c



c 
 





 

dela Cruz, Victor S




Abanto, Rizza Jane R.

Alvarez, Alona M.

Benedicto, Imee Karla R.

Calderon, Mary Joy B.

Canada, Candice C.

Mallari, Elmer T.

Sablad, Joan M.

Santiago, Jhoana Marie B.

  

Eilleen B. Bautista RN MSN

  March 1,2011
r  

The endocrine system is made up of glands that produce and secrete hormones. These
hormones regulate the body's growth, metabolism (the physical and chemical processes
of the body), and sexual development and function. The hormones are released into the
bloodstream and may affect one or several organs throughout the body.

The major glands of the endocrine system are the hypothalamus, pituitary, thyroid,
parathyroids, adrenals, pineal body, and the reproductive organs (ovaries and testes).
The pancreas is also a part of this system; it has a role in hormone production as well
as in digestion.


 

The thyroid gland is located in the lower front part of the neck. It produces thyroid
hormones that regulate the body's metabolism. It also plays a role in bone growth and
development of the brain and nervous system in children. The pituitary gland controls
the release of thyroid hormones. Thyroid hormones also help maintain normal blood
pressure, heart rate, digestion, muscle tone, and reproductive functions.

The thyroid gland is controlled by thyroid-stimulating hormone (TSH) produced by the

pituitary (to be specific, the anterior pituitary) and thyrotropin-releasing hormone (TRH)
produced by the hypothalamus. The thyroid gland gets its name from the Greek word
for "shield", after the shape of the related thyroid cartilage. The most common problems
of the thyroid gland consist of an overactive thyroid gland, referred to as
hyperthyroidism, and an underactive thyroid gland, referred to as hypothyroidism.


  

The adrenal glands are triangular-shaped glands located on top of each kidney.They
are surrounded by an adipose capsule and renal fascia. In humans, the adrenal glands
are found at the level of the 12th thoracic vertebra. The adrenal glands are made up of
two parts. The outer part is called the adrenal cortex, and the inner part is called the
adrenal medulla. The cortex mainly produces cortisol, aldosterone, and androgens,
while the medulla chiefly produces epinephrine and norepinephrine. The combined
weight of the adrenal glands in an adult human ranges from 7 to 10 grams.

The adrenal cortex is devoted to the synthesis of corticosteroid hormones. Specific

cortical cells produce particular hormones including cortisol, corticosterone, androgens
such as testosterone, and aldosterone. Under normal unstressed conditions, the human
adrenal glands produce the equivalent of 35±40 mg of cortisone acetate per day. In
contrast to the direct innervation of the medulla, the cortex is regulated by
neuroendocrine hormones secreted by the pituitary gland and hypothalamus, as well as
by the renin-angiotensin system.
The adrenal medulla is the core of the adrenal gland, and is surrounded by the adrenal
cortex. The chromaffin cells of the medulla, named for their characteristic brown staining
with chromic acid salts, are the body's main source of the circulating catecholamines
adrenaline (epinephrine) and noradrenaline (norepinephrine). Derived from the amino
acid tyrosine, these water-soluble hormones are major hormones underlying the fight-
or-flight response.To carry out its part of this response, the adrenal medulla receives
input from the sympathetic nervous system through preganglionic fibers originating in
the thoracic spinal cord from T5±T11. Because it is innervated by preganglionic nerve
fibers, the adrenal medulla can be considered as a specialized sympathetic ganglion.
Unlike other sympathetic ganglia, however, the adrenal medulla lacks distinct synapses
and releases its secretions directly into the blood.Cortisol also promotes epinephrin
synthesis in the medulla. Produced in the cortex, cortisol reaches the adrenal medulla
and at high levels, the hormone can promote the upregulation of phenylethanolamine -
methyltransferase (PNMT), thereby increasing epinephrine synthesis and secretion.

 

 

The pancreas is an elongated organ located toward the back of the abdomen behind
the stomach. The pancreas has digestive and hormonal functions. One part of the
pancreas, the exocrine pancreas, secretes digestive enzymes. The other part of the
pancreas, the endocrine pancreas, secretes hormones called insulin and glucagon.
These hormones regulate the level of glucose (sugar) in the blood.

The pancreas is an elongated, tapered organ located across the back of the abdomen,
behind the stomach. The right side of the organ (called the head) is the widest part of
the organ and lies in the curve of the duodenum (the first section of the small intestine).
The tapered left side extends slightly upward (called the body of the pancreas) and
ends near the spleen (called the tail).

The pancreas is made up of two types of tissue.The exocrine tissue secretes digestive
enzymes. These enzymes are secreted into a network of ducts that join the main
pancreatic duct, which runs the length of the pancreas.The endocrine tissue, which
consists of the islets of Langerhans, secretes hormones into the bloodstream.

The pancreas has digestive and hormonal functions.The enzymes secreted by the
exocrine tissue in the pancreas help break down carbohydrates, fats, proteins, and
acids in the duodenum. These enzymes travel down the pancreatic duct into the bile
duct in an inactive form. When they enter the duodenum, they are activated. The
exocrine tissue also secretes a bicarbonate to neutralize stomach acid in the
duodenum.The hormones secreted by the endocrine tissue in the pancreas are insulin
and glucagon (which regulate the level of glucose in the blood), and somatostatin
(which prevents the release of the other two hormones).
rr 



 


  

Hypothyroidism, or underactive thyroid, develops when the thyroid gland fails to

produce or secrete as much thyroxine (T4) as the body needs. Because T4 regulates
such essential functions as heart rate, digestion, physical growth, and mental
development, an insufficient supply of this hormone can slow life-sustaining processes,
damage organs and tissues in every part of the body, and lead to life-threatening
complications.

Hypothyroidism is one of the most common chronic diseases in the United States.
Symptoms may not appear until years after the thyroid has stopped functioning and they
are often mistaken for signs of other illnesses, menopause, or aging. Although this
condition is believed to affect as many as 11 million adults and children, as many as two
of every three people with hypothyroidism may not know they have the disease.

Nicknamed "Gland Central" because it influences almost every organ, tissue, and cell in
the body, the thyroid is shaped like a butterfly and located just below the Adam's apple.
The thyroid stores iodine the body gets from food and uses this mineral to create T4.
Low T4 levels can alter weight, appetite, sleep patterns, body temperature, sex drive,
and a variety of other physical, mental, and emotional characteristics.

There are three types of hypothyroidism. The most common is primary hypothyroidism,
in which the thyroid doesn't produce an adequate amount of T4. Secondary
hypothyroidism develops when the pituitary gland does not release enough of the
thyroid-stimulating hormone (TSH) that prompts the thyroid to manufacture T4. Tertiary
hypothyroidism results from a malfunction of the hypothalamus, the part of the brain that
controls the endocrine system. Drug-induced hypothyroidism, an adverse reaction to
medication, occurs in two of every 10,000 people, but rarely causes severe
hypothyroidism.
Hypothyroidism is at least twice as common in women as it is in men. Although
hypothyroidism is most common in women who are middle-aged or older, the disease
can occur at any age. Newborn infants are tested for congenital thyroid deficiency
(cretinism) using a test that measures the levels of thyroxine in the infant's blood.
Treatment within the first few months of life can prevent mental retardation and physical
abnormalities. Older children who develop hypothyroidism suddenly stop growing.

