CARE OF CLIENTS WITH PROBLEM ON ENDOCRINE

INTRODUCTION
The Endocrine system is involved in all the integrative aspects of life, including growth, sex
differentiation, metabolism and adaptation to an ever-changing environment.

The nervous system and the interconnected network of glands known as the endocrine
system control body systems. Disorders of the endocrine system are common and have the
potential to affect the function of every organ system in the body. Understanding the function of
each of the endocrine glands, and the consequences of hypofunction and hyperfunction of each
gland, enables the nurse to anticipate physiologic changes and to plan interventions to address
them. Nursing interventions that are essential in managing endocrine disorders are carried out in
every setting from the intensive care unit to the outpatient setting and the home.

OBJECTIVES
At the end of the module students will be able to:

1. Describe the functions of each of the endocrine glands and their hormones.
2. Identify the diagnostic tests used to determine alterations in function of each of the
endocrine glands and metabolic.
3. Identify the different Endocrine disorders: their causes, pathophysiology, clinical
manifestations, management, and nursing interventions.
4. Use the nursing process as a framework for care of patients with Endocrine and Metabolic
Disorders.
5. Identify the teaching needs of patients requiring different therapies.

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 Endocrine Anatomy and Physiology

The endocrine system has far-reaching

effects in the human body because of its
links with the nervous system and the
immune system. The hormones secreted
by the endocrine system are affected in
large part by structures in the central
nervous system, such as the
hypothalamus. Other structures located
in the brain, such as the pituitary gland,
are endocrine glands that influence the
function of a large number of other
endocrine glands. The effects of
hormones secreted by the endocrine
system affect the nervous system and
are, in turn, mediated by the nervous
system. The adrenal medulla, for
example, secretes a number of
substances (eg, norepinephrine and epinephrine) that act as neurotransmitters. The immune
system also interacts closely with the endocrine system. It responds to the introduction of foreign
agents by means of chemicals (eg, interleukins, interferons) and is regulated by hormones secreted
by the adrenal cortex.

In addition to the hormones secreted by the major endocrine glands, other tissues produce
hormones that are secreted into body fluids and act on nearby cells and tissues. The
gastrointestinal mucosa produces hormones (eg, gastrin, enterogastrone, secretin, and
cholecystokinin) that are important in the digestive process. The kidneys produce erythropoietin, a
hormone that stimulates the bone marrow to produce red blood cells. The white blood cells produce
cytokines that actively participate in inflflammatory and immune responses. Hormones are
important in regulation of the internal environment of the body and affect every aspect of life. Some
hormones target specific tissues; for example, adrenocorticotropic hormone (ACTH), or
corticotrophin, is secreted by the anterior pituitary gland and targets the adrenal cortex to increase
the secretion of the hormones of the adrenal cortex (ie, glucocorticoids, mineralocorticoids, and
androgens). Other hormones affect a wide variety of cells and tissues of the body. Thyroid hormone
is one example; it affects metabolic activity of cells throughout the body.

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GLANDS OF THE ENDOCRINE SYSTEM

The endocrine glands

include the pituitary,
thyroid, parathyroids,
adrenals, pancreatic islets,
ovaries, and testes.
Endocrine glands secrete
their products directly into
the blood stream, which
differentiates them from
exocrine glands, such as
sweat glands, which
secrete their products
through ducts onto
epithelial surfaces or into the gastrointestinal tract. The hypothalamus is the link between the
nervous system and the endocrine system.

FUNCTION AND REGULATION OF HORMONES

The chemical substances secreted by the endocrine glands are called hormones. Hormones help
to regulate organ function in concert with the nervous system. This dual regulatory system, in which
rapid action by the nervous system is balanced by slower hormonal action, permits precise control
of organ functions in response to varied changes within and outside the body. The endocrine glands
are composed of secretory cells arranged in minute clusters known as acini. No ducts are present,
but the glands have a rich blood supply so that the hormones they produce enter the bloodstream
rapidly. In the healthy physiologic state, hormone concentration in the bloodstream is maintained
at a relatively constant level. When the hormone concentration rises, further production of that
hormone is inhibited. When the hormone concentration falls, the rate of production of that hormone
increases. This mechanism for regulating hormone concentration in the bloodstream is called
negative feedback, which is important in the regulation of many biologic processes.

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Major Actions and Sources of selected Hormones

CLASSIFICATION AND ACTION OF HORMONES

Hormones are classified as steroid hormones (such as hydrocortisone), peptide or protein

hormones (such as insulin), and amine hormones (such as epinephrine). These different classes
of hormones act on the target tissues by different mechanisms. Hormones can alter the function of

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the target tissue by interacting with chemical receptors located either on the cell membrane or in
the interior of the cell. Peptide and protein hormones interact with receptor sites on the cell surface,
which results in the stimulation of the intracellular enzyme adenyl cyclase. This results in increased
production of cyclic 3′, 5′-adenosine monophosphate (cyclic AMP). The cyclic AMP inside the cell
alters enzyme activity. Thus, cyclic AMP is the “second messenger” that links the peptide hormone
at the cell surface to a change in the intracellular environment. Some of the protein and peptide
hormones may also act by changing membrane permeability. These hormones act within seconds
or minutes. The mechanism of action for amine hormones is similar to that for peptide hormones.
Steroid hormones, because of their smaller size and higher lipid solubility, penetrate the cell
membranes and interact with intracellular receptors. This steroid–receptor complex modifies cell
metabolism and formation of messenger ribonucleic acid (RNA) from deoxyribonucleic acid (DNA).
The messenger RNA then stimulates protein synthesis within the cell. Steroid hormones require
several hours to exert their effects because they exert their action by the modification of protein
synthesis.

PITUITARY FUNCTION
Commonly referred to as the master gland, the pituitary
secretes hormones that control the secretion of hormones
by other endocrine glands. The pituitary itself is controlled
by the hypothalamus, an adjacent area of the brain
connected to the pituitary by the pituitary stalk.

Posterior Pituitary
The important hormones secreted by the posterior lobe of
the pituitary gland are vasopressin (antidiuretic hormone
[ADH]) and oxytocin. These hormones are synthesized in
the hypothalamus and travel from the hypothalamus to the
posterior pituitary gland for storage. Vasopressin controls the excretion of water by the
kidney; its secretion is stimulated by an increase in the osmolality of the blood or by a decrease in
blood pressure. Oxytocin facilitates milk ejection during lactation and increases the force of uterine
contractions during labor and delivery. Oxytocin secretion is stimulated during pregnancy and at
childbirth.

Anterior Pituitary
The major hormones of the anterior pituitary gland are follicle stimulating hormone (FSH),
luteinizing hormone (LH), prolactin, ACTH, thyroid-stimulating hormone (TSH), and growth
hormone (also referred to as somatotropin). The secretion of these major hormones is controlled

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by releasing factors secreted by the hypothalamus. These releasing factors reach the anterior
pituitary by way of the bloodstream in a special circulation called the pituitary portal blood system.
Other hormones include melanocyte-stimulating hormone and beta-lipotropin; the function of
lipotropin is poorly understood. The hormones released by the anterior pituitary enter the general
circulation and are transported to their target organs. The main function of TSH, ACTH, FSH, and
LH is the release of hormones from other endocrine glands. Prolactin acts on the breast to stimulate
milk production. Growth hormone has wide spread effects on many target tissues and is discussed
later. Hormones that stimulate other organs and tissues are discussed in conjunction with their
target organs. Growth hormone is a protein hormone that increases protein synthesis in many
tissues, increases the breakdown of fatty acids in adipose tissue, and increases the glucose level
in the blood. These actions of growth hormone are essential for normal growth, although other
hormones, such as thyroid hormone and insulin, are required as well. Stress, exercise, and low
blood glucose levels increase the secretion of growth hormone. The halflife of growth hormone
activity in the blood is 20 to 30 minutes; the hormone is largely inactivated in the liver.

Thyroid Function

It consists of two lateral lobes connected by an isthmus. The gland is about 5 cm long and 3 cm
wide and weighs about 30 g. The blood flow to the thyroid is very high (about 5 mL/min per gram
of thyroid tissue), about five times the blood flow to the liver. This reflects the high metabolic activity
of the thyroid gland. The thyroid gland produces three hormones: thyroxine (T4), triiodothyronine
(T3), and calcitonin. Thyroxine and triiodothyronine are referred to collectively as thyroid hormone.

