REPORT HARD COPY

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Care of Pediatric Client

With Endocrine Disorder President:

dela Cruz, Victor S

Members:

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.

Submitted to:

Eilleen B. Bautista RN MSN

Date: March 1,2011


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I. Anatomy

The endocrine system is made up of glands that produce and secrete hormones. Thesehormones regulate the body's growth, metabolism (the physical and chemical processesof 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 wellas in digestion.

Thyroid Gland

The thyroid gland is located in the lower front part of the neck. It produces thyroidhormones 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 controlsthe release of thyroid hormones. Thyroid hormones also help maintain normal bloodpressure, heart rate, digestion, muscle tone, and reproductive functions.

The thyroid gland is controlled by thyroid-stimulating hormone (TSH) produced by thepituitary (to be specific, the anterior pituitary) and thyrotropin-releasing hormone (TRH)produced by the hypothalamus. The thyroid gland gets its name from the Greek wordfor "shield", after the shape of the related thyroid cartilage. The most common problemsof the thyroid gland consist of an overactive thyroid gland, referred to ashyperthyroidism, and an underactive thyroid gland, referred to as hypothyroidism.

Adrenal Glands

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 glandsare 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 theadrenal medulla. The cortex mainly produces cortisol, aldosterone, and androgens,while the medulla chiefly produces epinephrine and norepinephrine. The combinedweight 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. Specificcortical cells produce particular hormones including cortisol, corticosterone, androgenssuch as testosterone, and aldosterone. Under normal unstressed conditions, the humanadrenal glands produce the equivalent of 3540 mg of cortisone acetate per day. Incontrast to the direct innervation of the medulla, the cortex is regulated byneuroendocrine hormones secreted by the pituitary gland and hypothalamus, as well asby the renin-angiotensin system.


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The adrenal medulla is the core of the adrenal gland, and is surrounded by the adrenalcortex. The chromaffin cells of the medulla, named for their characteristic brown stainingwith chromic acid salts, are the body's main source of the circulating catecholaminesadrenaline (epinephrine) and noradrenaline (norepinephrine). Derived from the aminoacid 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 receivesinput from the sympathetic nervous system through preganglionic fibers originating inthe thoracic spinal cord from T5T11. Because it is innervated by preganglionic nervefibers, the adrenal medulla can be considered as a specialized sympathetic ganglion. Unlike other sympathetic ganglia, however, the adrenal medulla lacks distinct synapsesand releases its secretions directly into the blood.Cortisol also promotes epinephrinsynthesis in the medulla. Produced in the cortex, cortisol reaches the adrenal medullaand at high levels, the hormone can promote the upregulation of phenylethanolamine N -methyltransferase (PNMT), thereby increasing epinephrine synthesis and secretion.

Pancreas

The pancreas is an elongated organ located toward the back of the abdomen behindthe stomach. The pancreas has digestive and hormonal functions. One part of thepancreas, the exocrine pancreas, secretes digestive enzymes. The other part of thepancreas, 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) andends near the spleen (called the tail).

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

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


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II. Disorders

Hypothyroidism

A.

Definition

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

produce or secrete as much thyroxine (T 4) as the body needs. Because T 4 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 T 4.

Low T 4 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 T 4. Secondary

hypothyroidism develops when the pituitary gland does not release enough of the

thyroid-stimulating hormone (TSH) that prompts the thyroid to manufacture T 4. Tertiaryhypothyroidism 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.


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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.

B . Pathophysiology

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 . Clinical Manifestation

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


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were a foreign body. The attack by the immune system impairs thyroid function and

sometimes destroys the gland. Other causes of hypothyroidism include:

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

or radiation treatments for head or neck cancers can destroy the thyroid gland.y Surgery. Removal of the thyroid gland because of cancer or other thyroid

disorders can result in hypothyroidism.

y Viruses and bacteria. Infections that depress thyroid hormone production usually

cause permanent hypothyroidism.

y 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.y 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 T 4.

y Congenital defect. One of every 4,000 babies is born without a properly

functioning thyroid gland.

y Diet. Because the thyroid makes T 4 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.

y 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


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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 includesevere 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 besudden 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.

D. Diagnostic Exam

The correct diagnosis of hypothyroidism depends on the following.

Symptoms . Hypothyroidism doesnt 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 youve

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).

Medical and family history . Y ou should tell your doctor:

y about changes in your health that suggest that your body is slowing

down;

y if youve ever had thyroid surgery;


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y if youve ever had radiation to your neck to treat cancer;

y if youre taking any of the medicines that can cause

hypothyroidism amiodarone, lithium, interferon alpha, interleukin-

2, and maybe thalidomide;whether any of your family members have thyroid

disease.

Physical exam . The doctor will check your thyroid gland and look for

changes such as dry skin, swelling, slower reflexes, and a slower heart

rate.