Factors that increase a person's risk of developing hypothyroidism include age, weight,
and medical history. Women are more likely to develop the disease after age 50; men,
after age 60. Obesity also increases risk. A family history of thyroid problems or a
personal history of high cholesterol levels or such autoimmune diseases as lupus,
rheumatoid arthritis, or diabetes can make an individual more susceptible to
hypothyroidism.

  

On average, the normal thyroid releases about 100 mcg of thyroxine (T4) daily and only
small amounts of triiodothyronine (T3). Levothyroxine (either natural or synthetic T4), a
prohormone, is converted to liothyronine (natural or synthetic T3), the active hormone in
the peripheral tissues. Decreased production of T4 causes an increase in secretion of
TSH by the pituitary. TSH causes the thyroid to release more T3 by stimulating thyroid
T4-5'-deiodinase activity and stimulates hyperplasia and hypertrophy of the thyroid.
Decreasing levels of T4 and increasing thyroid production of T3 leads to preservation of
T3 levels and lowering of T4 levels early in the disease.

c c
  

Hypothyroidism is most often the result of Hashimoto's disease, also known as chronic
thyroiditis (inflammation of the thyroid gland). In this disease, the immune system fails to
recognize that the thyroid gland is part of the body's own tissue and attacks it as if it
were a foreign body. The attack by the immune system impairs thyroid function and
sometimes destroys the gland. Other causes of hypothyroidism include:

= Radiation. Radioactive iodine used to treat hyperthyroidism (overactive thyroid)

or radiation treatments for head or neck cancers can destroy the thyroid gland.
= Surgery. Removal of the thyroid gland because of cancer or other thyroid
disorders can result in hypothyroidism.
= Viruses and bacteria. Infections that depress thyroid hormone production usually
cause permanent hypothyroidism.
= Medication. Nitroprusside, lithium, or iodides can induce hypothyroidism.
Because patients who use these medications are closely monitored by their
doctors, this side effect is very rare.
= Pituitary gland malfunction. This is a rare condition in which the pituitary gland
fails to produce enough TSH to activate the thyroid's production of T4.
= Congenital defect. One of every 4,000 babies is born without a properly
functioning thyroid gland.
= Diet. Because the thyroid makes T4 from iodine drawn from food, an iodine-
deficient diet can cause hypothyroidism. Adding iodine to table salt and other
common foods has eliminated iodine deficiency in the United States. Certain
foods (cabbage, rutabagas, peanuts, peaches, soybeans, spinach) can interfere
with thyroid hormone production.
= Environmental contaminants. Certain man-made chemicals(such as PCBs) found
in the local environment at high levels may also cause hypothyroidism.

Hypothyroidism is sometimes referred to as a "silent" disease because early symptoms

may be so mild that no one realizes anything is wrong. Untreated symptoms become
more noticeable and severe, and can lead to confusion and mental disorders, breathing
difficulties, heart problems, fluctuations in body temperature, and death.
Someone who has hypothyroidism will probably have more than one of the following
symptoms fatigue,decreased heart rate,progressive hearing loss,weight gain,problems
with memory and concentration,depression,goiter (enlarged thyroid gland),muscle pain
or weakness,loss of interest in sex,numb, tingling hands,dry skin,swollen
eyelids,dryness, loss, or premature graying of hair,extreme sensitivity to
cold,constipation,irregular menstrual periods and hoarse voice

Hypothyroidism usually develops gradually. When the disease results from surgery or
other treatment for hyperthyroidism, symptoms may appear suddenly and include
severe muscle cramps in the arms, legs, neck, shoulders, and back.
It's important to see a doctor if any of these symptoms appear unexpectedly. People
whose hypothyroidism remains undiagnosed and untreated may eventually develop
myxedema. Symptoms of this rare but potentially deadly complication include enlarged
tongue, swollen facial features, hoarseness, and physical and mental sluggishness.

Myxedema coma can cause unresponsiveness; irregular, shallow breathing; and a drop
in blood pressure and body temperature. The onset of this medical emergency can be
sudden in people who are elderly or have been ill, injured, or exposed to very cold
temperatures; who have recently had surgery; or who use sedatives or anti-
depressants. Without immediate medical attention, myxedema coma can be fatal.

   
 

The correct diagnosis of hypothyroidism depends on the following.

 ˜ Hypothyroidism doesn¶t have any characteristic symptoms.

There are no symptoms that people with hypothyroidism always have
and many symptoms of hypothyroidism can occur in people with
other diseases. One way to help figure out whether your complaints
are symptoms of hypothyroidism is to think about whether you¶ve
always had a symptom (hypothyroidism is less likely) or whether the
symptom is a change from the way you used to feel (hypothyroidism
is more likely).

   
. oou should tell your doctor:
= about changes in your health that suggest that your body is slowing
down;
= if you¶ve ever had thyroid surgery;
 = if you¶ve ever had radiation to your neck to treat cancer;
= if you¶re taking any of the medicines that can cause
hypothyroidism² amiodarone, lithium, interferon alpha, interleukin-
2, and maybe thalidomide;whether any of your family members have thyroid
disease.

 . The doctor will check your thyroid gland and look for
changes such as dry skin, swelling, slower reflexes, and a slower heart
rate.
  . There are two blood tests that are used in the diagnosis
of hypothyroidism.
= TSH (thyroid-stimulating hormone) test. This is the most important
and sensitive test for hypothyroidism. It measures how much of the
thyroid hormone thyroxine (T4) the thyroid gland is being asked to
make. An abnormally high TSH means hypothyroidism: the thyroid
gland is being asked to make more T4 because there isn¶t enough T4
in the blood.

= T4 tests. Most of the T4 in the blood is attached to a protein called

thyroxine-binding globulin. The ³bound´ T4 can¶t get into body cells.
Only about 1%±2% of T4 in the blood is unattached (³free´) and can
get into cells. The free T4 and the free T4 index are both simple blood
tests that measure how much unattached T4 is in the blood and available to get into
cells.

 
 
   

The therapeutic management of hypothyroidism caused by deficient thyroid hormone

production is discussed. The therapeutic use of the following thyroid agents is reviewed:
levothyroxine sodium, Thyroid USP, thyroglobulin, liotrix, and liothyronine sodium.
Myxedema coma, neonatal hypothyroidism, primary hypothyroidism, and secondary and
tertiary hypothyroidism are specific hypothyroid states for which drug therapy is
discussed. Levothyroxine sodium is the preferred agent because of consistent potency,
restoration of normal, constant serum levels of thyroxine (T4) and triiodothyronine (T3)
and ease of interpretation of thyroid hormone levels. Other agents, because they
contain T3, result in postabsorptive elevated T3 serum concentrations that may cause
thyrotoxic symptoms and reduction of T4 levels. This, in turn, may give rise to
misleading estimates of thyroid dosage. Patients with the sick euthyroid or low T3
syndromes are not candidates for thyroid hormone therapy.