Thyroid Hormone
The two separate hormones, thyroxine (T4) and triiodothyronine (T3), that are produced by the
thyroid gland and that make up thyroid hormone, are amino acids that have the unique property of

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containing iodine molecules bound to the amino acid structure. T4 contains four iodine atoms in
each molecule, and T3 contains only three. These hormones are synthesized and stored bound to
proteins in the cells of the thyroid gland until needed for release into the bloodstream. About 75%
of bound thyroid hormone is bound to thyroxine-binding globulin (TBG); the remaining bound
thyroid hormone is bound to thyroid-binding prealbumin and albumin.

ROLE OF IODINE
Iodine is essential to the thyroid gland for synthesis of its hormones. In fact, the major use of iodine
in the body is by the thyroid, and the major derangement in iodine deficiency is alteration of thyroid
function. Iodide is ingested in the diet and absorbed into the blood in the gastrointestinal tract. The
thyroid gland is extremely efficient in taking up iodide from the blood and concentrating it within the
cells, where iodide ions are converted to iodine molecules, which react with tyrosine (an amino
acid) to form the thyroid hormones.

REGULATION OF THYROID HORMONE

The secretion of T3 and T4 by the thyroid gland is controlled by thyroid-stimulating hormone (TSH,
or thyrotropin) from the anterior pituitary gland. TSH controls the rate of thyroid hormone release.
In turn, the level of thyroid hormone in the blood determines the release of TSH. If thyroid hormone
concentration in the blood decreases, the release of TSH increases, which causes increased output
of T3 and T4. This is an example of negative feedback. Thyrotropin-releasing hormone (TRH),
secreted by the hypothalamus, exerts a modulating influence on the release of TSH from the
pituitary. Environmental factors, such as a decrease in temperature, may lead to increased
secretion of TRH, resulting in elevated secretion of thyroid hormones.

FUNCTION OF THYROXINE AND TRIIODOTHYRONINE

The primary function of the thyroid hormone is to control the cellular metabolic activity. T4, a
relatively weak hormone, maintains body metabolism in a steady state. T3 is about five times as
potent as T4 and has a more rapid metabolic action. These hormones accelerate metabolic
processes by increasing the level of specific enzymes that contribute to oxygen consumption and
altering the responsiveness of tissues to other hormones. The thyroid hormones influence cell
replication and are important in brain development. Thyroid hormone is also necessary for normal
growth. The thyroid hormones, through their widespread effects on cellular metabolism, influence
every major organ system.

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Calcitonin
Calcitonin, or thyrocalcitonin, is another important hormone secreted by the thyroid gland. It is
secreted in response to high plasma levels of calcium, and it reduces the plasma level of calcium
by increasing its deposition in bone.

PARATHYROID FUNCTION
Parathormone, the protein hormone from the
parathyroid glands, regulates calcium and
phosphorus metabolism. Increased secretion of
parathormone results in increased calcium
absorption from the kidney, intestine, and bones,
thereby raising the blood calcium level. Some
actions of this hormone are increased by the
presence of vitamin D. Parathormone also tends
to lower the blood phosphorus level. Excess
parathormone can result in markedly elevated
levels of serum calcium, a potentially life-threatening situation. When the
product of serum calcium and serum phosphorus (calcium × phosphorus) rises, calcium phosphate
may precipitate in various organs of the body and cause tissue calcification. The serum level of
ionized calcium regulates the output of parathormone. Increased serum calcium results in
decreased parathormone secretion, creating a negative feedback system.

ADRENAL FUNCTION
There are two adrenal glands in the human,
each attached to the upper portion of a
kidney. Each adrenal gland is, in reality, two
endocrine glands with separate, independent
functions. The adrenal medulla at the center
of the gland secretes catecholamines, and
the outer portion of the gland, the adrenal
cortex, secretes steroid hormones. The
secretion of hormones from the adrenal cortex is regulated by the hypothalamicpituitary-adrenal
axis. The hypothalamus secretes corticotropin releasing hormone (CRH), which in turn stimulates
the pituitary gland to secrete ACTH. ACTH then stimulates the adrenal cortex to secrete
glucocorticoid hormone (cortisol). Increased levels of the adrenal hormone then inhibit the
production or secretion of CRH and ACTH. This system is an example of a negative feedback
mechanism.

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Adrenal Medulla
The adrenal medulla functions as part of the autonomic nervous system. Stimulation of
preganglionic sympathetic nerve fibers, which travel directly to the cells of the adrenal medulla,
causes release of the catecholamine hormones epinephrine and norepinephrine. About 90% of the
secretion of the human adrenal medulla is epinephrine (also called adrenaline). Catecholamines
regulate metabolic pathways to promote catabolism of stored fuels to meet caloric needs from
endogenous sources. The major
effects of epinephrine release are to prepare to meet a challenge (fight-or-flight response).
Secretion of epinephrine causes decreased blood flow to tissues that are not needed in emergency
situations, such as the gastrointestinal tract, and causes increased blood flow to tissues that are
important for effective fight or flight, such as cardiac and skeletal muscle. Catecholamines also
induce the release of free fatty acids, increase the basal metabolic rate, and elevate the blood
glucose level.

Adrenal Cortex
A functioning adrenal cortex is necessary for life; adrenocortical secretions make it possible for the
body to adapt to stress of all kinds. The three types of steroid hormones produced by the adrenal
cortex are glucocorticoids, the prototype of which is hydrocortisone; mineralocorticoids, mainly
aldosterone; and sex hormones, mainly androgens (male sex hormones). Without the adrenal
cortex, severe stress would cause peripheral circulatory failure, circulatory shock, and prostration.
Survival in the absence of a functioning adrenal cortex is possible only with nutritional, electrolyte,
and fluid replacement and appropriate replacement with exogenous adrenocortical hormones.

GLUCOCORTICOIDS
The glucocorticoids are so named because they have an important influence on glucose
metabolism: increased hydrocortisone secretion results in elevated blood glucose levels. However,
the glucocorticoids have major effects on the metabolism of almost all organs of the body.
Glucocorticoids are secreted from the adrenal cortex in response to the release of ACTH from the
anterior lobe of the pituitary gland. This system represents an example of negative feedback. The
presence of glucocorticoids in the blood inhibits the release of corticotropin-releasing factor from
the hypothalamus and also inhibits ACTH secretion from the pituitary. The resultant
decrease in ACTH secretion causes diminished release of glucocorticoids from the adrenal cortex.
Glucocorticoids (in the form of corticosteroids) are administered frequently to inhibit the
inflammatory response to tissue injury and suppress allergic manifestations. Their side effects
include the development of diabetes mellitus, osteoporosis, peptic ulcer, increased protein
breakdown resulting in muscle wasting and poor wound healing, and redistribution of body fat.

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Large amounts of exogenously administered glucocorticoids in the blood inhibit the release of
ACTH and endogenous glucocorticoids. Because of this, the adrenal cortex can atrophy. If
exogenous glucocorticoid administration is discontinued suddenly, adrenal insufficiency results
because of the inability of the atrophied cortex to respond adequately.

MINERALOCORTICOIDS
Mineralocorticoids exert their major effects on electrolyte metabolism. They act principally on the
renal tubular and gastrointestinal epithelium to cause increased sodium ion absorption in exchange
for excretion of potassium or hydrogen ions. ACTH only minimally influences aldosterone secretion.
It is primarily secreted in response to the presence of angiotensin II in the bloodstream. Angiotensin
II is a substance that elevates the
blood pressure by constricting arterioles. Its concentration is increased when renin is released from
the kidney in response to decreased perfusion pressure. The resultant increased aldosterone levels
promote sodium reabsorption by the kidney and the gastrointestinal tract, which tends to restore
blood pressure to normal. The release of aldosterone is also increased by hyperkalemia.
Aldosterone is the primary hormone for the long-term regulation of sodium balance.

ADRENAL SEX HORMONES (ANDROGENS)

Androgens, the third major type of steroid hormones
produced by the adrenal cortex, exert effects similar to
those of male sex hormones. The adrenal gland may also
secrete small amounts of some estrogens, or female sex
hormones. ACTH controls the secretion of adrenal
androgens. When secreted in normal amounts, the
adrenal androgens probably have little effect, but when secreted in excess, in certain inborn
enzyme deficiencies, masculinization may result. This is termed the adrenogenital syndrome.

THE PANCREAS
The pancreas, located in the upper abdomen, has endocrine as well as exocrine functions. The
secretion of pancreatic enzymes into the gastrointestinal tract through the pancreatic duct
represents its exocrine function. The secretion of insulin, glucagon, and somatostatin directly into
the bloodstream represents its endocrine function.

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Exocrine Pancreas
The secretions of the exocrine portion of the pancreas are collected in the pancreatic duct, which
joins the common bile duct and enters the duodenum at the ampulla of Vater. Surrounding the
ampulla is the sphincter of Oddi, which partially controls the rate at which secretions from the
pancreas and the gallbladder enter the duodenum.

