REVIEW OF ANATOMY AND

PHYSIOLOGY OF ENDOCRINE SYSTEM

1. The endocrine system maintains the stability of internal environment.
2. It consists of glands (glands are the group of epithelial cells). They produce specialized secretions.
Glands are of two types:
a. EXOCRINE GLANDS:
i. They discharge their secretions onto the epithelial surface of an organ, either directly or
through a duct.
ii. They vary in size, shape and complexity.
b. ENDOCRINE GLANDS:
i. They discharge their secretions into the blood and lymph. 2200
ii. These are ductless glands, e.g. hormones.
iii. These glands may secrete single hormone or more than one hormone.
3. The science concerned with the structure and functions of the endocrine glands and the diagnosis
and treatment of the disorders of the endocrine system is called endocrinology.
4. The endocrine glands secrete their products, hormones, directly into the blood because they do not
have ducts, so they are also called ductless glands.
5. The endocrine system consists of a number of distinct glands.
PITUITARY GLAND
1. The pituitary gland also called hypophysis is the master endocrine gland.
2. It is situated in the cranial cavity.
a. Length: About 1.2 to 1.5 cm.
b. Weight: About 500 to 900 mg in normal adult humans.
3. It has a stem-like stalk called the infundibulum, which connects it to the hypothalamus of the
brain.
4. It secretes nine different hormones.
5. The pituitary looks like one gland, but it consists of two lobes, i.e. Anterior Pituitary Lobe and
Posterior Pituitary Lobe.

ANTERIOR PITUITARY LOBE

It is also called adenohypophysis, consists of connective tissue fibres. The releasing hormones
increase the secretion of the gland hormones. Releasing hormones and inhibiting hormones from
hypothalamus stimulate and suppress the secretions of anterior pituitary respectively called
hypothalamic hormones. The pituitary portal system of blood vessel passes the hormones to the
gland. The whole system is controlled by negative feedback mechanism.
1. Growth Hormone (GH): Growth Hormone (GH) is also known as Somatotropin Hormone
(STH). It helps in the growth of bone, muscle and other tissues. The increase rate of fat metabolism
causes the hyperglycemia. The time of stress, anxiety or low glucose level (hypoglycemia) increases
the release of growth hormone.
2. Thyroid Stimulating Hormone (TSH): This is also called thyrotropin. It helps in the growth
and development of target glands. TSH synthesizes and secretes the two hormones, i.e.
Triiodothyronine (T3) and Thyroxine (T4). Thyroid Releasing Hormone (TRH) depends upon the
amount of TSH and T3.
3. Adrenocorticotropic Hormone (ACTH): This hormone is synthesized by the anterior
pituitary gland. The hypothalamus secretes the Corticotropin Releasing Hormone (CRH) which
stimulates adrenal glands to produce ACTH. ACTH controls the synthesis and secretion of
glucocorticoids and mineralocorticoids. Large amount of ACTH can darken the skin. ACTH level is
low during day time and high at night time. The secretion of ACTH increases during exercise, stress
or when level of glucose decreases. It also increases the concentration of cholesterol and steroids.
4. Prolactin: It initiates and maintains the milk secretion by the mammary gland. The
hormone oxytocin prolactin promotes the production of milk. The prolactin secretion is high during
sleep, anxiety or stress.
5. Gonadotropins: They are also called sex hormones. They are synthesized by anterior
pituitary gland. The two sex hormones are:
a. Luteinizing Hormone (LH)
 b. Follicle Stimulating Hormone (FSH)
In females, LH along with FSH helps in the ovulation. LH supports FSH in stimulating the
maturation of follicles. FSH and LH are called gonadotropins because they stimulate the growth and
maintenance of the gonads (ovaries and testes).
In males, LH helps in the secretion of testosterone. FSH stimulates the development of seminiferous
tubules of the testes and maintains the sperm production.

POSTERIOR PITUITARY LOBE

It is also called neurohypophysis. It stores and releases the two hormones, i.e. ANTIDIURETIC
HORMONE (ADH) and OXYTOCIN (OT).
It does not synthesize any hormone. These hormones are secreted by neurosecretory cells. The blood
supply to the posterior pituitary gland is from inferior hypophyseal arteries. These hormones are
released by non-endocrine gland.
1. Antidiuretic Hormone (ADH): The word "Antidiuretic" means "Opposing the large
production of urine". It prevents the formation of a large volume of urine. It helps in the storage of
water in body. In absence of ADH, urine output increases than normal. It can lead to fluid imbalance.
It causes the smooth muscle contraction and vasoconstriction in the blood vessel of skin and
abdominal organs.
2. Oxytocin: It helps in the uterine contraction and it causes milk ejaculation from the breast
THYROID GLAND
1. The butterfly-shaped thyroid gland is one of the largest pure endocrine gland in the body.
2. It is located in the anterior neck, just inferior to the larynx.
3. It has two pyramidal shaped lobes with one on either side of the trachea at the level the 5th,
6th and 7th cervical and 1st thoracic vertebra. Its two lateral lobes are connected by a median
tissue mass called the isthmus anterior to trachea.
4. Each lobe is 5 cm long and 3 cm wide. Normal mass of the gland is 25-30 g.
5. Gland is covered by a fibrous capsule. The capsule has numerous septae which extend into
the gland and divide into lobules.
6. It has a very rich blood supply from the superior and inferior thyroid arteries. It receives
80-120 ml of blood per minute. It appears redder than its surrounding tissues.
HORMONES OF THYROID GLAND
Hormone secreted by thyroid gland are as follows:
1. Thyroid hormones (T3 and T4)
2. Calcitonin (Thyrocalcitonin)
THYROID HORMONES (T3 AND T4)
1. The follicular cells of thyroid gland secrete two iodine-containing amine hormones:
a. Triiodothyronine (T3)
b. Thyroxine (T4) or tetraiodothyronine.
2. These names refer to the fact that the two hormones contain three (T3) and four (T4) iodine atoms.
3. The term "thyroid hormone" refers to "T3 and T4" collectively.
4. T4 is the major hormone secreted by the thyroid follicles; most T3 is formed at the target tissues
by conversion of T4 to T3.
5. Very much like one another, the hormones are constructed from two linked tyrosine amino acids.
The principal difference is that T4 has four bound iodine atoms and T3 has three (thus, T4 and T3).
FUNCTIONS OF THYROID HORMONES (T3 AND T4)
These hormones are referred to as the body's major metabolic hormones.
1. The primary effect of TH is to increase the body's metabolic rate. As a result, it raises
oxygen consumption and has a calorigenic effect-it increases basal metabolic rate and body heat
production.
2. TH secretion rises in cold weather and thus helps to compensate for increased heat loss.
3. To ensure an adequate blood and oxygen supply to I meet this increased metabolic demand,
thyroid hormone also raises the heart rate and contraction strength and raises the respiratory rate.
4. It accelerates the breakdown of carbohydrates, fats and protein for fuel and stimulates the
appetite.
5. Thyroid hormone promotes alertness, bone growth and remodeling, the development of the
skin, hair, nails and teeth and fetal nervous system and skeletal development.
6. It also stimulates the pituitary gland to secrete growth hormone.
7. Except for the adult brain, spleen, testes, uterus and the thyroid gland itself, TH affects
nearly every cell in the body.
8. When children are born with thyroid hormone deficiency they have problems with physical
growth and developmental problems. Brain development can also be severely impaired.
CALCITONIN (THYROCALCITONIN)
1. Calcitonin is another hormone produced and released by the thyroid gland. Calcitonin is a
32 amino acid polypeptide hormone.
2. This hormone is secreted by C cells of the thyroid gland.
FUNCTIONS OF CALCITONIN
1. It contributes to the regulation of blood calcium levels.
2. Its most important effect is to lower blood Ca²+ levels. Most of the calcium removed from the
blood is stored in the bones.
3. It is a direct antagonist of parathyroid hormone.
4. Calcitonin's regulation of blood Ca2+ levels is short lived but extremely rapid.
5. Calcitonin targets the skeleton, where it:
a. Inhibits osteoclast activity and hence, bone resorption and release of Ca2+ from the bony
matrix.
b. Stimulates Ca2+ uptake and incorporation into bone matrix. Thus, calcitonin has a bone
sparing effect.
6. Calcitonin appears to be important only in childhood, when the skeleton grows quickly and the
bones change dramatically in mass, size and shape.
7. It has relatively little effect in adults. In adults, it is just a weak hypo calcemic agent.
8. Calcitonin can also be used therapeutically for the treatment of hypercalcemia or osteoporosis.
PARATHYROID GLANDS
1. The parathyroid glands are partially embedded in the posterior surface of the lateral lobes of
thyroid.
2. They are small, light-colored lumps that stick out from the surface of the thyroid gland
3. There are four glands:
a. Each about 3 to 8 mm long and 2 to 5 mm wide (about the size of a split pea).
b. They are lentiform in shape.
c. Each has a mass of about 40 mg.