!
c
   

= Assess the patient for manifestations of hypothyroidism an response to therapy

(eg: mental status, quality of skin and hair, subnormal temperature, bradycardia,
respiratory rate, BP, worsening heart failure, wt. gain or loss).
= Provide instructions for adhering to a low calorie diet until the patient's weight
stabilizes within an ideal range. Weight gain develops when the patient's appetite
improves with the start of therapy, but energy levels have not yet improved.
= Encourage activity as tolerated to reduce constipation
= Advise the pt. to drink 6-8 glasses of water daily and eat high fiber foods. A stool
softener may be needed if diet and exercise are ineffective. Reassure the pt. that
energy levels will return to normal after hormone therapy is begun.
= Maintain pt. airway, administering oxygen, and intravenous fluids for the patient
with myxedema coma.
= Monitor intake, output, and daily weights.
"#"#$rr

  

Too much thyroid hormone from an overactive thyroid gland is called hyperthyroidism, because
it speeds up the body's metabolism. This hormone imbalance occurs in about 1 percent of all
women, who get hyperthyroidism more often than men. One of the most common forms of
hyperthyroidism is known as Graves' disease. This autoimmune disorder tends to run in
families, although the exact nature of the genetic abnormality is unknown.Increase secretion of
T3 and T4 Graves disease or thyrotoxicosis is the most common type.Can be treated with
surgical removal of thyroid gland (thyroidectomy) radiation Iodine therapy and antithyroid drugs.

 $"r$%$"

In hyperthyroidism, serum T3 usually increases more than does T4, probably because of
increased secretion of T3 as well as conversion of T4 to T3 in peripheral tissues. In some
patients, only T3 is elevated (T3 toxicosis). T3 toxicosis may occur in any of the usual disorders
that produce hyperthyroidism, including Graves' disease, multinodular goiter, and the
autonomously functioning solitary thyroid nodule. If T3 toxicosis is untreated, the patient usually
also develops laboratory abnormalities typical of hyperthyroidism. The various forms of
thyroiditis commonly have a hyperthyroid phase followed by a hypothyroid phase.

c c%r!rc%!r r$!

Most symptoms and signs are the same regardless of the cause. Exceptions include
infiltrative ophthalmopathy and dermopathy, which occur only in Graves' disease.The
clinical presentation may be dramatic or subtle. A goiter or nodule may be present.
Many common symptoms and signs of hyperthyroidism are similar to those of
adrenergic excess, such as nervousness, palpitations, hyperactivity, increased
sweating, heat hypersensitivity, fatigue, increased appetite, weight loss, insomnia,
weakness, and frequent bowel movements (occasionally diarrhea). Hypomenorrhea
may be present. Signs may include warm, moist skin; tremor; tachycardia; widened
pulse pressure; atrial fibrillation; and palpitations.

Elderly patients, particularly those with toxic nodular goiter, may present atypically
(apathetic or masked hyperthyroidism) with symptoms more akin to depression or
dementia. Most do not have exophthalmos or tremor. Atrial fibrillation, syncope, altered
sensorium, heart failure, and weakness are more likely. Symptoms and signs may
involve only a single organ system.

Eye signs include stare, eyelid lag, eyelid retraction, and mild conjunctival injection and
are largely due to excessive adrenergic stimulation. They usually remit with successful
treatment. Infiltrative ophthalmopathy, a more serious development, is specific to
Graves' disease and can occur years before or after hyperthyroidism. It is characterized
by orbital pain, lacrimation, irritation, photophobia, increased retro-orbital tissue,
exophthalmos, and lymphocytic infiltration of the extraocular muscles, producing ocular
muscle weakness that frequently leads to double vision.

Infiltrative dermopathy, also called pretibial myxedema (a confusing term, because

myxedema suggests hypothyroidism), is characterized by nonpitting infiltration by
proteinaceous ground substance, usually in the pretibial area. It rarely occurs in the
absence of Graves' ophthalmopathy. The lesion is often pruritic and erythematous in its
early stages and subsequently becomes brawny. Infiltrative dermopathy may appear
years before or after hyperthyroidism.

   
 

Diagnosis is based on history, physical examination, and thyroid function tests. Serum
TSH measurement is the best test, because TSH is suppressed in hyperthyroid patients
except in the rare instance when the etiology is a TSH-secreting pituitary adenoma or
pituitary resistance to thyroid hormone. Screening selected populations for TSH level is
warranted. Free T4 is increased in hyperthyroidism. However, T4 can be falsely normal
in true hyperthyroidism in patients with a severe systemic illness (similar to the falsely
low levels that occur in euthyroid sick syndrome) and in T3 toxicosis. If free T4 level is
normal and TSH is low in a patient with subtle symptoms and signs of hyperthyroidism,
then serum T3 should be measured to detect T3 toxicosis; an elevated level confirms
that diagnosis.The cause can often be diagnosed clinically (eg, exposure to a drug, the
presence of signs specific to Graves' disease). When hyperthyroidism is due to
hormone overproduction, thyroid radioactive iodine uptake is usually elevated.

Physicians will look for physical signs and symptoms indicated by patient history. On
inspection, the physician may note symptoms such as a goiter or eye bulging. Other
symptoms or family history may be clues to a diagnosis of hyperthyroidism. An elevated
body temperature (basal body temperature) above 98.6 °F (37 °C) may be an indication
of a heightened metabolic rate (basal metabolic rate) and hyperthyroidism. A simple
blood test can be performed to determine the amount of thyroid hormone in the patient's
blood. The diagnosis is usually straightforward with this combination of clinical history,
physical examination, and routine blood hormone tests. Radioimmunoassay, or a test to
show concentrations of thyroid hormones with the use of a radioisotope mixed with fluid
samples, helps confirm the diagnosis. A thyroid scan is a nuclear medicine procedure
involving injection of a radioisotope dye which will tag the thyroid and help produce a
clear image of inflammation or involvement of the entire thyroid. Other tests can
determine thyroid function and thyroid-stimulating hormone levels. Ultrasonography,
computed tomography scans (CT scan), and magnetic resonance imaging (MRI) may
provide visual confirmation of a diagnosis or help to determine the extent of
involvement.

TSH receptor antibodies can be measured to detect Graves' disease, but measurement
is rarely necessary except during the 3rd trimester of pregnancy to assess the risk of
neonatal Graves' disease; TSH receptor antibodies readily cross the placenta to
stimulate the fetal thyroid. Most patients with Graves' disease have circulating
antithyroid peroxidase antibodies, and fewer have antithyroglobulin
antibodies.Inappropriate TSH secretion is uncommon. The diagnosis is confirmed when
hyperthyroidism occurs with elevated circulating free T4 and T3 concentrations and
normal or elevated serum TSH.If thyrotoxicosis factitia is suspected, serum
 thyroglobulin can be measured; it is usually low or low-normal²unlike in all other
causes of hyperthyroidism.In hyperthyroidism caused by excess iodine ingestion, low
radioactive iodine uptake is typical because thyroid radioactive iodine uptake is
inversely proportional to iodine intake.

 #&rc!!

> Monitor for signs and symptoms of thyrotoxicosis

> Provide calm cool environment
> Increase Protein and increase calorie diet
> Teach signs and symptoms of hypothyroidism, which may occur with treatment
> Give eye care (drops, patches) prn
> Thyrotoxicosis: Hypothermia blanket, oxygen, propranolol, steroids,
propylthiouracil, iodide

!
c
   

> Determine baseline vital signs

> Check serum T3, T4 and TSH levels.Report abnormal results.
> Note for drug interaction-anticoagulant, sympathomimetics and insulin.
> Asses for symptoms of thyroid crisis.
> Monitor vital signs.
> Instruct clients to take drug with meals.take vital signs note for tachycardia and palpitations.

 c'


  

Cushing's syndrome, also called hypercortisolism, has an adverse effect on all of the
processes described above. The syndrome occurs in approximately 10 to 15 out of
every one million people per year, usually striking adults between the ages of 20 and
50. An estimated 10 to 15 of every million people are affected each year. The term
³CUSHING SoNDROME´ is to describe a hormonal disorder resulting from long term
exposure to excessive glucocorticoids .A Cushing syndrome affects about 3 times more
women than males.The condition is reversible once steroids are gradually withdrawn.
People who are obese and have a type 2 diabetes, along with poorly controlled blood
glucose- and also called blood sugar-and have high blood pressure, have an increased
risk of developing this disorder.