The secretions of the exocrine pancreas are digestive enzymes high in protein content and an
electrolyte-rich fluid. The secretions are very alkaline because of their high concentration of sodium
bicarbonate and are capable of neutralizing the highly acid gastric juice that enters the duodenum.
The enzyme secretions include amylase, which aids in the digestion of carbohydrates; trypsin,
which aids in the digestion of proteins; and lipase, which aids in the digestion of fats. Other
enzymes that promote the breakdown of more complex foodstuffs are also secreted.

Hormones originating in the gastrointestinal tract stimulate the secretion of these exocrine
pancreatic juices. Secretin is the major stimulus for increased bicarbonate secretion from the
pancreas, and the major stimulus for digestive enzyme secretion is the hormone CCK-PZ. The
vagus nerve also influences exocrine pancreatic secretion.

Endocrine Pancreas
The islets of Langerhans, the endocrine part of the pancreas, are collections of cells embedded in
the pancreatic tissue. They are composed of alpha, beta, and delta cells. The hormone produced
by the beta cells is called insulin; the alpha cells secrete glucagon and the delta cells secrete
somatostatin.

INSULIN
A major action of insulin is to lower blood glucose by permitting entry of the glucose into the cells
of the liver, muscle, and other tissues, where it is either stored as glycogen or used for energy.
Insulin also promotes the storage of fat in adipose tissue and the synthesis of proteins in various

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body tissues. In the absence of insulin, glucose cannot enter the cells and is excreted in the urine.
This condition, called diabetes mellitus, can be diagnosed by high levels of glucose in the blood. In
diabetes mellitus, stored fats and protein are used for energy instead of glucose, with consequent
loss of body mass. The level of glucose in the blood normally regulates the rate of insulin secretion
from the pancreas.

GLUCAGON
The effect of glucagon (opposite to that of insulin) is chiefly to raise the blood glucose by converting
glycogen to glucose in the liver. Glucagon is secreted by the pancreas in response to a decrease
in the level of blood glucose.

SOMATOSTATIN
Somatostatin exerts a hypoglycemic effect by interfering with release of growth hormone from the
pituitary and glucagon from the pancreas, both of which tend to raise blood glucose levels.

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 PITUITARY DISORDERS

HYPOPITUITARISM
Hyposecretion of 1 or more of the pituitary hormones caused by tumors, trauma,
encephalitis, autoimmunity, or stroke. Hormones most often affected are growth hormone (GH) and
gonadotropic hormones (luteinizing hormone, follicle-stimulating hormone), but thyroid-stimulating
hormone (TSH), adrenocorticotropic hormone (ACTH), or antidiuretic hormone (ADH) may be
involved.

Clinical manifestations

▫ Mild to moderate obesity

▫ Reduced cardiac output
▫ Infertility, sexual dysfunction
▫ Fatigue, low blood pressure
▫ Tumors of the pituitary also may cause headaches and visual defects (the pituitary is
located near the optic nerve).

Management

1. Client may need hormone replacement for the specific deficient hormones.
2. Provide emotional support to the client and family.
3. Encourage the client and family to express feelings related to disturbed body image or
sexual dysfunction.
4. Client education is needed regarding the signs and symptoms of hypofunction and
hyperfunction related to insufficient or excess hormone replacement.

HYPERPITUITARISM (ACROMEGALY)
Hypersecretion of growth hormone by the anterior pituitary gland in an adult; caused
primarily by pituitary tumors.

Clinical Manifestations
▫ Large hands and feet ▫ Oily, rough skin
▫ Thickening and protrusion of the jaw ▫ Organomegaly
▫ Arthritic changes and joint pain, ▫ Hypertension, atherosclerosis,
impingement syndromes cardiomegaly, heart failure
▫ Visual disturbances ▫ Dysphagia
▫ Diaphoresis ▫ Deepening of the voice
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 ▫ Thickening of the tongue, narrowing ▫ Colon polyps, increased colon
of the airway, sleep apnea cancer risk
▫ Hyperglycemia

Management:

1. Provide pharmacological interventions to suppress GH or to block the action of GH

2. Prepare the client for radiation of the pituitary gland or for stereotactic radiosurgery if
prescribed.
3. Prepare the client for hypophysectomy if planned.
4. Provide pharmacological and nonpharmacological interventions for joint pain.
5. Provide emotional support to the client and family, and encourage the client and family to
express feelings related to disturbed body image.

Surgical Management

Hypophysectomy (pituitary adenectomy, sublabial transsphenoidal pituitary surgery)

Removal of a pituitary tumor via craniotomy or a sublabial transsphenoidal (endoscopic
trans nasal) approach (the latter approach is preferred because it is associated with fewer
complications).

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Post-operative care:
-Monitor V/S, neurological status & LOC
-Elevate head of bed
-Monitor for increased intracranial pressure & any
postnasal drip which might be CSF
-Avoid sneezing, coughing & blowing nose
-Monitor for temporary diabetes insipidus
-Monitor I & O & water intoxication
-Administer antibiotics, analgesics, antipyretics,
hormones & glucocorticoids if entire gland is removed

DIABETES INSIPIDUS
It is a disorder of the posterior lobe of the pituitary gland that is characterized by a
deficiency of ADH (vasopressin). Excessive thirst (polydipsia) and large volumes of dilute urine
characterize the disorder.

Causes
• It may occur secondary to • infections of the CNS (meningitis,) or
• head trauma, • tumors (eg, metastatic disease)
• brain tumor, or • failure of the renal tubules to respond
• surgical ablation or to ADH
• irradiation of the pituitary gland

Clinical Manifestations

▫ daily output of very dilute, waterlike urine with a specific gravity of 1.001 to 1.005 occurs
▫ urine contains no abnormal substances such as glucose or albumin
▫ patient tends to drink 2 to 20 L of fluid daily and craves cold water
▫ Severe dehydration and hypernatremia if water is restricted.

Diagnostics
• The fluid deprivation test
✓ withhold fluids for 8 to 12 hours or until 3% to 5% of the body weight
is lost.
✓ patient is weighed frequently during the test
✓ Plasma and urine osmolality studies are performed at the beginning
and end of the test

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 ✓ The inability to increase the specific gravity and osmolality of the urine
is characteristic of diabetes insipidus.
✓ The patient continues to excrete large volumes of urine with low
specific gravity and experiences weight loss, increasing serum
osmolality, and elevated serum sodium levels
✓ The patient’s vital signs should be monitored closely for signs of
hypovolemia

Management
The objectives of therapy are
1. to replace ADH (which is usually a long-term therapeutic program),
2. to ensure adequate fluid replacement, and
3. to identify and correct the underlying intracranial pathology.

Pharmacological Management
▫ Desmopressin inhalation
▫ IM vasopressin tannate in oil
 Warm or shake vigorously before administration.
 The injection is administered in the evening
 Abdominal cramps are a side effect of this medication.
 Rotation of injection sites is necessary to prevent lipodystrophy.

Nursing Management
o Monitor patient during Water deprivation test
o Inform about follow up care and emergency features
o Monitor for signs of hypovolemia
o Instruct drink adequate water
o Instruct to wear a medic alert bracelet
o Be cautious in giving Vasopressin with CAD patient.

SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE (SIADH)

▫ The syndrome of inappropriate antidiuretic hormone (SIADH) secretion includes excessive
ADH secretion from the pituitary gland even in the face of subnormal serum osmolality
▫ cannot excrete a dilute urine
▫ They retain fluids and develop a sodium deficiency known as dilutional hyponatremia.