B lood tests . There are two blood tests that are used in the diagnosis

of hypothyroidism.

y 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 isnt enough T4

in the blood.

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

thyroxine-binding globulin. The bound T4 cant get into body cells.Only about 1%2% of T4 in the blood is unattached (free) 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.

E . Therapeutic Management

The therapeutic management of hypothyroidism caused by deficient thyroid hormoneproduction 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,


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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.

F . Nursing Care Management

y 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).

y 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.

y Encourage activity as tolerated to reduce constipation

y 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. thatenergy levels will return to normal after hormone therapy is begun.

y Maintain pt. airway, administering oxygen, and intravenous fluids for the patient

with myxedema coma.

y Monitor intake, output, and daily weights.


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HYPERTHYRO IDISM

A. Definition

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.

B .PATHOPHYS IOLOGY

In hyperthyroidism, serum T 3 usually increases more than does T 4, probably because of

increased secretion of T 3 as well as conversion of T 4 to T 3 in peripheral tissues. In some

patients, only T 3 is elevated (T 3 toxicosis). T 3 toxicosis may occur in any of the usual disorders

that produce hyperthyroidism, including Graves' disease, multinodular goiter, and theautonomously functioning solitary thyroid nodule. If T 3 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 .CL INICAL MAN IFESTAT ION

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,


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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 byproteinaceous 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.

D. Diagnostic Exam

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 T 4 is increased in hyperthyroidism. However, T 4 can be falsely normal

in true hyperthyroidism in patients with a severe systemic illness (similar to the falsely


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low levels that occur in euthyroid sick syndrome) and in T 3 toxicosis. If free T 4 level is

normal and TSH is low in a patient with subtle symptoms and signs of hyperthyroidism,

then serum T 3 should be measured to detect T 3 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 simpleblood 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 T 4 and T 3 concentrations and

normal or elevated serum TSH.If thyrotoxicosis factitia is suspected, serum


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thyroglobulin can be measured; it is usually low or low-normalunlike 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.

E .. THERAPEUT IC MANAGEMENT

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


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.


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Cushings Syndrome

A. Definition

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

CUSHING S Y NDROME 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 increasedrisk of developing this disorder.

B . Pathophysiology

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) causes 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.


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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 cortisols 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 bythe adrenal glands is precisely balanced to meet the bodys 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 .Clinical Manifestation

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:

y a pituitary tumor producing abnormally large quantities of ACTH

y the abnormal production of ACTH by some source other than the pituitary


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y 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, thepancreas, 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:

y weight gain

y 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")

y purple and pink stretch marks across the abdomen and flanks

y high blood pressure

y weak, thinning bones (osteoporosis)

y weak muscles

y low energyy thin, fragile skin, with a tendency toward both bruising and slow healing

y abnormalities in the processing of sugars (glucose), with occasional development

of actual diabetes

y kidney stones


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y increased risk of infections

y emotional disturbances, including mood swings, depression, irritability, confusion,

or even a complete break with reality (psychosis)

y irregular menstrual periods in women

y decreased sex drive in men and difficulty maintaining an erection

y 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).

D. Diagnostic Examination

No single lab test is perfect and usually several are needed. The three most commontests used to diagnose Cushings 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 Cushings syndrome

from other causes of excess cortisol.

24- hour urinary free cortisol level . In this test, a persons urine is collected several

times over a 24-hour period and tested for cortisol. Levels higher than 50 to 100micrograms a day for an adult suggest Cushings syndrome. The normal upper limit

varies in different laboratories, depending on which measurement technique is used.

Midnight plasma cortisol and late -night salivary cortisol measurements . The

midnight plasma cortisol test measures cortisol concentrations in the blood. Cortisol

production is normally suppressed at night, but in Cushings syndrome, this suppression

doesnt occur. If the cortisol level is more than 50 nanomoles per liter (nmol/L),

Cushings syndrome is suspected. The test generally requires a 48-hour hospital stay toavoid 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.


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Low -dose dexamethasone suppression test (LDDST) . 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, Cushings 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 Cushings

syndrome. On the other hand, drugs such as phenytoin and phenobarbital may cause

cortisol levels to drop, falsely indicating that Cushings 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

Dexamethasone -corticotropin - releasing hormone (Crh) test . Some people have

high cortisol levels but do not develop the progressive effects of Cushings syndrome,

such as muscle weakness, fractures, and thinning of the skin. These people may have

pseudo-Cushings 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-Cushings does not have the same long-term effects on

health as Cushings syndrome and does not require treatment directed at the endocrine

glands. The dexamethasone-CRH test rapidly distinguishes pseudo-Cushings from mild

cases of Cushings. 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 pseudoCushings. Elevations of cortisol during this test suggest Cushings

syndrome.


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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:

Reducing corticosteroid use . 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.

Surgery . 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 thereplacement 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.


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Radiation therapy . If the surgeon can't totally remove a pituitary tumor, he or she will

usually prescribe radiation therapy to be used in conjunction with the operation.