  

The cause of Cushing's syndrome is usually divided into two broad categories:
Exogenous and endogenous.

> Exogenous (outside) causes- prolonged use of glucocorticoids (e.g. prednisone) for
diseases such as asthma and rheumatoid arthritis
- Food dependent: - in appropriate sensitivity of adrenal glands to normal postprandial
increases in secretion of gastric inhibitory polypeptide
> Endogenous (outside) cause¶s benign pituitary adenoma secretes ACTH. This is
responsible for 65% of endogenous Cushing's syndrome.
- Excess cortisol is produced by adrenal gland tumors, hyperplastic adrenal glands, or
adrenal glands with nodular adrenal hyperplasia (adrenocortical neoplasms)

First, the hypothalamus, a part of the brain about the size of a small sugar cube, sends
corticotropin-releasing hormone (CRH) to the pituitary gland. CRH causes the pituitary
to secrete adrenocorticotropin hormone (ACTH), which stimulates the adrenal glands.
When the adrenals, which are located just above the kidneys, receive the ACTH, they
respond by releasing cortisol into the bloodstream.

The hypothalamus sends CRH to the pituitary, which responds by secreting ACTH.
ACTH then causes the adrenals to release cortisol into the bloodstream.

One of cortisol¶s most important jobs is to help the body respond to stress. For this
reason, women in their last 3 months of pregnancy and highly trained athletes normally
have high levels of the hormone. People suffering from depression, alcoholism,
malnutrition, or panic disorders also have increased cortisol levels.

When the amount of cortisol in the blood is adequate, the hypothalamus and pituitary
release less CRH and ACTH. This process ensures the amount of cortisol released by
the adrenal glands is precisely balanced to meet the body¶s daily needs. However, if
something goes wrong with the adrenals or the regulating switches in the pituitary gland
or hypothalamus, cortisol production can go awry.

c c
  

The clinical manifestations are non-specific and overlap with much more common
disorders such as simple obesity, hypertension, type 2 DM and depression.

The most common cause of Cushing's syndrome is the long-term use of glucocorticoid
hormones in medications. Medications such as prednisone are used in a number of
inflammatory conditions. Such conditions include rheumatoid arthritis, asthma,
vasculitis, lupus, and a variety of other autoimmune disorders in which the body's
immune cells accidentally attack some part of the body itself. In these disorders, the
glucocorticoids are used to dampen the immune response, thereby decreasing damage
to the body.

Cushing's syndrome can also be caused by three different categories of disease:

= a pituitary tumor producing abnormally large quantities of ACTH

= the abnormal production of ACTH by some source other than the pituitary
 = a tumor within the adrenal gland overproducing cortisol

Although it is rare, about two-thirds of endogenous (occurring within the body rather
than from a source outside the body, like a medication) Cushing's syndrome which is
caused by excessive secretion of ACTH by a pituitary tumor, usually an adenoma
(noncancerous tumor). The pituitary tumor causes increased growth of the adrenal
cortex (hyperplasia) and increased cortisol production. Cushing's disease affects
women more often than men.
Tumors in locations other than the pituitary can also produce ACTH. This is called
ectopic ACTH syndrome ("ectopic" refers to something existing out of its normal place).
Tumors in the lung account for more than half of all cases of ectopic ACTH syndrome.
Other types of tumors that may produce ACTH include tumors of the thymus, the
pancreas, the thyroid, and the adrenal gland. Nearly all adrenal gland tumors are benign
(noncancerous), although in rare instances a tumor may actually be cancerous.

Symptoms of cortisol excess (resulting from medication or from the body's excess
production of the hormone) include:

= weight gain
= an abnormal accumulation of fatty pads in the face (creating the distinctive "moon
face" of Cushing's syndrome); in the trunk (termed "truncal obesity"); and over
the upper back and the back of the neck (giving the individual what has been
called a "buffalo hump")
= purple and pink stretch marks across the abdomen and flanks
= high blood pressure
= weak, thinning bones (osteoporosis)
= weak muscles
= low energy
= thin, fragile skin, with a tendency toward both bruising and slow healing
= abnormalities in the processing of sugars (glucose), with occasional development
of actual diabetes
= kidney stones
 = increased risk of infections
= emotional disturbances, including mood swings, depression, irritability, confusion,
or even a complete break with reality (psychosis)
= irregular menstrual periods in women
= decreased sex drive in men and difficulty maintaining an erection
= abormal hair growth in women (in a male pattern, such as in the beard and
mustache area), as well as loss of hair from the head (receding hair line).

   
  

No single lab test is perfect and usually several are needed. The three most common
tests used to diagnose Cushing¶s syndrome are the 24-hour urinary free cortisol test,
measurement of midnight plasma cortisol or late-night salivary cortisol, and the low-
dose dexamethasone suppression test. Another test, the dexamethasone-
corticotropinreleasing hormone test, may be needed to distinguish Cushing¶s syndrome
from other causes of excess cortisol.

> ¢







( In this test, a person¶s urine is collected several
times over a 24-hour period and tested for cortisol. Levels higher than 50 to 100
micrograms a day for an adult suggest Cushing¶s syndrome. The normal upper limit
varies in different laboratories, depending on which measurement technique is used.

>    


  
  (


 
  The
midnight plasma cortisol test measures cortisol concentrations in the blood. Cortisol
production is normally suppressed at night, but in Cushing¶s syndrome, this suppression
doesn¶t occur. If the cortisol level is more than 50 nanomoles per liter (nmol/L),
Cushing¶s syndrome is suspected. The test generally requires a 48-hour hospital stay to
avoid falsely elevated cortisol levels due to stress.
However, a late-night or bedtime saliva sample can be obtained at home, then tested
to determine the cortisol level. Diagnostic ranges vary, depending on the measurement
technique used.
> %)
   
  *%+ In the LDDST, a person is
given a low dose of dexamethasone, a synthetic glucocorticoid, by mouth every 6 hours
for 2 days. Urine is collected before dexamethasone is administered and several times
on each day of the test. A modified LDDST uses a onetime overnight dose.
Cortisol and other glucocorticoids signal the pituitary to release less ACTH, so the
normal response after taking dexamethasone is a drop in blood and urine cortisol levels.
If cortisol levels do not drop, Cushing¶s syndrome is suspected.

The LDDST may not show a drop in cortisol levels in people with depression,
alcoholism, high estrogen levels, acute illness, or stress, falsely indicating Cushing¶s
syndrome. On the other hand, drugs such as phenytoin and phenobarbital may cause
cortisol levels to drop, falsely indicating that Cushing¶s is not present in people who
actually have the syndrome. For this reason, physicians usually advise their patients to
stop taking these drugs at least 1 week before the test

>    






 
*c
+  Some people have
high cortisol levels but do not develop the progressive effects of Cushing¶s syndrome,
such as muscle weakness, fractures, and thinning of the skin. These people may have
pseudo-Cushing¶s syndrome, a condition sometimes found in people who have
depression or anxiety disorders, drink excess alcohol, have poorly controlled diabetes,
or are severely obese. Pseudo-Cushing¶s does not have the same long-term effects on
health as Cushing¶s syndrome and does not require treatment directed at the endocrine
glands. The dexamethasone-CRH test rapidly distinguishes pseudo-Cushing¶s from mild
cases of Cushing¶s. This test combines the LDDST and a CRH stimulation test. In the
CRH stimulation test, an injection of CRH causes the pituitary to secrete ACTH.
Pretreatment with dexamethasone prevents CRH from causing an increase in cortisol in
people with pseudoCushing¶s. Elevations of cortisol during this test suggest Cushing¶s
syndrome.