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Causes
SIADH is often of nonendocrine origin
▫ bronchogenic carcinoma
▫ severe pneumonia,
▫ pneumothorax, and other disorders of the lungs,
▫ malignant tumors that affect other organs (Porth, 2005).
▫ head injury,
▫ brain surgery or tumor, and infection

Management

1. Eliminate the underlying cause

2. restricting fluid intake
3. Diuretics such as furosemide (Lasix) may be used
4. Close monitoring of I&O,
5. daily weight,
6. urine and blood chemistries, and
7. neurologic status
8. Monitor for signs of fluid overload

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 THYROID DISORDERS

Diagnostic Procedures for Thyroid

1. Serum TSH
✓ Measurement of TSH has a sensitivity of 98% and specificity of greater than 92%
✓ the single best screening test of thyroid function
✓ NVof 0.4 to 6.15 µU/mL
✓ Elevated- hypothyroidism
✓ Decreased- hyperthyroidism
✓ Can be taken with thyroid hormone for comparison
2. Serum Free T4
✓ Free T4 levels correlate with metabolic status;
✓ NV of 0.9 to 1.7 ng/dL
✓ they are elevated in hyperthyroidism and decreased in hypothyroidism
3. Serum T3 &T4
✓ Measurement of total T3 or T4 includes protein-bound and free hormone levels that
occur in response to TSH secretion.
✓ T4 is 80% bound to TBG;
✓ T3 is bound less firmly.
✓ NV T4 is 4.5 to 11.5 µg/dL
✓ NV T3 is 70 to 220 ng/dL
✓ T3 level appears to be a more accurate indicator of hyperthyroidism,
4. T3 Resin uptake
✓ Its purpose is to determine the amount of thyroid hormone bound to TBG and the
number of available binding sites
✓ normal T3 uptake value is 25% to 35%
✓ Increased uptake indicates hyperthyrodism
✓ Decreased uptake indicates hypothyroidism
5. Thyroid antibodies
✓ Autoimmune thyroid diseases include both hypothyroid and hyperthyroid conditions.
6. Radioactive Iodine Uptake
✓ measures the rate of iodine uptake by the thyroid gland
✓ patient is administered a tracer dose of iodine 123 (123I)
✓ count is made over the thyroid gland with a scintillation counter,
✓ It measures the proportion of the administered dose that is present in the thyroid gland
at a specific time after its administration

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 ✓ hyperthyroidism exhibit a high uptake of the 123I

7. Fine-Needle Aspiration Biopsy

✓ s often the initial test for evaluation of thyroid masses. Results are reported as
a. negative (benign),
b. positive (malignant),
c. indeterminate (suspicious),
d. inadequate (nondiagnostic).
8. Thyroid Scan, Radioscan, or Scintiscan
✓ Scans are helpful in determining the location, size, shape, and anatomic function of
the thyroid gland
✓ Identifying areas of increased function (“hot” areas) or decreased function (“cold”
areas) can assist in diagnosis
9. Serum Thyroglobulin
✓ it is used to detect persistence or recurrence of thyroid carcinoma.

HYPOTHYROIDISM
Causes

• The most common cause of hypothyroidism in adults is autoimmune thyroiditis

(Hashimoto's disease), in which the immune system attacks the thyroid gland
o Hyperthyroidism followed by hypothyroidism
• Previous hyperthyroidism
o Treated with radioactive Iodine
o Post-thyroidectomy
• Dysfunction of thyroid gland itself (primary Hypothyroidism)
• Dysfunction of hypothalamus/hypophysis (Central hypothyroidism)
• Autoimmune disease (Hashimoto's thyroiditis, post–Graves' disease)
• Atrophy of thyroid gland with aging
• Therapy for hyperthyroidism
o Radioactive iodine (131I)
o Thyroidectomy
• Medications
o Lithium
o Iodine compounds
o Antithyroid medications
• Radiation to head and neck for treatment of head and neck cancers, lymphoma
• Infiltrative diseases of the thyroid (amyloidosis, scleroderma, lymphoma)

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 • Iodine deficiency and iodine excess.

Clinical Manifestations
▫ extreme fatigue
▫ hair loss,
▫ brittle nails, and dry skin are common, and
▫ numbness and tingling of the fingers
▫ may become husky
▫ menorrhagia or amenorrhea occur
▫ loss of libido
▫ Severe hypothyroidism results in a subnormal temperature and pulse rate
▫ gain weight even without an increase in food intake
▫ becomes thickened because of an accumulation of mucopolysaccharides in the
subcutaneous tissues (myxedema)
▫ complains of being cold even in a warm environment.
▫ mental processes become dulled, and the patient appears apathetic
▫ Speech is slow, the tongue enlarges, and hands and feet increase in size
▫ frequently complains of constipation
▫ Deafness may also occur
▫ Dementia
▫ Inadequate ventilation and sleep apnea
▫ respiratory muscle weakness
▫ elevated serum cholesterol level, atherosclerosis, coronary artery disease, and poor left
ventricular function.
▫ hypothermic and abnormally sensitive to sedatives, opioids, and anesthetic agents

Myxedema coma describes the most extreme, severe stage of hypothyroidism, in which the patient
is hypothermic and unconscious. Increasing lethargy may progress to stupor and then coma

Management

1. primary objective is to restore a normal metabolic state by replacing the missing hormone
• levothyroxine (Synthroid or Levothroid)
▫ Prevent cadiac dysfunction
▫ Monitor for Myocardial Infarction

2. Provide supportive care in case of Myxedema coma

a. Monitor ABG to detect CO2 retention

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 b. Monitor O2 Saturation with pulse oxymetry
c. Avoid application of external heat
d. Administer fluid cautiously to avoid water intoxication
e. Administer glucose if hypoglycemic
f. Monitor V/S closely
3. Give low fat, low cholesterol diet
4. Encourage high fiber diet and Increase fluids
5. Provide for comfort and safety:
6. monitor for infection or trauma;
7. provide warmth,
8. prevent heat loss & vascular collapse
9. Prevent complications of immobility

HYPERTHYROIDISM
• Graves' disease, the most common type of hyperthyroidism, results from an excessive
output of thyroid hormones caused by abnormal stimulation of the thyroid gland by
circulating immunoglobulins.
• Can also be caused by stress, infection, or excessive use of thyroid hormone

Clinical Manifestations:
Subjective data:
▫ nervousness, mood swings, palpitations, heat intolerance, dyspnea, weakness.
Objective data:
▫ Eyes: exophthalmos, characteristic stare, lid lag.
▫ Skin: warm, moist, velvety; increased sweating; increased melanin pigmentation; pretibial
edema with thickened skin & hyperpigmentation
▫ Weight loss despite increased appetite
▫ V/S: increased systolic BP, widened pulse pressure, tachycardia
▫ Goiter: thyroid gland noticeable & palpable
▫ Gyne: abnormal menstruation
▫ GI: frequent bowel movements
▫ Activity pattern: fatigue which leads to depression
▫ Lab data: elevated T3 & T4 level; elevated RAIU; elevated metabolic rate (BMR);
decreased WBC caused by decreased granulocytosis (<4500).
▫ Osteoporosis and fractures
▫ Tachycardia, dysrythmia and atrial fibrilation can lead to cardiac arrest

49
Diagnostics and assessment

✓ Enlarged thyroid gland

✓ Thrill can be palpated
✓ Bruit can be auscultated
✓ decrease in serum TSH,
✓ increased free T4, and
✓ increase in radioactive iodine uptake.

Management

1. antithyroid agents,
• Antithyroid agents block the utilization of iodine by interfering with the
iodination of tyrosine and the coupling of iodotyrosines in the synthesis of
thyroid hormones.
• commonly, propylthiouracil (PTU) or
• methimazole (Tapazole)
• it may take several weeks until relief of symptoms occurs

2. radioactive iodine
• The goal of radioactive iodine therapy (131I) is to destroy the overactive
thyroid cells. Almost all the iodine that enters and is retained in the body
becomes concentrated in the thyroid gland
• The patient is instructed about what to expect with this tasteless, colorless
radioiodine
• Contraindicated during pregnancy and breastfeeding
• Instruct patient not to get pregnant for 6 months

3. Surgery
• Thyroidectomy
Preoperative preparation
• PTU is administered until signs of hyperthyroidism have disappeared.
• beta-adrenergic blocking agent (propranolol) may be used to reduce the heart rate and
other signs and symptoms of hyperthyroidism
• Iodine (Lugol's solution or KI) may be prescribed in an effort to reduce blood loss
• palatable if diluted with water, milk or juice
 - give through straw to prevent staining of teeth

50
  - takes 2-4 weeks before results are evident
• Avoid Stimulants and Foods that prolong clotting time
• High caloric diet, vitamin C and thiamine days before the surgery
• Demonstrate how to support the neck with the hands after surgery

Pre-operative Care:
✓ Assess V/S, weight, electrolyte & glucose level
✓ Teach DBE & coughing as well as how to support neck in post-op period when coughing
& moving
✓ Administer antithyroid meds etc. to prevent thyroid storm

Post operative Care:

✓ Monitor for respiratory distress & have tracheostomy set, O2 & suction machine at bed
side
✓ Maintain semi-Fowler’s position to reduce edema
✓ Immobilize head with pillows/sandbags; prevent flexion & hyperextension of neck
✓ Check surgical site for edema & bleeding
✓ Limit client talking & assess for hoarseness
✓ Assess for laryngeal nerve damage…high-pitched voice, stridor, dysphagia, dysphonia &
restlessness
✓ Monitor for signs of hypocalcemia & tetany & have calcium gluconate at bed side
✓ Give cold water when nausea subsides.
✓ Provide bedside table to provide easy access to things frequently needed
✓ Encourage early ambulation

Monitor for complications

• Hemorrhage
• Hematoma formation
• Edema of the glottis
• Injury to the Laryngeal nerves
• Tetany

THYROID STORM
Clinical Manifestations
• High fever (hyperpyrexia) above 38.5°C (101.3°F)

51
 • Exaggerated symptoms of hyperthyroidism with disturbances of a major system—for
example, gastrointestinal (weight loss, diarrhea, abdominal pain), or cardiovascular
(edema, chest pain, dyspnea, palpitations)
• Altered neurologic or mental state, which frequently appears as delirium psychosis,
somnolence, or coma
• Extreme tachycardia (more than 130 beats/min)
Life-threatening thyroid storm is usually precipitated by stress, such as
✓ injury,
✓ infection,
✓ thyroid and nonthyroid surgery,
✓ tooth extraction,
✓ insulin reaction,
✓ diabetic ketoacidosis, pregnancy,
✓ digitalis intoxication,
✓ abrupt withdrawal of antithyroid medications, extreme emotional stress, or vigorous
palpation of the thyroid.