FRONT VIEW BACK VIEW

4. Microscopically, gland is composed of two major types of cells that make up parathyroid tissues:
a. Chief (principal) cells:
i. The more numerous cells are chief (principal) creatic cells. They are more in young people.
ii. These cells are arranged in tightly-packed nests around small blood vessels.
iii. Chief cells produce parathyroid hormone.
b. Oxyphil cells:
i. Other types of cells are called oxyphil cells.
ii. Their function is basically unknown.
iii. Their number increases with age.
PARATHYROID HORMONE (PTH) OR PARATHORMONS
1. Parathyroid hormone is secreted from four parathyroid glands.
2. It is released directly into the bloodstream and travels to its target cells which are often
quite far away.
3. The major target cells of PTH are in bone, kidneys, and the gastrointestinal system.
FUNCTIONS
1. It is the major regulator of the levels of calcium, magnesium and phosphate ions in the blood. It
opposes the effect of calcitonin.
2. PTH raises blood calcium levels by:
a. Stimulating osteoclasts (bone resorbing cells) to digest some of the bony matrix and release
ionic calcium and phosphates to the blood.
b. Enhancing reabsorption of Ca2+ (and excretion of PO) by the kidneys.
c. Increasing absorption of Ca2+ by the intestinal mucosal cells.