  
 
   

Treatments for Cushing's syndrome are designed to lower the high level of cortisol in
your body. The best treatment for you depends on the cause of the syndrome.
Treatment options include:

> #



 
 If the cause of Cushing's syndrome is long-term use of
corticosteroid medications, your doctor may be able to keep your Cushing's signs and
symptoms under control by reducing the dosage of the drug over a period of time, while
still adequately managing your asthma, arthritis or other condition. For many of these
medical problems, your doctor can prescribe noncorticosteroid drugs, which will allow
him or her to reduce the dosage or eliminate the use of corticosteroids altogether.

Don't reduce the dose of corticosteroid drugs or stop taking them on your own. Do so
only under your doctor's supervision. Abruptly discontinuing these medications could
lead to deficient cortisol levels. Slowly tapering off corticosteroid drugs allows your body
to resume normal cortisol production.

> 

 If the cause of Cushing's syndrome is a tumor, your doctor may recommend
complete surgical removal. Pituitary tumors are typically removed by a neurosurgeon,
who may perform the procedure through your nose. If a tumor is present in the adrenal
glands, lungs or pancreas, the surgeon can remove it through a standard operation or in
some cases by using minimally invasive surgical techniques, with smaller incisions.

After the operation, you'll need to take cortisol replacement medications to provide your
body with the correct amount of cortisol. In most cases, you'll eventually experience a
return of normal adrenal hormone production, and your doctor can taper off the
replacement drugs. However, this process can take up to a year or longer. In some
instances, people with Cushing's syndrome never experience a resumption of normal
adrenal function; they then need lifelong replacement therapy.
l #   
 If the surgeon can't totally remove a pituitary tumor, he or she will
usually prescribe radiation therapy to be used in conjunction with the operation.
Additionally, radiation may be used for people who aren't suitable candidates for
surgery. Radiation can be given in small doses over a six-week period, or by a
technique called stereotactic radiosurgery or gamma-knife radiation. In the latter
procedure, administered as a single treatment, a large dose of radiation is delivered to
the tumor, and the radiation exposure to surrounding tissues is minimized.
l 
 Medications can be used to control cortisol production when surgery and
radiation don't work. Medications may also be used before surgery in people who have
become very sick with Cushing's syndrome. Doctors recommend drug therapy before
surgery to improve signs and symptoms and minimize surgical risk. Medications to
control excessive production of cortisol include ketoconazole (Nizoral), mitotane
(Lysodren) and metyrapone (Metopirone).

In some cases, the tumor or its treatment will cause other hormones produced by the
pituitary or adrenal gland to become deficient and your doctor will recommend hormone
replacement medications.

If none of these treatment options is effective, your doctor may recommend surgical
removal of your adrenal glands (bilateral adrenalectomy). This procedure will cure
excess production of cortisol. However, your ACTH levels will remain high, possibly
causing excess pigmentation of your skin.

!
c
   

= Monitor intake and output, daily weights, and serum glucose and electrolytes.
= Monitor for signs of infection because risk is high with excess glucocorticoids.
= After hypophysectomy, monitor for diabetes insipidus, hypothyroidism, and other
endocrine changes.
= Assess the skin frequently to detect reddened areas, skin breakdown or tearing,
excoriation, infection or edema.
= Handle skin and extremity gently to prevent trauma; prevent falls by using siderails.
= Avoid using adhesive tape on the skin to reduce trauma on its removal.
= Encourage the patient to turn in bed frequently or ambulate to reduce pressure on bony
prominences and areas of edema.
= Assist the patient with ambulation and hygiene when weak and fatigued. Use assistive
devices during ambulation to prevent falls and fractures.
= Help the patient to schedule exercise and rest. Advise the patient how to recognize
signs and symptoms of excessive exertion.
= Instruct the patient to correct body mechanics to avoid pain or injury during activities.
= Provides foods low in sodium to minimize edema and provide foods high in potassium
(bananas, orange juice, tomatoes) and administer potassium supplements as
prescribed to counteract weakness re;ated to hypokalemia.
= Report edema and signs of fluid retention.
= Encourage the patient to verbalize concerns about the illness, changes in appearance,
and alters role function.
= Explain to female patient who has benign adenoma or hyperplasia that, with proper
treatment, evidence of masculinization can be reversed.
   

  
Diabetes Mellitus is a disease in which the body does not produce or properly use
insulin to regulate the amount of glucose or sugar in the blood. It starts out as a
dysfunction in pancreas, but ends up wrecking eyes , feet and heart, causing great
disabilities˜ Diabetes is a disorder of the metabolism described as high levels of blood
glucose caused by a imperfection in creating insulin, failure to respond to insulin¶s
effects (insulin resistance), or both. Low blood sugar occurs from occasionally in many
people with diabetes. Diabetes is one of the most common lifelong ailments in children.

"$ r%%r&

Type I diabetes, sometimes called juvenile diabetes, begins most commonly in

childhood or adolescence. In this form of diabetes, the body produces little or no insulin.
It is characterized by a sudden onset and occurs more frequently in populations
descended from Northern European countries (Finland, Scotland, Scandinavia) than in
those from Southern European countries, the Middle East, or Asia. In the United States,
approximately three people in 1,000 develop Type I diabetes. This form also is called
insulin-dependent diabetes because people who develop this type need to have daily
injections of insulin.

Brittle diabetics are a subgroup of Type I where patients have frequent and rapid swings
of blood sugar levels between hyperglycemia (a condition where there is too much
glucose or sugar in the blood) and hypoglycemia (a condition where there are
abnormally low levels of glucose or sugar in the blood). These patients may require
several injections of different types of insulin during the day to keep the blood sugar
level within a fairly normal range.

The more common form of diabetes, Type II, occurs in approximately 3-5% of
Americans under 50 years of age, and increases to 10-15% in those over 50. More than
90% of the diabetics in the United States are Type II diabetics. Sometimes called age-
onset or adult-onset diabetes, this form of diabetes occurs most often in people who are
overweight and who do not exercise. It is also more common in people of Native
American, Hispanic, and African-American descent. People who have migrated to
Western cultures from East India, Japan, and Australian Aboriginal cultures also are
more likely to develop Type II diabetes than those who remain in their original countries.

Type II is considered a milder form of diabetes because of its slow onset (sometimes
developing over the course of several years) and because it usually can be controlled
with diet and oral medication. The consequences of uncontrolled and untreated Type II
diabetes, however, are the just as serious as those for Type I. This form is also called
noninsulin-dependent diabetes, a term that is somewhat misleading. Many people with
Type II diabetes can control the condition with diet and oral medications, however,
insulin injections are sometimes necessary if treatment with diet and oral medication is
not working.