Management
1. A hypothermia mattress or blanket, ice packs, a cool environment, hydrocortisone, and
acetaminophen (Tylenol). Salicylates (eg, aspirin) are not used because they displace
thyroid hormone from binding proteins and worsen the hypermetabolism.
2. Humidified oxygen is administered to improve tissue oxygenation and meet the high
metabolic demands. Arterial blood gas levels or pulse oximetry may be used to monitor
respiratory status.
3. Intravenous fluids containing dextrose are administered to replace liver glycogen stores
that have been decreased in the hyperthyroid patient
4. PTU or methimazole is administered to impede formation of thyroid hormone and block
conversion of T4 to T3, the more active form of thyroid hormone.
5. Hydrocortisone is prescribed to treat shock or adrenal insufficiency.
6. Iodine is administered to decrease output of T4 from the thyroid gland. For cardiac problems
such as atrial fibrillation, dysrhythmias, and heart failure, sympatholytic agents may be
administered. Propranolol, combined with digitalis, has been effective in reducing severe
cardiac symptoms.

Possible complications of anti-thyroid medication

• medication sensitization,
• fever,

52
 • rash,
• urticaria,
• agranulocytosis and thrombocytopenia

Nursing Management
o Protect from stress: private room, restrict visitors, quiet environment.
o Promote physical & emotional equilibrium:

1. cool, quiet, cool well ventilated environment.

2. eye care: sunglasses to protect from photophobia, protective drops
(methylcellulose) to soothe cornea
3. diet: high calorie, protein, vit. B; avoid stimulants
o Prevent complications: give medications as ordered.
o Monitor for thyroid storm.
o Health teaching: stress reduction techniques; importance of medications; methods to
protect eyes from environment; s/sx of thyroid storm.

53
 PARATHYROID DISORDERS

HYPERPARATHYROIDISM
• caused by overproduction of parathormone by the parathyroid glands, is characterized by
bone decalcification and the development of renal calculi (kidney stones) containing
calcium.

Clinical Manifestation
▫ Primarily, It has no symptoms
▫ Apathy, fatigue, muscle weakness, nausea, vomiting, constipation, hypertension,
and cardiac dysrhythmias may occur
▫ Signs of Hypercalcemia
▫ decrease in the excitation potential of nerve and muscle tissue.
▫ Apathy, fatigue, muscle weakness, nausea, vomiting, constipation,
hypertension, and cardiac dysrhythmias may occur
Complications
▫ Related to the presence of Renal Calculi
▫ Fractures secondary to demineralized bones

Diagnostics
• Elevated Serum Calcium levels • UTZ
• Elevated Serum Parathormone • MRI
Levels • Fine needle biopsy
• Bone changes on X-Ray

Management
1. Parathyroidectomy
2. Increased fluid intake to prevent kidney stones
3. Cranberry juice to acidify the urine
4. Monitor for flank pain or blood in the urine
5. Encourage frequent ambulation
6. Instruct to avoid high calcium foods
7. Encourage High Fiber diet
8. Basically, the same with thyroidectomy
9. Avoid dehydration
10. Monitor Tetany (early Postop complication)

54
HYPERCALCEMIC CRISIS
• Serum calcium levels greater than 15 mg/dL (3.7 mmol/L) result in neurologic,
cardiovascular, and renal symptoms that can be life-threatening
• Treatment includes
• rehydration with large volumes of IV fluids,
• diuretic agents to promote renal excretion of excess calcium, and
• phosphate therapy to correct hypophosphatemia and decrease serum calcium levels by
promoting calcium deposition in bone and reducing the gastrointestinal absorption of
calcium
• A combination of calcitonin and corticosteroids has been administered in emergencies to
reduce the serum calcium level by increasing calcium deposition in bone

HYPOPARATHYROIDISM
Inadequate secretion of the parathyroid gland
Causes
• interruption of the blood supply or
• surgical removal of parathyroid gland tissue
▫ during thyroidectomy,
▫ parathyroidectomy, or radical neck dissection

Electrolyte changes
• Increased Serum phosphate level
• Decreased blood calcium level
• Decreased intestinal absorption of calcium
• Decreased calcium resorption from bones
• Decreased calcium resorption from kidneys
• Decreased Renal phosphate excretion

Clinical Manifestation
▫ Hypocalcemia causes irritability of the neuromuscular system and contributes to the chief
symptom of hypoparathyroidism—TETANY
▫ Hyportonia
▫ Uncoordinated muscle movements
▫ numbness,
▫ tingling, and cramps in the extremities
▫ include bronchospasm,
▫ laryngeal spasm,

44
 ▫ carpopedal spasm (flexion of the elbows and wrists and extension of the carpophalangeal
joints and dorsiflexion of the feet),
▫ dysphagia,
▫ photophobia,
▫ cardiac dysrhythmias, and
▫ seizures

Assessment and Diagnostics

• Chvosteck’s sign • Increased serum Phosphate
• Trousseau's sign • Increased bone density
• Decreased serum calcium

Management
1. IV Calcium Gluconate to replenish calcium in the blood
2. Phenobarbital to prevent seizures
3. IV parathormone
4. environment should be free of noise, drafts, bright lights, or sudden movement
5. Tracheostomy or bronchodilators if spasm is present
6. High Calcium, Low phosphorus diet
7. Instruct to take Vitamin D

45
 ADRENAL DISORDERS

PHEOCHROMOCYTOMA
• Pheochromocytoma is a tumor that is usually benign and originates from the chromaffin
cells of the adrenal medulla
• Results in exaggeration of sympathetic response

Clinical Manifestation
▫ Triad of the patient in ▫ air hunger, and
hypertensive patient ▫ dyspnea.
 Palpitations ▫ Severe Hypertension
 headache, and ▫ polyuria,
 Diaphoresis ▫ nausea,
▫ Hyperglycemia ▫ vomiting,
▫ Anxiety ▫ diarrhea, abdominal pain,
▫ Nervousness ▫ feeling of impending doom
▫ headache, ▫ Palpitations and tachycardia
▫ vertigo, .
▫ blurring of vision,
▫ tinnitus,
Assessment and Diagnostic Findings

✓ Pheochromocytoma is suspected if signs of sympathetic nervous system overactivity occur

in association with marked elevation of blood pressure
5 “h” of phaeochromocytoma
Hypertension,
Headache,
Hyperhidrosis (excessive sweating),
Hypermetabolism, and
Hyperglycemia
• Measurements of urine and plasma levels of catecholamines and metanephrine (MN), a
catecholamine metabolite, are the most direct and conclusive tests for overactivity of the
adrenal medulla
• 24 hr urine collection to determine free catecholamine or MN
▫ Restrict
 coffee and tea (including decaffeinated varieties),
 bananas,

44
  chocolate,
 vanilla, and
 Aspirin
• Total plasma catecholamine concentration
▫ Let patient rest lying supine on bed for 30 min
▫ Insert the needle to the vein 30 min before blood extraction
• Clonidine suppression Test
• CT Scan
• MRI
• UTZ
• 131I-metaiodobenzylguanidine (MIBG) scintigraphy may be required to determine the
location of the pheochromocytoma

Management

1. Encourage rest and relaxation exercises during acute episodes

2. Decrease BP quickly
 Phentolamine (Regitine)
 Sodium Nitropruside (Nipride)
Alpha Blocker -Phenoxybenzamine (Dibenzyline)
Calcium Channel Blocker- nifedipine (Procardia)
Beta Adrenergic Blocker- propranolol (Inderal)

Surgical management
Adrenalectomy

✓ Control BP Before the surgery

✓ Maintain hydration throughout the surgery
✓ Keep antihypertensive during the surgery
✓ Watch for possible hypotension and hypoglycemia postop
✓ The patient needs lifelong Steroid replacement if adrenalectomy is bilateral
✓ Continue monitoring for signs of phaeochromocytoma

ADDISON’S DISEASE
• Addison's disease, or adrenocortical insufficiency, occurs when adrenal cortex function is
inadequate to meet the patient's need for cortical hormones.