ADRENAL (SUPRARENAL) GLANDS

1. Adrenal glands are two in number. Both of these are situated superior to each kidney.
a. These are 3-5 cm in height, width is 2-3 cm and thickness is 1 cm.
b. Its weight is about 3-5 gm.
2. According to its functions and structure, adrenal gland is divided into two regions:
a. Outer adrenal cortex
b. Inner adrenal medulla
3. The arterial blood supply to the glands is by branches from the abdominal aorta and renal arteries.
ADRENAL CORTEX
Adrenal cortex produces the steroid hormones called corticosteroid. They are:
GLUCOCORTICOIDS
1. Protein catabolism.
2. Formation of glucose.
3. Lipolysis.
4. Resistance to stress.
5. Anti-inflammatory effect
6. Depression of immune response.
MINERALOCORTICOIDS (ALDOSTERONE)
It maintains the fluid and electrolyte balance in human body. It increases the reabsorption of Na+,
which helps in retention of water. At the same time, aldosterone increases excretion of K+ in urine.
This reduces the acid in body.
ANDROGENS
It is the male sex hormone. The female sex hormone secreted by this is estrogen. In males, this
hormone exerts masculinizing effect, but not in females. In females, this hormone helps in the
growth of pubic hairs.
ADRENAL MEDULLA
It produces two catecholamine hormones, i.e. adrenaline and noradrenaline.
EPINEPHRINE AND NOREPINEPHRINE
These are not so essential for human body like adrenal cortex. They help in fight or flight response.
The sympathetic nervous system stimulates to secrete these hormones. Their functions in the body
are as follows:
1. Help in contraction of blood vessels.
2. Increase the blood pressure.
3. Increase the heart rate.
4. Dilate the airway to the lungs.
5. Decrease the rate of digestion.
6. Increase the blood glucose level, of goodies
7. Stimulate cellular metabolism
8. Dilate the pupils
9. Supply the blood to the essential organs including the heart, brain and skeletal muscles.
NURSING ASSESSMENT
HISTORY DATA COLLECTION
Thorough history collection, the nurse gathers information about the patient's present condition and
previous medical history. The history begins with biographic data and proceeds to the chief
complaints including additional subjective data are collected about the patient's past medical history,
family history, major diseases and hospitalizations, psychosocial history and life and a careful review
of systems.
A nurse should assess the patient's presenting symptoms which may be specific or non-specific.
SPECIFIC SYMPTOMS
Specific symptoms for certain endocrine disorders are:
1. Mental status changes: The patient may report increased nervousness, mood changes, confusion
and depression. Coma may occur in uncontrolled diabetes mellitus.
2. Vital signs:
a. Increased body temperature and pulse rate in hyperthyroidism.
b. Deep rapid breathing is a classic sign of diabetic ketoacidosis.
c. Tumors of adrenal glands, causing increased secretion of epinephrine, can result in
hypertension.
 d. Insufficient antidiuretic hormone from the pituitary gland can cause dehydration and over
secretion can cause excessive retention of body water.
3. Palpitations: In hyperthyroidism and in pheochromocytoma, there is an increased heart rate with
sweating and flushing.
4. Tremors: Uncontrolled tremors in hyperthyroidism.
5. Fatigue: Due to pathophysiological changes and emotional stress.
6. Weakness: May be generalized or local.
7. Appetite changes: Polyphagia or anorexia associated with diabetes mellitus.
8. Weight changes: Eating more but frequent weight loss indicates diabetes mellitus or
hyperthyroidism. Weight gain may indicate hypothyroidism.
9. Polydipsia and polyuria: It may indicate diabetes mellitus.
10. Changes in bowel status: Frequent loose stools in hyperthyroidism and constipation can indicate
hypothyroidism.
11. Abnormalities involving the sexual organs and libido: Irregular menstruation, amenorrhea,
loss of libido, premature development of secondary sexual characteristics, impotence and infertility
are the sexual changes which are the characteristics of endocrine disorders.
12. Changes in physical appearance: Enlargement of hands and feet, coarsening of the facial
features in acromegaly.
13. Adrenocortical hyperfunction: It is manifested by moon like face, thin extremities and truncal
obesity.
14. Growth abnormalities: Delayed growth, dwarfism, gigantism or inappropriate growth.
15. Skin and tissue changes: Hyperpigmentation in Addison's disease. Hypopigmentation or vitiligo
may indicate other endocrine disorders. Delayed tissue healing in diabetes mellites. Non-pitting
edema in hypothyroidism.
16. Eyes: Bulging eyes in hyperthyroidism. Partial or total vision loss due to pituitary tumor.
Temporary blurred vision or permanent blindness due to diabetes mellitus.
17. Bone and joints: Bone pain, cysts, fractures in hyperparathyroidism. Rapid breakdown of bone
in Cushing's syndrome.
18. Renal changes: Colic or renal stone development may follow the bone disorder, found in
hyperpara- thyroidism.
19. Hair changes: Excessive hair in women indicates ovarian disorders. Axillary and pubic hair loss
indicates pituitary disorders. Hair becomes soft and silky in hyperthyroidism. Brittle, coarse and dry
hair in hyperthyroidism.
NON-SPECIFIC SYMPTOMS
Common non-specific symptoms include
1. Fatigue and depression.
2. Altered alertness, decrease energy
3. Disturbed sleeping pattern.
4. Weight changes.
5. Altered mood and affect
6. Changes in the condition of the skin and hair.
7. Altered general appearance.
8. Sexual dysfunction.
DIAGNOSTIC TESTS
THYROID FUNCTION TESTS
A number of tests are available to assess thyroid function.
The most important tests are:
1. Serum thyroxin (T4), triiodothyronine (T3)
2. Serum thyroid stimulating hormone (TSH)
3. Radioiodine uptake test
4. T3 resin uptake
5. Thyrotropin releasing hormone stimulation test.
6. Serological tests: Many thyroid disorders are presumed to have an autoimmune basis, such
as Hashimoto's thyroiditis, some types of myxedema and in graves disease. Consequently,
serological tests may be performed to determine, if the patient's blood contains any
antithyroid antibodies.
PARATHYROID FUNCTION TESTS
1. Parathyroid Hormone (PTH): It is used to detect the measurement of PTH concentration
in blood using radioimmunoassay technique.
2. Total serum calcium level: Used to detect the alterations in calcium metabolism caused
by parathyroid disease or any malignancy.
3. Ionized serum calcium level: Approximately 45-50% of total serum calcium is in
biologically active ionized form. This test is used to detect the changes in calcium
metabolism caused by parathyroid disease, malignancies or neck surgery.
4. Serum phosphate: This test is used to measure the level of inorganic phosphorous in the b
lood and to detect metabolic abnormalities that affect calcium metabolism.
ADRENAL FUNCTION TESTS
1. Plasma cortisol: Useful to assess adrenal dysfunction.
2. 24-hour urinary free cortisol test: It is useful to establish diagnosis of hypercortisolism.
In this test, measurement of cortisol production during a 24-hour period is done.
 3. Dexamethasone Suppression Test (DST): It is used to evaluate adrenal hyperfunction.
4. Adrenocorticotropic Hormone (ACTH) stimulation test: It is useful to determine, if
hypercortisolism is ACTH dependent (bilateral hyperplasia) or ACTH independent (adrenal
tumor).
5. Corticotropin stimulation test: This test is used to measure the responsiveness of
pituitary gland to ocorticotropin-releasing factor, a hypothalamic nod hormone that regulates
pituitary secretion of ACTH.
6. Clonidine suppression test: It is useful to differentiate pheochromocytoma from essential
hypertension when test results are inconclusive.
7. Urine or blood test for aldosterone: It is useful to diagnose primary aldosteronism.
PITUITARY FUNCTION TESTS
1. Serum prolactin: Direct radioimmunoassay measurement of prolactin secreted by the
anterior pituitary gland and useful to detect pituitary tumors.
2. Serum Growth Hormone (GH): Useful to diagnose acromegaly, gigantism, pituitary
tumors or pituitary related growth failure in children.
3. Adrenocorticotropic Hormone (ACTH): It is useful to diagnose the cause of adrenal
abnormalities when compared with serum cortisol levels.
4. Insulin tolerance test: It is useful to detect the functional hypopituitarism that is caused by
pituitary disease or that appears after pituitary surgery.
5. Glucose suppression test: Postprandial elevations of glucose inhibit the secretion of
growth hormone by the pituitary gland. Failure to suppress the growth hormone levels after
ingestion of glucose suggests a growth-hormone secreting tumor.
6. Water deprivation test: It is useful to determine the diagnose and etiology of diabetes
insipidus.
EXOCRINE PANCREATIC FUNCTION TESTS
1. Urine test: In this test, oral bentiromide is given to the patient after overnight fast, then
urine sample is collected for 6 hours. Then, pancreatic chymotrypsin splits bentiromide, Para-
aminobenzoic acid (PABA) is a breakdown product which is excreted in urine. Less PABA
may indicate pancreatic insufficiency.
2. Angiography: This X-ray procedure allows the visualization of the visceral vessels in
order to identify the abnormalities of vascular structure and function of pancreas. In this
procedure, a contrast medium is injected through femoral artery.
3. Radionuclide scanning/Scintigraphy: It involves the infusion of I/V infusion of gamma-
emitting isotopes. Following infusion, a scintillation detector passes over the abdomen to
detect a tumor or abscess formation in the pancreas.
 DISORDERS OF THYROID GLAND
HYPOTHYROIDISM
Hypothyroidism is an underactivity of the thyroid, hyposecretion of thyroid hormone, and decreased
body metabolism and heat production.
TYPES OF HYPOTHYROIDISM
1. Primary hypothyroidism (thyroid failure): It is defined as "Low levels of blood thyroid
hormone due to destruction of the thyroid gland". It is the most common endocrine disease. It may be
caused by the following:
a. Cretinism.
b. Defective hormone synthesis.
c. Iodine deficiency.
d Antithyroid drugs.
e. Radiation therapy for hyperthyroidism.
2. Secondary hypothyroidism (pituitary): It involves decreased activity of the thyroid caused by
failure of the pituitary gland. It is caused by disorders of the pituitary gland or hypothalamus.
3. Tertiary hypothyroidism (hypothalamic): It may develop, if tumors or lesions in the
hypothalamic area interfere with normal hypothalamic function and cause it not to produce
Thyrotropin Releasing Hormone (TRH)
4. Subclinical hypothyroidism: Hypothyroidism with an elevated TSH level but a normal to low
normal T4 level.
ETIOLOGY
1. Autoimmune thyroiditis
2. Congenital disease
3. Pituitary disease
4. Pregnancy
5. Thyroid dysgenesis
6. Radiation therapy for the treatment of head and neck cancer and hyperthyroidism.
7. Severe long standing hypothyroidism display myxedema causes: Puffiness, periorbital edema, and
mask like affect, prominent tongue, course, sparse hair, etc.