Another form of diabetes called gestational diabetes can develop during pregnancy and
generally resolves after the baby is delivered. This diabetic condition develops during
the second or third trimester of pregnancy in about 2% of pregnancies. In 2004,
incidence of gestational diabetes were reported to have increased 35% in 10 years.
Children of women with gestational diabetes are more likely to be born prematurely,
have hypoglycemia, or have severe jaundice at birth. The condition usually is treated by
diet, however, insulin injections may be required. These women who have diabetes
during pregnancy are at higher risk for developing Type II diabetes within 5-10 years.

Diabetes also can develop as a result of pancreatic disease, alcoholism, malnutrition, or

other severe illnesses that stress the body.

  

Insulin is the principal hormone that regulates uptake of glucose from the blood into
most cells (primarily muscle and fat cells, but not central nervous system cells).
Therefore deficiency of insulin or the insensitivity of its receptors plays a central role in
all forms of diabetes mellitus. Humans are capable of digesting some carbohydrates, in
particular those most common in food; starch, and some disaccharides such as
sucrose, are converted within a few hours to simpler forms most notably the
monosaccharide glucose, the principal carbohydrate energy source used by the body.
The rest are passed on for processing by gut flora largely in the colon. Insulin is
released into the blood by beta cells (ȕ-cells), found in the Islets of Langerhans in the
pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is
used by about two-thirds of the body's cells to absorb glucose from the blood for use as
fuel, for conversion to other needed molecules, or for storage. Insulin is also the
principal control signal for conversion of glucose to glycogen for internal storage in liver
and muscle cells. Lowered glucose levels result both in the reduced release of insulin
from the beta cells and in the reverse conversion of glycogen to glucose when glucose
levels fall. This is mainly controlled by the hormone glucagon which acts in the opposite
manner to insulin. Glucose thus forcibly produced from internal liver cell stores (as
glycogen) re-enters the bloodstream; muscle cells lack the necessary export
mechanism. Normally liver cells do this when the level of insulin is low (which normally
correlates with low levels of blood glucose). Higher insulin levels increase some
anabolic ("building up") processes such as cell growth and duplication, protein
synthesis, and fat storage. Insulin (or its lack) is the principal signal in converting many
of the bidirectional processes of metabolism from a catabolic to an anabolic direction,
and vice versa. In particular, a low insulin level is the trigger for entering or leaving
ketosis (the fat burning metabolic phase). If the amount of insulin available is
insufficient, if cells respond poorly to the effects of insulin (insulin insensitivity or
resistance), or if the insulin itself is defective, then glucose will not have its usual effect
so that glucose will not be absorbed properly by those body cells that require it nor will it
be stored appropriately in the liver and muscles. The net effect is persistent high levels
of blood glucose, poor protein synthesis, and other metabolic derangements, such as
acidosis. When the glucose concentration in the blood is raised beyond its renal
threshold (about 10 mmol/L, although this may be altered in certain conditions, such as
pregnancy), reabsorption of glucose in the proximal renal tubuli is incomplete, and part
of the glucose remains in the urine (glycosuria). This increases the osmotic pressure of
the urine and inhibits reabsorption of water by the kidney, resulting in increased urine
production (polyuria) and increased fluid loss. Lost blood volume will be replaced
osmotically from water held in body cells and other body compartments, causing
dehydration and increased thirst.

c c
  
The symptomatology of diabetes is more readily recognizable in children than in adults,
so it is surprising that the diagnosis may sometimes be missed or delayed, Diabetes is a
great imitator: influenza, gastroenteritis, and appendicitis are the conditions more often
diagnosed, only to find that the disease was really diabetes. Those families with a
strong family history of diabetes should suspect diabetes, especially if there is one child
in the family with diabetes. Main manifestations are polyuria, polydipsia, polyphagia,
progressive cachexia, glucosuria, hyperglycemia, and increasing of specific gravity of
urine.The sequence of chemical events described previously results in hyperglycemia
and acidosis, which in turn produce the three "P¶s" of diabetes- polyphagia, polydipsia,
and polyuria- the cardinal symptoms of the disease.In non-insulin-dependent diabetes
(which has also been found in older children), the insulin values are found to be
overweight, and there is often tiredness and frequent infections (such as monilial
infections in females).The insulin-dependent diabetic has markedly decreased insulin
levels and, as diabetes becomes complete, there is no demonstrable, insulin at all.The
child may start wetting the bed, become grouchy and "not himself" or act overly tired.

The causes of diabetes mellitus are unclear, however, there seem to be both hereditary
(genetic factors passed on in families) and environmental factors involved. Research
has shown that some people who develop diabetes have common genetic markers. In
Type I diabetes, the immune system, the body's defense system against infection, is
believed to be triggered by a virus or another microorganism that destroys cells in the
pancreas that produce insulin. In Type II diabetes, age, obesity, and family history of
diabetes play a role.

In Type II diabetes, the pancreas may produce enough insulin, however, cells have
become resistant to the insulin produced and it may not work as effectively. Symptoms
of Type II diabetes can begin so gradually that a person may not know that he or she
has it. Early signs are lethargy, extreme thirst, and frequent urination. Other symptoms
may include sudden weight loss, slow wound healing, urinary tract infections, gum
disease, or blurred vision. It is not unusual for Type II diabetes to be detected while a
patient is seeing a doctor about another health concern that is actually being caused by
the yet undiagnosed diabetes.

Individuals who are at high risk of developing Type II diabetes mellitus include people
who:

= are obese (more than 20% above their ideal body weight)
= have a relative with diabetes mellitus
= belong to a high-risk ethnic population (African-American, Native American,
Hispanic, or Native Hawaiian)
= have been diagnosed with gestational diabetes or have delivered a baby
weighing more than 9 lbs (4 kg)
= have high blood pressure (140/90 mmHg or above)
= have a high density lipoprotein cholesterol level less than or equal to 35 mg/dL
and/or a triglyceride level greater than or equal to 250 mg/dL
= have had impaired glucose tolerance or impaired fasting glucose on previous
testing

Several common medications can impair the body's use of insulin, causing a condition
known as secondary diabetes. These medications include treatments for high blood
pressure (furosemide, clonidine, and thiazide diuretics), drugs with hormonal activity
(oral contraceptives, thyroid hormone, progestins, and glucocorticorids), and the anti-
inflammation drug indomethacin. Several drugs that are used to treat mood disorders
(such as anxiety and depression) also can impair glucose absorption. These drugs
include haloperidol, lithium carbonate, phenothiazines, tricyclic antidepressants, and
adrenergic agonists. Other medications that can cause diabetes symptoms include
isoniazid, nicotinic acid, cimetidine, and heparin. A 2004 study found that low levels of
the essential mineral chromium in the body may be linked to increased risk for diseases
associated with insulin resistance.
Symptoms of diabetes can develop suddenly (over days or weeks) in previously healthy
children or adolescents, or can develop gradually (over several years) in overweight
adults over the age of 40. The classic symptoms include feeling tired and sick, frequent
urination, excessive thirst, excessive hunger, and weight loss.

Ketoacidosis, a condition due to starvation or uncontrolled diabetes, is common in Type

I diabetes. Ketones are acid compounds that form in the blood when the body breaks
down fats and proteins. Symptoms include abdominal pain, vomiting, rapid breathing,
extreme lethargy, and drowsiness. Patients with ketoacidosis will also have a sweet
breath odor. Left untreated, this condition can lead to coma and death.

With Type II diabetes, the condition may not become evident until the patient presents
for medical treatment for some other condition. A patient may have heart disease,
chronic infections of the gums and urinary tract, blurred vision, numbness in the feet
and legs, or slow-healing wounds. Women may experience genital itching.