44
Causes
▪ Autoimmune or idiopathic atrophy
▪ surgical removal of both adrenal glands
▪ infection of the adrenal glands
▪ Therapeutic use of corticosteroids

Clinical Manifestations
▫ by muscle weakness;
▫ anorexia;
▫ gastrointestinal symptoms;
▫ fatigue;
▫ emaciation;
▫ dark pigmentation of the mucous membranes and the skin, especially of the knuckles,
knees, and elbows; hypotension;
▫ low blood glucose, low serum sodium, and high serum potassium levels
▫ Mental status changes such as depression, emotional lability, apathy, and confusion are
present in 60% to 80% of patients

ADDISONIAN CRISIS
This condition is characterized by cyanosis and the classic signs of circulatory shock: pallor,
apprehension, rapid and weak pulse, rapid respirations, and low blood pressure.
In addition, the patient may complain of headache, nausea, abdominal pain, and diarrhea and may
show signs of confusion and restlessness. Even slight overexertion, exposure to cold, acute
infection, or a decrease in salt intake may lead to circulatory collapse, shock, and death

Diagnostic Tests
• early-morning serum cortisol and plasma ACTH
• Heme glucose test
• Serum Na and K

Medical Management
✓ combating circulatory shock: restoring blood circulation, administering fluids and
corticosteroids, monitoring vital signs, and placing the patient in a recumbent position with
the legs elevated
✓ Hydrocortisone (Solu-Cortef) is administered intravenously, followed by 5% dextrose in
normal saline. Vasopressor amines may be required if hypotension persists.

45
Nursing management
o Monitor Fluid Balance and Signs of Circulatory compromise
o Minimze physical and psychological stressors
o Keep IV, glucose and electrolytes at bedside
o Educate the patient and the family about hormone replacement theory

CUSHING SYNDROME
• Cushing's syndrome results from excessive, rather than deficient, adrenocortical activity.
Causes
• use of corticosteroid medications
• excessive corticosteroid production secondary to hyperplasia of the adrenal cortex
• tumor of the pituitary gland that produces ACTH and stimulates the adrenal cortex
• Primary hyperplasia of the adrenal glands
• ectopic production of ACTH by malignancies

Clinical Manifestations
▫ arrest of growth, obesity, and musculoskeletal changes occur along with glucose
intolerance
▫ central-type obesity, with a fatty “buffalo hump” in the neck and supraclavicular areas, a
heavy trunk, and relatively thin extremities
▫ The skin is thin, fragile, and easily traumatized; ecchymoses (bruises) and striae develop
▫ Excessive protein catabolism occurs, producing muscle wasting and osteoporosis
▫ Kyphosis, backache, and compression fractures of the vertebrae may result
▫ Retention of sodium and water occurs as a result of increased mineralocorticoid activity,
producing hypertension and heart failure.
▫ The patient develops a “moon-faced” appearance and may experience increased oiliness
of the skin and acne.
▫ There is increased susceptibility to infection
▫ Hyperglycemia or overt diabetes may develop
▫ report weight gain, slow healing of minor cuts, and bruises
▫ Virilization -the appearance of masculine traits and the recession of feminine traits
▫ There is an excessive growth of hair on the face (hirsutism), the breasts atrophy, menses
cease, the clitoris enlarges, and the voice deepens. Libido is lost in men and women.

Diagnostic Tests
• overnight dexamethasone suppression test
• a 24-hour urinary free cortisol level

46
Medical Management
1. Hypophysectomy if the cause is pituitary
2. Adrenalectomy if the cause is the adrenal glands
3. Adrenal enzyme inhibitors (eg, metyrapone, aminoglutethimide, mitotane, ketoconazole)
may be used to reduce hyperadrenalism if the syndrome is caused by ectopic ACTH

Nursing Management
o decreased risk of injury,
o decreased risk of infection,
o increased ability to carry out self-care activities,
o improved skin integrity,
o improved body image,
o improved mental function, and
o absence of complications.
o Manage patients undergone transphenoidal hypophysectomy
o Manage patients with hyperclycemia
o Manage patients with peptic ulcer
o Monitor for Addisonian crisis

47
 DIABETES MELLITUS
 Diabetes mellitus is a group of metabolic diseases characterized by increased levels of
glucose in the blood (hyperglycemia) resulting from defects in insulin secretion, insulin
action, or both
 The cells may stop responding to insulin or the pancreas may stop producing insulin
entirely. This leads to hyperglycemia, which may result in acute metabolic complications
such as diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic
syndrome (HHNS).
 Long-term effects of hyperglycemia contribute to macrovascular complications (coronary
artery disease, cerebrovascular disease, and peripheral vascular disease), chronic
microvascular complications (kidney and eye disease), and neuropathic complications
(diseases of the nerves).

Types of Diabetes Mellitus

1. TYPE 1 DIABETES MELLITUS

➢ Type 1 diabetes is characterized by destruction of the pancreatic beta cells.
Combined genetic, immunologic, and possibly environmental (eg, viral) factors are
thought to contribute to beta cell destruction.
➢ There is also evidence of an autoimmune response in type 1 diabetes
➢ Diabetic Ketoacidosis is possible

2. TYPE II DIABETES MELLITUS

➢ There is insulin resistance and/or impaired insulin secretion
➢ Hyperosmolar Hyperglycemic nonketotic syndrome may occur
➢ Can be prevented with appropriate lifestyle changes

3. GESTATIONAL DIABETES MELLITUS

➢ Gestational diabetes mellitus (GDM) is any degree of glucose intolerance with its
onset during pregnancy. Hyperglycemia develops during pregnancy because of
the secretion of placental hormones, which causes insulin resistance.

Clinical Manifestation
➢ Polydipsia ➢ Possible Microvascular and
➢ Polyuria Macrovascular
➢ Polyphagia Complications
➢ Weight Loss ➢ Neuropathy
➢ Hypertension

48
Diagnostics
 Abnormally high glucose level
◼ FBS of 126 mg/dL or higher
◼ RBS of 200 mg/dL or higher
◼ HgbA1C (A1C)
◼ Fasting lipid profile
◼ Test for microalbuminuria
◼ Serum creatinine level
◼ Urinalysis
◼ Electrocardiogram

Criteria for diagnosing DM

1. Symptoms of diabetes plus casual plasma glucose concentration equal to or greater

than 200 mg/dL (11.1 mmol/L). Casual is defined as any time of day without regard to
time since last meal. The classic symptoms of diabetes include polyuria, polydipsia,
andpolyphagia.
2. Fasting plasma glucose greater than or equal to 126 mg/dL (7.0 mmol/L). Fasting is
defined as no caloric intake for at least 8 hours.
3. Two-hour postload glucose equal to or greater than 200 mg/dL (11.1 mmol/L) during
an oral glucose tolerance test. The test should be performed as described by the World
Health Organization, using a glucose load containing the equivalent of 75 g anhydrous
glucose dissolved in water.