RISK FACTORS
Factors that increase the risk of developing hypothyroidism include:
1. Being female.
2. Being of an older age
3. Being Caucasian or Asian. depression and guilt
4. Family history of Hashimoto's thyroiditis or another autoimmune disease, such as type 1 diabetes
or celiac disease.
5. Sporadic goitre: Ingestion of goitrogenic glycosides may cause sporadic goitre.
6. Genetic defects involving faulty iodine metabolism cause hypothyroidism.
7. Being pregnant or postpartum.
8. Treated with certain medicines, such as lithium.
9. Underwent thyroid surgery.

PATHOPHYSIOLOGY
1. Hypothyroidism may reflect a malfunction of the hypothalamus, pituitary or thyroid gland, or all
of which are part of the same negative feedback mechanism.
2. Lack of iodine in diet prevents thyroid gland from producing the three thyroid hormones, i.e.:
a. T4 (Thyroxine)
b. T3 (Triiodothyronine)
c. Calcitonin (Thyrocalcitonin)
Decrease production of thyroid hormones slows the body's metabolic rate.
3. Chronic autoimmune thyroiditis associated with goitre is known as Hashimoto's thyroiditis. The
cause of this autoimmune process is unknown, although heredity has a role and specific human
leukocyte antigen subtypes are associated with greater risk.
4. To restore thyroid hormone production to normal levels, the anterior pituitary mainly increases
production of TSH, causing the thyroid gland to enlarge.
a. Enlargement causes development of goitre
b. This enlargement compresses structures present in the neck and chest, resulting in respiratory
problems and dysphagia.

CLINICAL MANIFESTATION:
1. Cardiovascular system:
a. Heart rate: Slows to normal. Slow rate may contribute to decrease cardiac output.
b. Rhythm: Dysrhythmias are rare.
c. Blood pressure: Normal to slight elevation of systolic or diastolic.
2. Hematologic system:
a. Easy bruising.
b. Normocytic or macrocytic anemia.
3. Respiratory system:
a. Dyspnea.
b. Reduced hypoxic drive.
c. Respiratory muscle weakness.
 d. Hypercapnic ventilatory drive.
4. Renal system:
a. Fluid retention
b. Decreased urinary output.
c. Increased total body water.
d. Decreased production of erythropoietin
5. Gastrointestinal system:
a. Anorexia.
b. Increased weight gain.
c. Constipation.
d. Decreased bowel sounds.
e. Decreased protein metabolism.
f. Increased serum lipids.
g. Delayed glucose uptake.
h. Decreased glucose absorption.
6. Musculoskeletal system:
a. Muscle cramps or stiffness.
b. Slow movements.
c. Increased bone density.
d. Transient pain.
7. Integumentary system:
a. Skin: Dry, worse, scaly.
b. Hair: Falls out.
c. Nails: Expressionless.
d. Cold intolerance.
8. Endocrine system:
a. Normal to enlarged thyroid.
9. Neurologic system:
a. Decreased tendon reflexes.
b. Muscle sluggishness.
c. Speech: Slow, deliberate.
d. Lethargy.
10. Reproductive system:
a. Males: Decreased libido, impotence.
b. Females: Menorrhagia, irregular menses, decreased libido.
DIAGNOSTIC EVALUATION
1. Medical history or physical examination
2. Blood tests: Hypothyroidism can be confirmed by following blood tests.
a. Thyroid Stimulating Hormone (TSH): TSH test helps to measure the amount of T4
(Thyroxine) that the thyroid is being signaled to make. High level of TSH indicates patient
has hypothyroidism.
b. T4 (Thyroxine) test: Free T4 and free T4 index are the blood test that in combination with
TSH test helps the physician to know how patient's thyroid is functioning.
3. Additional laboratory test: It may be indicated to confirm the effects of hypothyroidism on other
body systems.
4. Radioactive Iodine Uptake Test (RAIU):
a. RAIU shows increased TSH levels in primary hypothyroidism.
b. Decreased level in secondary hypothyroidism.
5. ECG: ECG may reveal changes related to hypothyroidism.
6. Needle biopsy: Needle biopsy may be performed to check for malignancies.

MANAGEMENT
MEDICAL MANAGEMENT
The main aim of medical management for hypothyroidism is to restore or maintain patient's thyroid
state for life.
Non-pharmacologic Interventions
1. Sufficient physical and emotional rest and emotional support.
2. Adequate bowel elimination
3. Balanced diet with increased fibre.
Pharmacologic Interventions
1. Thyroid hormone supplements:
a. Thyroid USP (desiccated thyroid, thyroid extract) which contains T4 and T3. It may cause
side effects similar to hyperthyroidism and may exacerbate angina.
b. Synthetic T4 (thyroxine, levothyroxine or sodium L-thyroxine). It has fewer side effects
than thyroid USP.
2. Thyroid hormone replacement: Thyroid hormone replacement must be gradual and monitored
by monthly measurements of TSH.