   
 
Diabetes is suspected based on symptoms. Urine tests and blood tests can be used to
confirm a diagnose of diabetes based on the amount of glucose found. Urine can also
detect ketones and protein in the urine that may help diagnose diabetes and assess
how well the kidneys are functioning. These tests also can be used to monitor the
disease once the patient is on a standardized diet, oral medications, or insulin.

&
  

Clinistix and Diastix are paper strips or dipsticks that change color when dipped in urine.
The test strip is compared to a chart that shows the amount of glucose in the urine
based on the change in color. The level of glucose in the urine lags behind the level of
glucose in the blood. Testing the urine with a test stick, paper strip, or tablet that
changes color when sugar is present is not as accurate as blood testing, however it can
give a fast and simple reading.
Ketones in the urine can be detected using similar types of dipstick tests (Acetest or
Ketostix). Ketoacidosis can be a life-threatening situation in Type I diabetics, so having
a quick and simple test to detect ketones can assist in establishing a diagnosis sooner.
Another dipstick test can determine the presence of protein or albumin in the urine.
Protein in the urine can indicate problems with kidney function and can be used to track
the development of renal failure. A more sensitive test for urine protein uses
radioactively tagged chemicals to detect microalbuminuria, small amounts of protein in
the urine, that may not show up on dipstick tests.

  
> 



 ± blood glucose levels are checked after fasting for
between 12 and 14 hours. oou can drink water during this time, but should
strictly avoid any other beverage. Patients with diabetes may be asked to delay
their diabetes medication or insulin dose until the test is completed.
> O 



 ± blood glucose levels are checked at various
times during the day, and it doesn¶t matter when you last ate. Blood glucose
levels tend to stay constant in a person who doesn¶t have diabetes.
> å 
   
 ± a high-glucose drink is given. Blood samples are
checked at regular intervals for two hours.


 
 
   
= Children with diabetes need their parents' help to keep their blood sugar levels in
a safe range and to exercise safely. It is important for children to learn the
symptoms of both high and low blood sugar so they can tell others when they
need help.
= Management involves nutrition management, increased physical activity, and
blood glucose testing.
= Type 2 diabetes is different from type 1 in that the child's life is generally not in
immediate danger without treatment.
= Metformin is the only oral medication that's approved for children and
adolescents (age 10 and older) who have type 2 diabetes.
 = Aspirin; Diet Control; LDL cholesterol; ACE Inhibitors

!
c
   
± Monitor VS, body weight,
± Daily care routines are described,
± Proper nutrition, the benefits of exercise, hygiene, psychosocial factors, and self
monitoring of blood glucose levels
± Long-term financial aspects of the disease, and whether the patient can obtain
adequate medical and life insurance.
± Support of family˜

  
, 


  

Diabetic ketoacidosis is a dangerous complication of diabetes mellitus in which the

chemical balance of the body becomes far too acidic..Diabetic ketoacidosis (DKA)
results from dehydration during a state of relative insulin deficiency, associated with
high blood levels of sugar level and organic acids called ketones. Diabetic ketoacidosis
is associated with significant disturbances of the body's chemistry, which resolve with
proper therapy. Diabetic ketoacidosis usually occurs in people with type 1 (juvenile)
diabetes mellitus (T1DM), but diabetic ketoacidosis can develop in any person with
diabetes. Since type 1 diabetes typically starts before age 25 years, diabetic
ketoacidosis is most common in this age group, but it may occur at any age. Males and
females are equally affected.

Diabetic ketoacidosis (DKA) always results from a severe insulin deficiency. Insulin is
the hormone secreted by the body to lower the blood sugar levels when they become
too high. Diabetes mellitus is the disease resulting from the inability of the body to
produce or respond properly to insulin, required by the body to convert glucose to
energy. In childhood diabetes, DKA complications represent the leading cause of death,
mostly due to the accumulation of abnormally large amounts of fluid in the brain
(cerebral edema). DKA combines three major features: hyperglycemia, meaning
excessively high blood sugar kevels; hyperketonemia, meaning an overproduction of
ketones by the body; and acidosis, meaning that the blood has become too acidic.
Insulin deficiency is responsible for all three conditions: the body glucose goes largely
unused since most cells are unable to transport glucose into the cell without the
presence of insulin; this condition makes the body use stored fat as an alternative
source instead of the unavailable glucose for energy, a process that produces acidic
ketones, which build up because they require insulin to be broken down. The presence
of excess ketones in the bloodstream in turn causes the blood to become more acidic
than the body tissues, which creates a toxic condition.
  

Insulin deficiency causes the body to metabolize triglycerides and muscle instead of
glucose for energy. Serum levels of glycerol and free fatty acids (FFAs) rise because of
unrestrained lipolysis, as does alanine from muscle catabolism. Glycerol and alanine
provide substrate for hepatic gluconeogenesis, which is stimulated by the excess of
glucagon that accompanies insulin deficiency. Glucagon also stimulates mitochondrial
conversion of FFAs into ketones. Insulin normally blocks ketogenesis by inhibiting the
transport of FFA derivatives into the mitochondrial matrix, but ketogenesis proceeds in
the absence of insulin. The major ketoacids produced, acetoacetic acid and ȕ-
hydroxybutyric acid, are strong organic acids that create metabolic acidosis. Acetone
derived from the metabolism of acetoacetic acid accumulates in serum and is slowly
disposed of by respiration.

Hyperglycemia caused by insulin deficiency produces an osmotic diuresis that leads to

marked urinary losses of water and electrolytes. Urinary excretion of ketones obligates
additional losses of Na and K. Serum Na may fall from natriuresis or rise due to
excretion of large volumes of free water. K is also lost in large quantities, sometimes >
300 mEq/24 h. Despite a significant total body deficit of K, initial serum K is typically
normal or elevated because of the extracellular migration of K in response to acidosis. K
levels generally fall further during treatment as insulin therapy drives K into cells. If
serum K is not monitored and replaced as needed, life-threatening hypokalemia may
develop.

c c
  

DKA is most commonly seen in individuals with type I diabetes, under 19 years of age
and is usually caused by the interruption of their insulin treatment or by acute infection
or trauma. A small number of people with type II diabetes also experience ketoacidosis,
but this is rare given the fact that type II diabetics still produce some insulin naturally.
When DKA occurs in type II patients, it is usually caused by a decrease in food intake
and an increased insulin deficiency due to hyperglycemia.

Symptoms and signs of DKA include those of hyperglycemia with the addition of
nausea, vomiting, and²particularly in children²abdominal pain. Lethargy and
somnolence are symptoms of more severe decompensation. Patients may be
hypotensive and tachycardic from dehydration and acidosis; they may breathe rapidly
and deeply to compensate for acidemia (Kussmaul's respirations). They may also have
fruity breath due to exhaled acetone. Fever is not a sign of DKA itself and, if present,
signifies underlying infection. In the absence of timely treatment, DKA progresses to
coma and death.

Acute cerebral edema, a complication in about 1% of DKA patients, occurs primarily in

children and less often in adolescents and young adults. Headache and fluctuating level
of consciousness herald this complication in some patients, but respiratory arrest is the
initial manifestation in others. The cause is not well understood but may be related to
too-rapid reductions in serum osmolality or to brain ischemia. It is most likely to occur in
children < 5 yr when DKA is the initial presentation of DM. Children with the highest
BUN and lowest Paco2 at presentation appear to be at greatest risk. Delays in
correction of hyponatremia and the use of HCO3 during DKA treatment are additional
risk factors.