Management
 The main goal of diabetes treatment is to normalize insulin activity and blood glucose levels
to reduce the development of vascular and neuropathic complications
 Diabetes management has five components

Nutritional therapy
Goals of Nutritional Therapy
 Providing all the essential food constituents (eg, vitamins, minerals) necessary for
optimal nutrition
 Meeting energy needs
 Achieving and maintaining a reasonable weight

43
  Preventing wide daily fluctuations in blood glucose levels, with blood glucose levels
as close to normal as is safe and practical to prevent or reduce the risk for
complications
 Decreasing serum lipid levels, if elevated, to reduce the risk for macrovascular
disease
 Meal Planning
 50% to 60% from glucose
 20% to 30% from fats
 10% to 20% from proteins
 Reduce Cholesterol intake
 Increase Dietary Fibers
 Food exchange List
 Nutritional Label
 Food pyramid guide

Glycemic Index- The term “glycemic index” is used to describe how much a given food increases
the blood glucose level compared with an equivalent amount of glucose.
 Combining starchy foods with protein- and fat-containing foods tends to
slow their absorption and lower the glycemic response.
 In general, eating foods that are raw and whole results in a lower glycemic
response than eating chopped, puréed, or cooked foods.
 Eating whole fruit instead of drinking juice decreases the glycemic
response, because fiber in the fruit slows absorption.
 Adding foods with sugars to the diet may result in a lower glycemic
response if these foods are eaten with foods that are more slowly
absorbed
 Alcohol consumption
 Sweeteners

Exercise
 Increases glucose uptake
 Improve insulin utilization
 Increases HDL and decreases LDL
 Increases lean muscle mass
 Loss weigth
 Stress reduction
 Enhances well being

44
General Precautions
 Avoid exercise if ketone is present in the urine
 Use proper footwear and, if appropriate, other protective equipment.
 Avoid exercise in extreme heat or cold.
 Inspect feet daily after exercise.
 Avoid exercise during periods of poor metabolic control
 Instruct to take snack before and after exercise or reduce the dosage of insulin
 Inform other people that he is diabetic or wear a medic alert bracelet
 Exercise during the safe time
 Alter exercise regimen to adapt with neuropathy or retinopathy
 Monitor blood pressure and watch for angina/heart attack

 Monitoring
The objective is to prevent fluctuations in blood glucose level
 Self-Monitoring of blood glucose
 Helpful in monitoring the effectiveness of diet, exercise and medication
 Helping detect hyperglycemia and hypoglycemia
 Prevent complications
 Frequency of monitoring
 Usually three times a day specially for patients taking insulin
 For non-insulin, 2 -3 times, including 2 hr postprandial
 If hypoglycemia or hyperglycemia is suspected
 Responding to SMBG result
 Instruct to keep logbook to monitor pattern
 Monitor 2 hrs postprandial to identify need for adjustment
 Continuous Glucose monitoring
 Contains glucometer
 It also contains insulin infusion pump
 Glycated Hemoglobin (HgB A1C)
 Urine Glucose Testing
 Testing for Ketones

Pharmacologic therapy
 Insulin therapy
 Injection of insulin to a patient
✓ Management of type 1 DM
✓ For pregnant patients

45
 ✓ Surgery
✓ Emergency for hyperglycemia

 Categories of Insulin
 Rapid Acting insulin
✓ O5-15min;P60-90min;D2-4 hrs
 Short Acting Insulin (Regular Insulin)
✓ O30-1hr;P2-3hr;D4-6hr
 Intermediate Acting (NPH Insulin)
✓ O3-4hr;P4-12hr;D16-20hr
 Long Acting Insulin
✓ O6-8;P12-16;D20-30
 Peakles or Very long acting
✓ acidic
 Complications of Insulin therrapy
✓ Local allergic reaction
✓ Insulin lipodystrophy
✓ Resistance to injected insulin
✓ Morning hyperglycemia
 Storing Insulin
✓ Refrigerate vials that are not in use
✓ Keep away from freezing, high temperature and direct sunlight
✓ The vial in use should be kept to room temperature (1mo)
✓ Roll or invert repeatedly cloudy insulin prior to use
✓ If the bottle is frosted or whitish, do not use
 Selecting syringe
✓ Use syringe appropriate to measure insulin accurately
✓ Dispose syringe in a puncture proof container after use
 Preparing the injection
✓ Draw up the regular insulin first if you mix two types of insulin
✓ Avoid contaminating insulin vials
 Withdrawing insulin
✓ Inject air to the vial with the same amount of insulin to be drawn
 Selecting and rotating injection sites
✓ Don’t inject at the same site in 2-3 weeks
✓ Don’t exercise the site of injection
 Preparing the skin

46
 ✓ Avoid using alcohol
✓ If alcohol is used, allow it to dry before injection
 Inserting needle
✓ Injection is through the subcutaneous route
✓ Aspiration for blood is not recommended
 Disposing Needles
✓ Dispose in a puncture proof container

 Oral Hypoglycemic Agent

 Sulfonylureas
◼ Stimulates directly the pancreas to secrete insulin
◼ Chlorpropamide (Diabenese)
 Biguanides
◼ Increase body tissues’ sensitivity to insulin
◼ Inhibit glucose production by the liver
◼ e.g. Metformin (Glucophage)
 Alpha-Glucosidase Inhibitors
◼ Delay absorption of complex carbohydrate in the intestine
◼ e.g. Acarbose (Precose)
 Thiazolidinediones
◼ Sensitizes body tissue to insulin
◼ e.g. Rosiglitazone (Avandia)

Education
 Seven Tips for managing DM
 Healthy Eating
 Being active
 Monitoring
 Taking Medicines
 Problem Solving
 Reducing risk
 Healthy coping
 Preventive care
 Foot care
 Eye Care
 General Hygiene
 Risk factor management

47
 Acute Complications of DM

Hypoglycemia(Insulin Reaction)
Caused by too much insulin or oral hypoglycemic agents, too little food, or excessive
physical activity.

Clinical Manifestation
Adrenergic symptoms and CNS symptoms

o Mild hypoglycemia
▫ Sympathetic stimulation
▫ Sweating, tremor, tachycardia, palpitations, nervousness, hunger

o Moderate hypoglycemia
▫ Glucose deprivation in the brain
▫ Inability to concentrate, headache, lightheadedness, confusion,
memory lapse, numbness of lips and tongue, slurred speech,
impaired coordination, irrational or combative behavior, diplopia

o Severe Hypoglycemia
▫ CNS severely impaired
▫ Disoriented behavior, seizures, difficulty arousing, lost of
consciousness

Management of Hypoglycemia

1. Give fast acting concentrated source of glucose

✓ Three or four commercially prepared glucose tablets
✓ 4 to 6 oz of fruit juice or regular soda
✓ 6 to 10 hard candies
✓ 2 to 3 teaspoons of sugar or honey
2. Monitor Blood sugar every 15min and retreat if it is less than 70 to 75 mg/dL
3. Give additional snack if the condition resolves and avoid high fat snacks
4. Emergency Measures
✓ Inject 1mg of glucagon subQ or IM for unconscious patient
✓ Administer 25 to 50mL D50W IV

48
Diabetic Ketoacidosis (DKA)
DKA is caused by an absence or markedly inadequate amount of insulin

o The three main clinical features of DKA are

✓ Hyperglycemia
✓ Dehydration and electrolyte loss
✓ Acidosis

o Three main causes of DKA are

✓ decreased or missed dose of insulin,
✓ illness or infection, and undiagnosed and
✓ untreated diabetes

Clinical Manifestation
▫ Polyuria ▫ Nausea
▫ Polydipsia ▫ Abdominal pain
▫ Blurred vision ▫ ACETONE Breath
▫ Headache ▫ Lethargic
▫ Orthostatic hypotension ▫ Kussmaul’s Respiration
▫ Anorexia

Diagnostic findings
o Serum glucose of 300 to 800 mg/dL
o Low serum Bicarbonate and Low pH
o Ketone in the urine
o Elevated BUN, Creatinine, Hematocrit

Prevention

✓ Continue Insulin during illness

Management

1. Rehydration
✓ Use PNSS
2. Restoring Electrolytes
✓ Monitor and correct serum potassium
3. Reversing acidosis

49
 ✓ Use Regular insulin IV. Flush the IV line
4. Monitor and prevent hypokalemia
5. Monitor for fluid overload

Hyperglycemic Hyperosmolar Nonketotic syndrome

o HHNS is a serious condition in which hyperosmolarity and hyperglycemia predominate, with
alterations of the sensorium (sense of awareness)
o Ketoacidosis is absent or rare
o glycosuria and dehydration, hypernatremia and increased osmolarity occur
o Insulin is present

Clinical Manifestation
▫ hypotension,
▫ profound dehydration (dry mucous membranes,
▫ poor skin turgor),
▫ tachycardia, and
▫ variable neurologic signs (eg, alteration of sensorium, seizures, hemiparesis).