SURGICAL MANAGEMENT
1. Surgery is performed to remove goiter endangering neck structures
2. Needle biopsy:
a. It is also performed to rule out malignancy.
b. During this procedure, thyroid area is cleansed or draped.
c. Local anesthesia may be administered.
d. Patient's neck is hyperextended and a 23-gauge needle is used to aspirate from the nodule
e. Mild pressure is placed over the site when the needle is removed.
f. In the end, adhesive bandage is applied.
NURSING MANAGEMENT
1. Modification of activity: The patient experiences decrease energy and lethargy. Therefore, risk
for complications from immobility increases. Moreover, due to cardiovascular and pulmonary
dysfunction, the patient activities decrease. Nurse should therefore assist with care and hygiene and
encourage the patient to participate in activities.
2. Monitor physical status: The patient's vital signs, cognitive levels are monitored closely to detect
deterioration of physical and mental status and complications of therapy.
3. Promote physical comfort: Extra clothing and blankets are provided as patient feels chilling and
intolerance of cold but use of heating pads and electric blankets should be avoided.
4. Patient experiences: Patient experiences severe emotional reactions due to changes in appearance
and body image. Therefore, patient needs emotional support while experiencing depression and guilt.
5. Patient's family: Patient's family and friends should be informed about the symptoms and
disorder.
6. Self-care including: Self-care including instructions about therapy, its complications, patient's
response is to be taught.
7. Dietary instructions: Dietary instructions to promote weight loss should be initiated along with
the medication.
8. Precautions: Precautions must be taken during the therapy because thyroid hormones interact
with other medications, it may increase blood glucose level, bone loss and may cause respiratory
depression.

COMPLICATIONS
1. Difficulty in swallowing.
2. Difficulty in breathing.
3. Infertility.

NURSING CARE PLAN

NURSING ASSESSMENT
1. Assess the vital signs of the patient.
2. Ask the patient regarding bowel movement, record color and consistency of fecal matter following
bowel movement.
3. Monitor and record symptoms associated with passage of bowel movement:
a. Any straining, pain or headache.
b. Any rectal bleeding or fissures.
4. Monitor the activity level of the patient. It provides baseline data for planning of activities.
NURSING DIAGNOSIS
1. Constipation related to decreased gastrointestinal function.
2. Activity intolerance related to fatigue or decrease cognitive process.
3. Deficient knowledge regarding therapeutic regimen for thyroid replacement therapy.
PLANNING
NURSING GOALS
1. To improve gastrointestinal function.
2. To maintain activity intolerance.
3. To enhance knowledge.
NURSING INTERVENTIONS
Improve Gastrointestinal Function
1. Assist the patient in developing a palatable diet high in fibre and liquids.
2. Monitor patient's bowel patterns and sounds.
3. Encourage increased mobility within patient's exercise tolerance.
4. Provide stool softeners and cathartics as ordered.

Maintain Activity Intolerance

1. Teach patient to space activities to promote rest and exercise as tolerated.
2. Help patient in establishing a relaxing atmosphere.
3. Provide thyroid supplements as ordered.
4. Explain that energy and interests will return as thyroid hormone level rise as a result of thyroid
supplements.
Enhance knowledge
1. Teach patient about the causes, sign and symptoms and management of hypothyroidism.
2. Describe the effects of thyroid hormone medications to patient.
3. Emphasize the necessity of lifelong treatment with thyroid supplements to enhance quality of life.
4. Assist the patient in adjusting the treatment program to provide continuous relief from symptoms
of hypothyroidism.
PATIENT EDUCATION AND HEALTH MAINTENANCE EDUCATE PATIENT AND
FAMILY TO:
1. Eat a high fibre, low calorie diet which helps to relieve constipation.
2. Maintain healthy weight.
3. Exercise regularly.
4. Avoid use of external heat sources.
5. Administer medications as ordered by physician on same time every day.
6. Get plenty of rest and sleep.
7. Increase fluid intake.
8. Contact health care provider, if any of these occurs:
a. Extreme tiredness.
b. Chest pain.
c. Irregular heartbeat.
d. Loss of consciousness.
EVALUATION: EXPECTED OUTCOMES
1. Gastrointestinal function is improved.
2. Activity intolerance is maintained.
3. Knowledge is maintained.