Additionally, radiation may be used for people who aren't suitable candidates for

surgery. 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.

Medications . 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.


y Monitor intake and output, daily weights, and serum glucose and electrolytes.

y Monitor for signs of infection because risk is high with excess glucocorticoids.

y After hypophysectomy, monitor for diabetes insipidus, hypothyroidism, and other endocrine changes.

y Assess the skin frequently to detect reddened areas, skin breakdown or tearing,

excoriation, infection or edema.

y Handle skin and extremity gently to prevent trauma; prevent falls by using siderails.


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y Avoid using adhesive tape on the skin to reduce trauma on its removal.

y Encourage the patient to turn in bed frequently or ambulate to reduce pressure on bony

prominences and areas of edema.

y Assist the patient with ambulation and hygiene when weak and fatigued. Use assistive

devices during ambulation to prevent falls and fractures.

y Help the patient to schedule exercise and rest. Advise the patient how to recognize

signs and symptoms of excessive exertion.

y Instruct the patient to correct body mechanics to avoid pain or injury during activities.

y 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.

y Report edema and signs of fluid retention. y Encourage the patient to verbalize concerns about the illness, changes in appearance,

and alters role function.

y Explain to female patient who has benign adenoma or hyperplasia that, with proper

treatment, evidence of masculinization can be reversed.


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Diabetes Mellitus

A. Definition

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 insulins

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.

TYPES OF D IAB ETES MELL ITUS

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


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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.

B .Pathophysiology

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


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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 ( -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 oppositemanner 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


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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 . Clinical manifestation:

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 "Ps" 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


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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:

y are obese (more than 20% above their ideal body weight)

y have a relative with diabetes mellitus

y belong to a high-risk ethnic population (African-American, Native American,

Hispanic, or Native Hawaiian)y have been diagnosed with gestational diabetes or have delivered a baby

weighing more than 9 lbs (4 kg)

y have high blood pressure (140/90 mmHg or above)

y 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

y 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.


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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 presentsfor 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.

D. Diagnostic Exam

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.

Urine tests

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.


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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.

B lood tests

Fasting blood glucose test blood glucose levels are checked after fasting for

between 12 and 14 hours. Y ou can drink water during this time, but shouldstrictly avoid any other beverage. Patients with diabetes may be asked to delay

their diabetes medication or insulin dose until the test is completed.

R andom blood glucose test blood glucose levels are checked at various

times during the day, and it doesnt matter when you last ate. Blood glucose

levels tend to stay constant in a person who doesnt have diabetes.

Or al glucose tole r ance test a high-glucose drink is given. Blood samples are

checked at regular intervals for two hours.


y 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.

y

Management involves nutrition management, increased physical activity, andblood glucose testing.

y Type 2 diabetes is different from type 1 in that the child's life is generally not in

immediate danger without treatment.

y Metformin is the only oral medication that's approved for children and

adolescents (age 10 and older) who have type 2 diabetes.


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y Aspirin; Diet Control; LDL cholesterol; ACE Inhibitors


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 .


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Diabetic Ketoacidosis

A. Definition

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.


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B . Pathophysiology

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 alanineprovide 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 -

hydroxybutyric acid, are strong organic acids that create metabolic acidosis. Acetone

derived from the metabolism of acetoacetic acid accumulates in serum and is slowlydisposed 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. Klevels 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 . Clinical Manifestation

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.


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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, andparticularly in childrenabdominal pain. Lethargy andsomnolence 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 Paco 2 at presentation appear to be at greatest risk. Delays in

correction of hyponatremia and the use of HCO 3 during DKA treatment are additionalrisk factors.

D. Diagnostic Examination

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 gassample (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.


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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 -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 laboratoryabnormalities 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).


y Immediate Diagnosis and Management

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,


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but also considered in patients with acute myocardial infarction or other acute vascular

disease and in those with severe sepsis or septis shock.

y Fluid Resuscitation

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 Ringers solution in adults, although it can be

argued that;Ringers 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.

y Insulin Therapy

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.

y Electrolyte Replacement

P otassium

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


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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.

Ph osp h ate

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.

Magnesium

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

for.

Sodium

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.

y Treating infection

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 broad 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.


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y Ongoing acidocis

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 shockand treatt appropriately. Occasionally, in such circumstances, raised lactate levels may

contribute to acidosis.

y Integrated Management goals

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.

y Long - term Management

Poor compliance with insulin therapy is a common precipitant of DKA, and other

patients who become ill inappropriately stop taking their insulin. Good follow- upeducationis thus vital, as is regular home glucose monitoring using an electronic

glucose meter. Patients may need careful tuning of their insulin- therapy newer

insulins such as insulin glargine ( for basal therapy ) and insulin lispro for boluses may

be of value.


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.


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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 physicians discreption.

Check urine for ketones with each void.

Strict input and output.

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