Long Term Complications of DM

 Macrovascular Complications
✓ Atherosclerosis
✓ Increased BP
✓ Heart attack
✓ Stroke
✓ Peripheral vascular disease
 Microvascular complication
✓ Diabetic Retinopathy
o Changes in the microvasculature include
o microaneurysms,
o intraretinal hemorrhage,
o hard exudates, and
o focal capillary closure
o Retinopathy has three main stages:

1. nonproliferative (background),

44
 ✓ macular edema, occurs and may lead to visual distortion
and loss of central vision
2. preproliferative,
✓ is considered to be a precursor to the more serious
proliferative retinopathy
✓ there are more widespread vascular changes and loss of
nerve fibers
3. Proliferative
✓ characterized by the proliferation of new blood vessels
growing from the retina into the vitreous
✓ The visual loss associated with proliferative retinopathy is
caused by this vitreous hemorrhage, retinal detachment
Management
1. Other strategies that may slow the progression of diabetic retinopathy include the
following:
2. Control of hypertension
3. Control of blood glucose
4. Cessation of smoking
5. argon laser photocoagulation
6. Avoid weight bearing activities
7. Vitrectomy

✓ Nephropathy
o the kidney's filtration mechanism is stressed, allowing blood proteins to
leak into the urine. As a result, the pressure in the blood vessels of the
kidney increases. It is thought that this elevated pressure serves as the
stimulus for the development of nephropathy
Diagnostics
• Microalbuminuria
• Creatinie
• BUN

Management
1. Control HPN
2. Control of UTI
3. Avoid nephrotoxic substances
4. Low sodium, low protein

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 5. Hemodialysis

✓ Diabetic Neuropathy
▪ May be due to
✓ Hyperglycemia for years
✓ Capillary basement membrane thickening
✓ Vascular closure
✓ Demyelination due to hyperglycemia
▪ Sensorymotor neuropathy (peripheral neuropathy)

✓ Paresthesia
✓ Burning sensation
✓ Intermittent claudication
✓ Decrease proprioception
▪ Autonomic neuropathy

✓ related to the cardiac, gastrointestinal, and renal systems

▪ Cardiovascular symptoms range from a fixed, slightly tachycardic heart rate
and orthostatic hypotension to silent, or painless, myocardial ischemia and
infarction
▪ Delayed gastric emptying may occur with the typical gastrointestinal symptoms
of early satiety, bloating, nausea, and vomiting. “Diabetic” constipation or
diarrhea (especially nocturnal diarrhea) may occur as a result
▪ Urinary retention, a decreased sensation of bladder fullness, and other urinary
symptoms of neurogenic bladder result from autonomic neuropathy
✓ Hypoglycemic Unawareness
✓ Sudomotor neuropathy
Refers to a decrease or absence of sweating (anhidrosis) of the extremities, with a
compensatory increase in upper body sweating. Dryness of the feet increases the risk for the
development of foot ulcers
✓ Sexual dysfunctionn
✓ Foot and Leg problems
▫ Neuropathy
▫ Peripheral vascular disease
▫ Immunocompromised
✓ Management of foot problems
▪ Inspect foot daily
▪ Don’t wallk barefooted

46
▪ Avoid ill fitting shoes
▪ Use mirror to assess bottom of feet
▪ Properly bathing, drying, and lubricating the feet, taking care not to allow
moisture (water or lotion) to accumulate between the toes
▪ Trimming toenails straight across and filing sharp corners to follow the
contour of the toe
▪ Avoid smoking

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 Activity
Research Article Digest
Instructions:

1. Select then downloads worthy scholarly full-text article published from year 2016 to present from
a reputable online journal
2. Topics of the research journal should be Adult Nursing limited to Endocrine or Metabolic
Disorders only.
3. Ensure that it is a research paper and not an editorial or a philosophical paper
4. Read thoroughly the research article
5. Digest and synthesize the research article; and;
6. Make a write-up (at least maximum of 2000 words, minimum of 1,300 words) as regards your
digest/synthesis in the following format
a. Title Page
b. INTRODUCTION
✓ What was it all about? What is the focus?
✓ What was the problem all about?
✓ What are the unsatisfactory/unacceptable points presented by the author/s?
c. DISCUSSION
✓ Describe and justify scientifically the unsatisfactory/unacceptable points which you
have identified
✓ Personally, how could the research itself be improved? Provide answers for every
unsatisfactory/unacceptable points
d. CONCLUSION
✓ Give a general statement on how you see it fit for the research concluded to be
scientifically improved?
e. REFERENCES
✓ See your research manual in writing your reference using APA style of citation.
✓ Watch the video for your guide in doing your reference.
https://youtube.com/watch?v=9pbUoNa5tyY&feature=share
✓ Although this requirement is partially based on your understanding and perspective,
support your claims using pertinent online references. Use APA 6 or 7h Edition
format in your citations and reference page.

Deadline of Submission: Submit your file using MS word office ARIAL font with 1-inch margin
all-around the A4 paper. Send it at email (Instructor’s email address) on or before the midterm

48
 examination. Note: Copy paste of digest/synthesis paper is strictly discouraged and will have a
mark of failing grade for this activity. This is 30 points.

Instruction: Cross the box that corresponds as your objective judgment on the paper you are
evaluating. 5 is the perfect score for each category and a total of 30 as overall rating.

KEY RESULT AREA

5 4 3 2 1
EXCELLENT PROFICIENT ADEQUATE LIMITED NOT EVIDENT
CRITERIA
Engaging and Clear and Straightforwar Simplistic and There is no
insightful thoughtful d and emerging presentation of
CONTENT presentation presentatio developing presentation thoughts and
of thoughts n thoughts presentation of thoughts supporting
and and of thought and details
supporting supporting and supporting
details. details. supporting details.
details.
Introduction Introduction Introduction Introduction Introduction
details details details details details
arrangement arrangement arrangement arrangement arrangement
ORGANIZATION
transition transition transition transition transition
conclusion and conclusion conclusion conclusion conclusion
coherence coherence coherence coherence coherence
are superior are very are are limited are not
good. satisfactory present
Purpose clearly Purpose clearly Purpose Purpose is Purpose is does
ACHIEVEMENT established and established and established vaguely not established
OF PURPOSE effectively generally but may not established and and may not be
sustained sustained be sustained. may not sustained.
be
sustained.
Precise and Carefully Generally Vague imprecise There is poor
sophisticated chosen and precise and or inappropriate vocabulary used.
VOCABULARY/ vocabulary complex straightforward vocabulary is Mainly simple
USE OF
used. vocabulary is vocabulary is used. Mainly sentences
LANGUAGE (
DICTION ,
Sentences vary used. used. simple lacking of
SENTENCES) in pattern and Sentences Sentences sentences association are
length often vary in sometimes vary lacking in variety used.
pattern and in pattern are used.
length and length
Great attention Great attention Less attention Little Great There is no
has been paid to has been paid has been paid attention has attention that
correctness. to correctness. correctness. been paid to has been paid
CORRECTNESS Text contains Text contains Text contains correctness. to correctness.
essentially no minor error error which Text contains Text contains
errors which none of which interfere with many errors many errors
interfere with interfere with clarity of which limit the which limit the
clarity of clarity of communication clarity of clarity of
communication. communication communication. communication.

The paper has The paper has The paper has The paper has The entire
ORIGINALITY zero 10% 50% 50% above paper has no
plagiarized plagiarized plagiarized score upon originality at all.
score upon score upon score upon plagiarized
checking checking checking checking

49
SELF ASSESSMENT QUESTIONNAIRE
MATCHING TYPE. Match Column A with the correct answer on Column B. Write the letter of
the correct answer in the space provided before the number.

COLUMN A COLUMN B
____ 1. It is the Hypo secretion of 1 or more of the A. Hyperpituitarism
pituitary hormones caused by tumors, trauma, B. Syndrome of
encephalitis, autoimmunity, or stroke.
inappropriate Anti
Diuretic Hormone
____ 2. A disorder which results from an excessive
C. Pheochromocytoma
output of thyroid hormones caused by abnormal D. Myexedema Coma
stimulation of the thyroid gland by circulating E. Hypopituitarism
immunoglobulins. F. Hyperthyroidism
____ 3. It is a tumor that is usually benign and originates G. Hyperparathyroidism
from the chromaffin cells of the adrenal medulla.
H. Diabetes Insipidus
I. Cushing syndrome
____ 4. A disorder which results from excessive, rather
J. Addisons Disease
than deficient, adrenocortical activity.
____ 5. A disorders which occurs when adrenal cortex
function is inadequate to meet the patient's need for
cortical hormones.
____ 6. It is a disorder of the posterior lobe of the pituitary
gland that is characterized by a deficiency of ADH
(vasopressin).
____ 7. It describes the most extreme, severe stage of
hypothyroidism, in which the patient is hypothermic
and unconscious. Increasing lethargy may progress
to stupor and then coma.
____ 8. A disorder which caused by overproduction of
parathormone by the parathyroid glands, is
characterized by bone decalcification and the
development of renal calculi (kidney stones)
containing calcium.
____ 9. It is the Hyper secretion of growth hormone by
the anterior pituitary gland in an adult; caused
primarily by pituitary tumors.
____ 10. It is a disorder in the secretion includes
excessive ADH secretion from the pituitary gland
even in the face of subnormal serum osmolality.

REFERENCE
Brunner & Suddarth’s (2011). Textbook of Medical-Surgical Nursing (11th Edition).

50