HYPERTHYROIDISM
 An excessive secretion of thyroid hormone which accelerates many body functions causing a
hyperthyroidism. Grave's disease is the most common type of hyperthyroidism. It results from an
excessive output of thyroid hormone by an abnormal stimulation of thyroid gland by circulating
immunoglobulins.
ETIOLOGY
1. It is caused by over functioning of the entire gland or less commonly by single or multiple
functioning adenomas of thyroid cancer.
2. Grave's disease: An autoimmune disorder which is the most common cause of hyperthyroidism.
3. Acute thyroiditis: It is a rare disorder, i.e. bacterial in origin produces fever or pain in the thyroid
which radiates to ears.
4. Sub-acute thyroiditis: More common condition, i.e. viral in origin.
5. Stress
6. Pituitary adenoma
7. Pituitary resistance to T4 (Thyroxine)
8. Iodine induced hyperthyroidism.
RISK FACTORS
1. Being female.
2. Being over age 60.
3. Pituitary disorders.
4. Hypothalamic disorder.
5. Overtreatment for hypothyroidism.
6. Radioiodine therapy of partial thyroidectomy causing a rebound effect which can produce
hyperthyroidism symptom
PATHOPHYSIOLOGY
1. Thyroid gland secretes thyroid precursor, T4 (thyroxine), thyroid hormone or triiodothyronine
(T3) and calcitonin.
a. T4 and T3: It stimulates protein, lipid ad carbohydrate metabolism primarily through
catabolic pathways.
b. Calcitonin: It removes calcium from blood and incorporates it into bone.
2. Hyperthyroidism results when conditions, such as autoimmune disorders and thyroiditis disrupt
the normal regulatory control over thyroid hormone secretion.
3. Excessive amount of thyroid hormone over stimulates the body causing hypermetabolism,
increased sympathetic nervous system activity, alteration of production and release of hormones
produced in the gonads, hypothalamus and pituitary.
4. If hyperthyroidism occurs:
 a. Before puberty: Sexual development is delayed in both sexes.
b. After puberty: It results in the following:
i. Decreased libido in men and women.
ii. Menstrual irregularities and decreased fertility also occurs in women.
1. Cardiovascular system:
a. Increased strength of myocardial contraction demonstrated by precordial thrust.
b. Tachycardia
c. Rhythm: Abnormal heart rhythms.
d. Blood pressure: Elevates systolic pressure, decreased diastolic giving a widened pulse
pressure.
2. Hematologic system:
a. No specific changes.
3. Respiratory system:
a. Shortness of breath.
b. Increased respiratory rate and depth.
4. Renal system:
a. Fluid retention.
b. Decreased output.
5. Gastrointestinal system:
a. Increased peristalsis.
b. Increased appetite.
c. Weight loss.
d. Diarrhea.
e. Increased use of adipose and protein stores.
f. Decreased serum lipids.
g. Vomiting or abdominal pain.
6. Musculoskeletal system:
a. Malnutrition.
b. Fatigue
C. Muscle weakness
d. Proximal muscle wasting.
7. Integumentary system:
 a. Hair: Fine, oily may have patchy alopecia.
b. Skin: Soft, moist, diaphoretic, warm.
c. Heat intolerance.
8. Endocrine system:
a. Thyroid usually enlarged.
b. Bruit over thyroid.
9. Neurologic system:
a. Increased tendon reflexes.
b. Fine tremors.
c. Nervousness.
d. Anxiety.
10. Reproductive system:
a. Males: Impotence, decreased sexual development, pre-puberty.
b. Females: Amenorrhea, irregular menses, decreased fertility, tendency for spontaneous
abortion.
DIAGNOSTIC EVALUATION
1. Decreased serum TSH and increased T3, T4 and FT.
2. Elevated serum calcium level reflecting hypercalcemia secondary to alteration in calcium
metabolism from hyperthyroidism.
3. Complete blood count: Increased red blood cell count secondary to increased formation of
erythrocytes, decreased white blood cells due to decline in neutrophils.
4. 24 hours radioactive iodine uptake test is performed to distinguish grave's disease from other
causes of hyperthyroidism.
5. Thyroid scan: During this test, a radioactive isotope is injected into the vein of patient's elbow or
sometimes into the vein of patient's hand. After injection of radioactive isotope, patient lies on a table
with head stretched backward while a special camera produces an image of patient's thyroid gland on
a computer screen. This test shows how iodine collects in patient's thyroid.
6. Thyroid ultrasound: It uses high frequency sound Plan waves to produce images of the thyroid. It
may be better at detecting thyroid nodes and there's no exposure to any radiation.
MANAGEMENT
MEDICAL MANAGEMENT
The main aim of medical management is to restore and maintain patient's euthyroid state for life.
1. Antithyroids such as propylthiouracil, methimazole and carbimazole inhibit hormone synthesis
and depletes hormone stores.
2. Radioactive iodine therapy: It helps to destroy overactive thyroid cells. Patient is instructed to
accept tasteless, colorless radioiodine after treatment.
3. Dexamethasone: It inhibits secretion of thyroid hormone and peripheral conversion of T4 to T3. 8
4. Beta-adrenergic antagonists: It helps to manage the cardiac side effects of hyperthyroidism.
Propranolol controls tachycardia, hypertension and atrial fibrillation.
5. Adjunctive therapy: In this, iodine to iodide compounds are used. It decreases the release of
Enthyroid hormones; compounds of potassium iodide may also be used.
SURGICAL MANAGEMENT
THYROID BIOPSY
Thyroid biopsy is performed for the following:
1. To distinguish between benign from malignant thyroid disease.
2. To diagnose disorders such as:
a. Sub-acute thyroiditis
b. Hashimoto's disease (a condition in which immune system attacks the thyroid gland).
c. Multinodular goitre (a goitre where there are many lumps [nodules] that appear within the gland
Thyroidectomy (see table 8.3)
1. It is performed when pharmacologic therapies fails to remove thyroid cancer.
2. Patients who undergo this surgery must take thyroid hormone on a permanent basis.
NURSING MANAGEMENT
1. Educate patient about hyperthyroidism.
2. Monitor vital signs of patient.
3. Monitor patient's intake/output.
4. Auscultate heart sounds.
5. Assess patient's level of anxiety in relationship to declining thyroid hormone levels.
6. Assess patient for other causes of anxiety which may augmenting this nervous state.
7. Assess nutritional status of patient.
8. Ask patient about visual difficulties, fatigue, weakness, tremors or insomnia.
9. Create a quiet, non-stressful environment.
10. Provide emotional support to patient and family members.
11. Reduce thyroid hyperactivity to relieve symptoms.
12. Instruct patient to eat well balanced high calorie diet.
13. Avoid eating food which increases peristalsis and results in diarrhea.
14. Be always gentle and polite to patient.
15. Encourage frequent short walks during the day and maintenance of usual bed time rituals at
night.
16. Elevate head of bed at night to drainage of fluid from the periorbital area
17. Encourage patient to do indoor activities.
18. Maintain personal hygiene of patient.
19. Provide plenty of fluid and encourage patient to take plenty of fluids.
20. Encourage patient to do prayer or read any book before going to bed.
21. Encourage patient to ventilate his/her doubts, perceptions
22. Encourage patient for frequent blood testing to check TSH, T₂ level.
23. Instruct patient to eat a well-balanced diet.
24. Encourage patient or significant others to talk about their concerns and ask questions.
25. Instruct patient to come for regular follow-up.
COMPLICATIONS
1. Thyrotoxic crisis
2. Brittle bones
3. Thyroid storm
NURSING CARE PLAN
NURSING ASSESSMENT
1. Assess the vital signs of patient.
2. Monitor skin and mucous membrane integrity every 2 hourly.
3. Monitor the activity level of the patient.
4. Assess the thinking process (determine orientation to place, person, or time) to get the information
regarding the extent of interference with sensory processing.
NURSING DIAGNOSIS
1. Risk for imbalanced nutrition: Less than body requirement related to increased metabolism rate
and increased appetite.
2. Risk of disturbed thought process related to physiological changes, such as increased CNS
stimulation/accelerated mental activity.
3. Risk for injury related to exophthalmos.
4. Ineffective airway clearance related to hemorrhage, edema or laryngeal spasm.
5. Anxiety related to stress or threat.
PLANNING
NURSING GOALS
1. To maintain nutritional balance.
2. To improve physiological changes.
3. To reduce the risk for injury.
4. To improve airway clearance.
5. To reduce anxiety.
NURSING INTERVENTIONS
MAINTAIN NUTRITIONAL BALANCE
1. Monitor daily food intake.
2. Weight daily and report losses.
3. Encourage patient to eat and increase the number of meals and snacks to help in keeping caloric
intake.
4. Provide a balanced diet to promote weight gain. Provide a diet high in calories, protein,
carbohydrates, and vitamins to ensure adequate intake of nutrients.
5. Instruct patient to avoid food that increase peristalsis and fluids that cause diarrhea.
IMPROVE PHYSIOLOGICAL CHANGES
1. Assess the thinking process.
2. Assess the level of patient's anxiety.
3. Provide calm and quiet environment to reduce external stimuli to decrease hyperactivity or CNS
irritability.
4. Encourage visits by family and relatives for
maintaining socialization and orientation.
5. Provide safety measures.
6. Administer medication as prescribed to promote relaxation and reduces CNS hyperactivity.
REDUCE RISK FOR INJURY
1. Administer isotonic solution or eye lubricants to keep the eyes moist.
2. At night, elevate the head of bed, which may assist in keeping the eyelids closed or cover the eyes
with eye guards to prevent drying.
3. Suggest to patient that dark or tinted wrap around the glasses may protect his/her eyes from wind
or airborne particles.
IMPROVE AIRWAY CLEARANCE
1. Assess for hoarseness.
2. Keep intubation and tracheostomy kits readily available.
3. Keep suctioning equipment ready.
4. Complete respiratory assessment frequently.
5. Monitor for respiratory distress and laryngeal spasms.
REDUCE ANXIETY
1. Assess patient's level of anxiety.
2. Monitor physical response, noting palpitations, repetitive movements, hyperventilation and
insomnia
3. Stay with the patient.
4. Maintain a calm environment around the patient.
5. Speak in brief statements. Use simple words.
6. Administer anti-anxiety agents or sedatives and monitor effects.
PATIENT EDUCATION AND HEALTH MAINTENANCE EDUCATE PATIENT AND
FAMILY TO:
1. Weight his/her body daily.
2. Avoid smoking.
3. Reduce the level of stress which helps to relieve the symptoms of anxiety, nervousness, poor
concentration and fast heartbeat.
4. Take medicines as directed by physician.
5. Avoid stressful and heavy physical activities.
6. Eat food high in protein.
7. Do not stop taking medicines without talking to his/her health care provider first.
8. Contact health care provider, if they notice the following:
a. Fever above 100.5°F.
b. Shortness of breath.
c. Bulging eyes.
d. Diarrhea
e. Weight loss for no obvious reason.
f. Sore throat.
EVALUATION: EXPECTED OUTCOMES
1. Nutritional balance is maintained.
2. Physiological changes are improved.
3. Risk for injury is reduced.
4. Airway clearance is improved.
5. Anxiety is reduced.