   
  

The diagnosis of diabetic ketoacidosis is typically made after the health care practitioner
obtains a history, performs a physical examination, and reviews the laboratory
tests.Blood tests will be ordered to document the levels of sugar, potassium, sodium,
and other electrolytes. Ketone level and kidney function tests along with a blood gas
sample (to assess the blood acid level, or pH) are also commonly performed.Other tests
may be used to check for conditions that may have triggered the diabetic ketoacidosis,
based on the history and physical examination findings. These may include chest X-ray,
electrocardiogram (ECG), urine analysis, and possibly a CT scan of the brain.
In patients suspected of having DKA, serum electrolytes, BUN and creatinine, glucose,
ketones, and osmolarity should be measured. Urine should be tested for ketones.
Those who appear significantly ill and those with positive ketones should have ABG
measurement. DKA is diagnosed by an arterial pH < 7.30 with an anion gap > 12 (see
Sidebar 1: Acid-Base Regulation and Disorders: The Anion Gap) and serum ketones in
the presence of hyperglycemia. A presumptive diagnosis can be made when urine
glucose and ketones are strongly positive. Urine test strips and some assays for serum
ketones may underestimate the degree of ketosis because they detect acetoacetic and
not ȕ-hydroxybutyric acid, which is usually the predominant ketoacid.Signs and
symptoms of a triggering illness should be pursued with appropriate studies (eg,
cultures, imaging studies). Adults should have an ECG to screen for acute MI and to
help determine the significance of abnormalities in serum K.Other laboratory
abnormalities include hyponatremia, elevated serum creatinine, and elevated serum
osmolarity. Hyperglycemia may cause dilutional hyponatremia, so measured serum Na
is corrected by adding 1.6 mEq/L for each 100 mg/dL elevation of serum glucose over
100 mg/dL. To illustrate, for a patient with serum Na of 124 mEq/L and glucose of 600
mg/dL, add 1.6 ([600-100]/100) = 8 mEq/L to 124 for a corrected serum Na of 132
mEq/L. As acidosis is corrected, serum K drops. An initial K level < 4.5 mEq/L indicates
marked K depletion and requires immediate K supplementation. Serum amylase and
lipase are often elevated, even in the absence of pancreatitis (which may be present in
alcoholic DKA patients and in those with coexisting hypertriglyceridemia).

 
 
   

= r      

Initial evaluation of the patient presenting with DKA should be at confirming the
diagnosis. Adverse outcomes and litigation associated with DKA are often related to
delays in diagnosis and management. DKA should obviously be suspected in any
patient presenting with typical features such as dehydration, polyuria, and polydypsia,
nausea and vomiting, acidotic respiration, and severe impaired level of consciousness,
but also considered in patients with acute myocardial infarction or other acute vascular
disease and in those with severe sepsis or septis shock.

= #
 

It is not clear what the optimal rate or nature of fluid resuscitation is in diabetic
ketoacidosis. Conventionally, normal saline is used. One can make a fairly strong
physiological case for the use of Lactated Ringer¶s solution in adults, although it can be
argued that;Ringer¶s lactate is somewhat hypotonic compaired to normal saline, and
could increase the likehood of cerebral edema.There is potential for RL to be
metabolised to glucose, increasing glucose levels in someone who is already
hyperglycemic.RL is racemic mixture of D- lactate and L- lactate. There is a theoretical
possibility that the D- lactate might not be adequately metabolised in a critically ill
patient with DKA, resulting in worsening obtundation.

= r


The best method of insulin administration is continuous intravenous infusion of

approximately 0.1 U/kg/hour of short- acting insulin (about 6-8 U/hour in an average
adult). It is important to note that in the rare patient with DKA who presents with initial
hypokalemia, insulin administration may further lower the potassium, resulting in
profound muscular weakness, and even respiratory embarassment. There is no good
reason to give an initial bolus of insulin before an insulin is started.

= 

 #
 

p 



Several regimens of potassium replacement have been proposed. If the serum

potassium is over about 5.5 ± 6 mmol/L, no potassium is added to replacement fluids,
but soon after insulin therapy starts, potassium levels often drop precipitately, about 10
± 20mmol/L should be addded to replacement solutions as soon as the serum
potassium drops below 5.5 mmol/L. Once the serum potassium level has dropped to
under 4 mmol/L, 30 ± 40 mmol/L can be added to the replacement solution, provided
serum K+ levels are diligently monitored.

p
  

Routine phosphate replacement is deleterious in DKA. However, levels should be

checked several times during the first 24 hours, and if moderate to marked
hypophosphataemia ( >0.5mmol/L ) develops, this should be carefully corrected, as
profound hypophosphataemia may result in muscular weakness, neurological
dysfunction, and even haemolysis or rhabdomyolysis. Insulin therapy will usually lower
serum phosphate levels, just as it lowers serum potassium.

 


DKA may be associated with substantial hypomagnesemia, and this should be looked
for.




Attention should be paid to alterations in serum sodium levels during therapy. Initially, if
marked hyperglycaemia is present, then serum sodium will be spuriously low.

= 
 


The two major features of infection ( pyrexia and leukocytosis ) are both obscured in
DKA. Patients with DKA are commonly mildly hypothermic and rarely pyrexial even in
the face of severe infection; DKA itself causes a raised white cell count. Common sites
off infection are urinary tract and skin, but every patient should also have a chest x-ray
to look for evidence of pneumonia. Wherever possible, treatment of infection should be
directed at likely organisms in a particular site, rather than ³broad spectrum´ shotgun
therapy.

DKA may be complicated by mucormycosis. The infection is rare, but those managing
DKA should always be aware of it, owing to its rampant progresssion and the possibility
of immediate surgical intervention being curative.
 = $



The treatment of acidocis is to continue with fluid and insulin, and administer enough
sugar to prevent hypoglycaemia. If acidocis still persist, especially if other parameters
are unfavourable, then one should consider the possibility of severe sepsis/septic shock
and treatt appropriately. Occasionally, in such circumstances, raised lactate levels may
contribute to acidosis.

= r 
    

Unless management goals in DKA are well- defined right from the start, things can
rapidly become chaotic, especially in an acute- care ward. Some such patients clearly
belong in an ICU setting. All therapeutic interventions should be meticulously
documented, especially fluid balances. Glass Coma Score should be monitored
regularly right from when the patient is first seen.

= %
 
   

Poor compliance with insulin therapy is a common precipitant of DKA, and other
patients who become ill inappropriately stop taking their insulin. Good follow- up
educationis thus vital, as is regular home glucose monitoring using an electronic
glucose meter. Patients may need careful ³tuning´ of their insulin- therapy ± newer
insulins such as insulin glargine ( for basal therapy ) and insulin lispro for boluses may
be of value.

!
c
   

± Blood glucose by meter and/or lab every 30 ± 60minutes

± .Electrolytes, lab glucose, blood ketones, capillary gas every 2hours as ordered.
± Record nursing results on DKA floowsheet.
± Neurovital signs every 15minutes until stable, then every hour until
order is discontinued.
 ± Close neurological observation and frequent rousing.
± Monitor for head ache, abnormal respirations, or behavioral
changes.
± NPO until rehydrated and glucose is stabilized.
± Ice chips may be allowed at physician¶s discreption.
± Check urine for ketones with each void.
± Strict input and output.