

High blood pressure has many risk factors, including:

● Age. The risk of high blood pressure increases as you age. Until about
age 64, high blood pressure is more common in men. Women are more
likely to develop high blood pressure after age 65.
● Race. High blood pressure is particularly common among people of
African heritage, often developing at an earlier age than it does in whites.
Serious complications, such as stroke, heart attack and kidney failure,
also are more common in people of African heritage.
● Family history. High blood pressure tends to run in families.
● Being overweight or obese. The more you weigh, the more blood you
need to supply oxygen and nutrients to your tissues. As the amount of
 blood blow through your blood vessels increases, so does the pressure
on your artery walls.
● Not being physically active. People who are inactive tend to have higher
heart rates. The higher your heart rate, the harder your heart must work
with each contraction and the stronger the force on your arteries. Lack of
physical activity also increases the risk of being overweight.
● Using tobacco. Not only does smoking or chewing tobacco immediately
raise your blood pressure temporarily, but the chemicals in tobacco can
damage the lining of your artery walls. This can cause your arteries to
narrow and increase your risk of heart disease. Secondhand smoke also
can increase your heart disease risk.
● Too much salt (sodium) in your diet. Too much sodium in your diet can
cause your body to retain fluid, which increases blood pressure.
● Too little potassium in your diet. Potassium helps balance the amount of
sodium in your cells. A proper balance of potassium is critical for good
heart health. If you don't get enough potassium in your diet, or you lose
too much potassium due to dehydration or other health conditions,
sodium can build up in your blood.
● Drinking too much alcohol. Over time, heavy drinking can damage your
heart. Having more than one drink a day for women and more than two
drinks a day for men may affect your blood pressure.
If you drink alcohol, do so in moderation. For healthy adults, that means
up to one drink a day for women and two drinks a day for men. One drink
equals 12 ounces of beer, 5 ounces of wine or 1.5 ounces of 80-proof
liquor.
● Stress. High levels of stress can lead to a temporary increase in blood
pressure. Stress-related habits such as eating more, using tobacco or
drinking alcohol can lead to further increases in blood pressure.
● Certain chronic conditions. Certain chronic conditions also may increase
your risk of high blood pressure, including kidney disease, diabetes and
sleep apnea.
● Sometimes pregnancy contributes to high blood pressure as well.
Signs and symptoms

Hypertension is generally a silent condition. Many people won’t experience any

symptoms. It may take years or even decades for the condition to reach levels
severe enough that symptoms become obvious. Even then, these symptoms may be
attributed to other issues.

Symptoms of severe hypertension can include:

● headaches
● shortness of breath
● nosebleeds
● flushing
● dizziness
● chest pain
● visual changes
● blood in the urine

Diagnostic Examination

Diagnosing hypertension is as simple as taking a blood pressure reading. Most

doctors’ offices check blood pressure as part of a routine visit.

If a patient’s blood pressure is elevated, the doctor may request more readings over
the course of a few days or weeks. A hypertension diagnosis is rarely given after just
one reading. The doctor needs to see evidence of a sustained problem. That’s
because the environment can contribute to increased blood pressure and blood
pressure levels change throughout the day.

If blood pressure remains high, the doctor will likely conduct more tests to rule out
underlying conditions. These tests can include:

● urine test
 ● cholesterol screening and other blood tests
● test of the heart’s electrical activity with an electrocardiogram (EKG,
sometimes referred to as an ECG)
● ultrasound of the heart or kidneys

Medical Intervention

Primary hypertension treatment options

With primary hypertension, lifestyle changes may help reduce high blood pressure. If
lifestyle changes alone aren’t enough, or if they stop being effective, the doctor may
prescribe medication.

Secondary hypertension treatment options

If the doctor discovers an underlying issue causing hypertension, treatment will focus
on that other condition. For example, if a medicine is causing increased blood
pressure, the doctor will try other medicines that don’t have this side effect.

Sometimes, hypertension is persistent despite treatment for the underlying cause. In

this case, the doctor may work with the patient to develop lifestyle changes and
prescribe medications to help reduce the blood pressure.

Medications

● Beta-blockers: Beta-blockers make your heart beat slower and with less force.
This reduces the amount of blood pumped through your arteries with each
beat, which lowers blood pressure. It also blocks certain hormones in your
body that can raise your blood pressure.
● Diuretics: High sodium levels and excess fluid in your body can increase
blood pressure. Diuretics, also called water pills, help your kidneys remove
 excess sodium from your body. As the sodium leaves, extra fluid in your
bloodstream moves into your urine, which helps lower your blood pressure.
● ACE inhibitors: Angiotensin is a chemical that causes blood vessels and
artery walls to tighten and narrow. ACE (angiotensin converting enzyme)
inhibitors prevent the body from producing as much of this chemical. This
helps blood vessels relax and reduces blood pressure.
● Angiotensin II receptor blockers (ARBs): While ACE inhibitors aim to stop the
creation of angiotensin, ARBs block angiotensin from binding with receptors.
Without the chemical, blood vessels won’t tighten. That helps relax vessels
and lower blood pressure.
● Calcium channel blockers: These medications block some of the calcium from
entering the cardiac muscles of your heart. This leads to less forceful
heartbeats and a lower blood pressure. These medicines also work in the
blood vessels, causing them to relax and further lowering blood pressure.
● Alpha-2 agonists: This type of medication changes the nerve impulses that
cause blood vessels to tighten. This helps blood vessels to relax, which
reduces blood pressure.

Pathophysiology
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