THYROID CANCER
A cancer which starts in the thyroid gland is known as thyroid cancer. The thyroid gland is located
inside the front of the lower neck.
Thyroid cancer represents 90% of endocrine malignancies and 1% of all cancers.
TYPES OF THYROID CANCER
1. Anaplastic thyroid cancer: Anaplastic thyroid cancer is a fast growing, poorly differentiated
thyroid cancer that may start from differentiated thyroid cancer or a benign thyroid tumor. It is rare,
accounting for about 1% of thyroid cancer.
2. Follicular thyroid cancer: Follicular thyroid cancer is also a differentiated thyroid cancer. It can
rarely spread to lymph nodes. It develops from follicular cells and usually grows slowly.
3. Medullary thyroid cancer: Medullary thyroid cancer develops in the C cells and is sometimes the
result of genetic syndrome is called Multiple Endocrine Neoplasia type 2 (MEN2).
4. Papillary adenocarcinoma: It develops from follicular 2 cells and usually grow slowly. It is the
most common type of thyroid cancer.
STAGES OF THYROID CANCER ANXIETY.
STAGE I AND II
1. In these stages, thyroid cancer is confined to the thyroid but it may include multiple sites of cancer
within the thyroid.
2. Thyroid cancer spread to nearby lymph nodes is considered to be in these stages when patient is
younger than 45 years of age as the presence of cancer is lymph nodes does not worsen the prognosis
these younger patients.
STAGE III
1. Thyroid cancer is greater than 4 cm in diameter.
2. Lymph nodes near trachea may be affected.
3. This stage is also referred to as locally advanced tissue.
STAGE IV
1. In this stage, cancer spread beyond the thyroid to soft tissues of neck, lymph nodes in the neck or
distant locations in the body.
2. Papillary carcinoma: Most frequently, it spreads to regional lymph nodes than to distant sites.
3. Follicular carcinoma: It invades blood vessels spread to distant locations.
ETIOLOGY
1. The exact etiology of thyroid cancer is unknown.
2. Certain factors can raise patient's odds of getting it, such as:
a Inherited genetic syndrome.
b. Iodine deficiency.
c. Radiation exposure.
RISK FACTORS
1. Females are more often prone to thyroid cancer than males.
2. Exposure to high level of radiation.
3. Family history of thyroid disease.
4. Enlarged goiter.
5. Low iodine intake.
6. Obesity.
7. Gene mutations that cause endocrine diseases, such as Multiple Endocrine Neoplasia type 2A
(MEN2A) or type 2B (MEN2B) syndrome.
PATHOPHYSIOLOGY

Due to etiological factor

Dysfunction in differentiation and proliferation of

Target cells, such as follicular cells

Development of cancerous cells

Proliferation of cancerous cells

Cancer cells invade organ and spreads in adjacent organs

Distant metastasis through lymphatic and hematogenous route

CLINICAL MANIFESTATIONS
1. A hard, painless nodule in an enlarged thyroid gland shows as 'cold' on an ultrasound.
2. Palpable lymph nodes.
3. Sore neck or tenderness palpation.
4. Difficulty in swallowing.
5. Cough.
6. Hoarseness or changing voice.
7. Possible bruit or thrill.
8. Displaced trachea.
DIAGNOSTIC EVALUATION
1. Physical examination: It may reveal a lump in the thyroid or swollen lymph nodes in the neck.
2. Complete blood count: Performed to identify thyroid gland is functionally normal or not.
3. Ultrasound of thyroid: It helps a physician to determine whether a thyroid nodule is likely to be
benign (non-cancerous) or whether there is a risk that it might be cancerous.
4. CT, MRI: Performed to identify whether cancer spread beyond patient's thyroid or not.
MANAGEMENT
MEDICAL MANAGEMENT
The main aim of medical management includes:
1. Early recognition and medical diagnosis to delay or end metastasis.
2. Improved prognosis.
THYROID HORMONE THERAPY
Patients who are treated for papillary, follicular and medullary thyroid cancer by surgery requires
THT, i.e., Levothyroxine.
RADIOACTIVE LODINE
1. It is used after thyroidectomy which helps to destroy any remaining healthy thyroid tissue or
microscopic areas of thyroid cancer which were not removed during surgery.
2. Usually, it is used to treat thyroid cancer which recurs after treatment.
EXTERNAL BEAM RADIATION THERAPY
1. It can be helpful, if surgery is not an option and cancer continues to grow after radioactive iodine
treatment.
2. It can also be helpful after surgery, if cancer will recur.
CHEMOTHERAPY
1. Chemotherapy is a drug treatment.
2. It is used to kill cancer cells and to treat thyroid cancer, e.g. Cisplatin.
3. It may be combined with radiation therapy.
SURGICAL MANAGEMENT
THYROIDECTOMY
1. Thyroidectomy is performed to remove thyroid gland which may involve removal of all of the
thyroid tissue or most of the thyroid tissue.
2. The surgeon often leaves small rims of thyroid tissue around the parathyroid glands to reduce the
risk of damage to the parathyroid glands which regulate the calcium level in the blood.
THYROID LOBECTOMY
During this surgery, surgeon removes half of patient's thyroid
NURSING MANAGEMENT
1. Educate patient or significant others about causes, signs and symptoms and management of
thyroid cancer.
2. Monitor vital signs of patient frequently.
3. Auscultate breath sounds.
4. Assess for dyspnea, stridor or cyanosis.
5. Assess the level of patient's anxiety.
6. Assess patient's difficulty in swallowing.
7. Review patient's or significant others previous experience with cancer.
8. Encourage patient and family members to share their thoughts and feelings.
9. Provide an open environment in which patient feels safe to discuss feelings.
10. Caution patient to avoid bending neck, support head with pillows. It reduces likelihood of tension
on surgical wood.
11. Educate patient about the importance of eating a diet high in carbohydrate and protein.
12. Provide accurate, consistent information regarding diagnosis or prognosis.
13. Place patient in semi-fowler's position and support head and neck in neutral position with small
pillow as required in immediate post-operative phase.
14. Provide steam inhalation, humidify room air because it reduces discomfort of sore throat and
tissue edema.
15. Reduce patient's anxiety level.
16. High calorie diet may be prescribed to promote weight gain.
17. The intensity of pain is assessed and analgesic agents are administered as prescribed.
18. IV fluids are administered during the immediate post-operative period.
19. Maintain quiet environment.
20. Encourage patient to talk about his/her fears and ask questions.
21. Be gentle and polite.
22. Provide emotional or psychological support to patient and family members.
23. Carefully support the patient's head and avoid tension on the sutures when moving and turning
the patient.
24. Instruct patient to expect temporary voice loss or hoarseness for several days after surgery.
25. Instruct patient on thyroid hormone replacement and follow-up blood tests.
COMPLICATIONS
1. Cancer can spread to lungs, bones or any other part of the body.
2. Injury to the voice box and hoarseness after surgery.
3. Low calcium levels from accidental removal of the parathyroid glands during surgery.
NURSING CARE PLAN
NURSING ASSESSMENT
1. Monitor vital signs noting elevated temperature, tachycardia, arrhythmias, respiratory distress and
Okcyanosis.
2. Monitor for pain at least every 2 hourly and ask the patient to rank pain on scale of 0-10 at episode
of pain.
3. Assess speech periodically to assess the baseline data regarding hoarseness and sore throat which
occurs secondary to tissue edema.
NURSING DIAGNOSIS
1. Acute pain related to surgical procedure.
2. Risk of injury related to excessive CNS stimulation.
3. Impaired verbal communication related to tissue edema; pain/discomfort.
4. Deficient knowledge related to lack of exposure recall or misinterpretation.
PLANNING
NURSING GOALS
1. To reduce the level of pain.
2. To minimize the risk of injury
3. To establish communication.
4. To enhance knowledge.
NURSING INTERVENTIONS
1. Discuss with the patient about intensity, severity, tolerance and precipitating factors of pain.
2. Monitor sleep-rest pattern.
3. Monitor vital signs noting elevated temperature, tachycardia, arrhythmias, respiratory distress and
cyanosis to get the baseline data after the thyroidectomy.
4. Monitor serum calcium level.
5. Provide calm and quite environment.
6. Promote relaxation by decreasing the sensory stimuli.
7. Fatigue contributes to an increased pain response, or pain can contribute to interrupted sleep.
8. Apply hot or cold application according to what the patient states provides best pain relief.
9. Provide alternative methods of communication. It facilitates the expression of needs.
10. Provide an answer call bell. It prevents patient from straining the voice.
11. Maintain a quiet environment to promote rest for the patient.
12. Administer medications as prescribed by physician.
13. Discuss need for well balanced, nutritious diet.
14. Instruct the patient regarding incisional care.
15. Review surgical procedure and future expectations.
16. Encourage progressive general exercise program.
17. Review post-operative exercises to be instituted after incision heal.
18. Administer pain medication as ordered to reduce pain response.
19. Decrease anxiety and muscle tension.
20. Provide ROM exercises at least every 4 hourly.
PATIENT EDUCATION AND HEALTH MAINTENANCE
1. Advice patient to take high caloric diet.
2. Take medicines as ordered by physician.
3. Avoid smoking because it increases the risk for new or returning thyroid cancer.
4. Advice patient to drink extra liquids which helps to prevent dehydration.
5. Avoid doing strenuous physical activities for 3 to 5 weeks after surgery.
6. Instruct patient and family members to call health care provider, if they notice any of the
following:
a. Trouble eating or swallowing.
b. Sore throat.
c. Fever of 100.5°F (38°C) or higher.
d. Chills.
e. Choking or trouble breathing.
f. Lump in the neck.
EVALUATION: EXPECTED OUTCOMES
1. Pain is reduced.
2. Minimized risk for infection.
3. Established communication.
4. Knowledge is enhanced.
 DISORDERS OF PARATHYROID GLAND
HYPOPARATHYROIDISM
Hypoparathyroidism is a condition of decreased secretion or peripheral action of Parathyroid
Hormones (PTH) with lessened PTH in bones and kidneys contributing to hypocalcemia and
hyperphosphatemia.
TYPES OF HYPOPARATHYROIDISM
1. Acquired hypoparathyroidism: The damage to or the removal of the parathyroid gland leads to
acquired hypoparathyroidism. Chemotherapy and radiation therapy given to treat cancer may also
damage the parathyroid glands, resulting in acquired hypo-parathyroidism.
2. Autoimmune hypoparathyroidism: If the immune system mistakenly begins to attack the
parathyroid glands or the PTH itself, autoimmune hypo-parathyroidism develops.
3. Congenital and idiopathic hypoparathyroidism: Hypoparathyroidism from birth is called
congenital hypoparathyroidism. It occurs as a result of mutations in the genes involved in making
PTH.
4. Familial hypoparathyroidism: It usually occurs in the absence of other endocrine diseases or
developmental problems.
RISK FACTORS
1. Thyroid surgery.
2. Parathyroid surgery.
3. Family history of hypoparathyroidism.
4. Addison's disease.
5. Pregnancy.
6. Lactation.
PATHOPHYSIOLOGY
1. Under production of parathyroid hormone causes:
a. Hypocalcemia
b. Hyperphosphatemia
2. Surgical manipulation of neck may damage the parathyroid gland, possibly by causing ischemia.
3. Degree of hypoparathyroidism: It varies from decreased reserve to frank tetany.
4. Hypomagnesemia can prevent PTH secretion in patient with GI magnesium losses and nutritional
deficiencies.
5. Due to reduce PTH secretions, bone resorption slows, serum calcium level falls and severe
neuromuscular irritability develops.
CLINICAL MANIFESTATIONS
1. Cardiovascular system:
 a. Palpitations
b. Cyanosis
2. Gastrointestinal system:
a. Nausea
b. Vomiting
c. Abdominal pain
3. Integumentary system:
a. Vitiligo
b. Hair: Thin
c. Skin: Dry, scaly
d. Nails: Horizontal ridges on nails, brittle nails
4. Neurologic system:
a. Paresthesia of lips, tongue or fingers
b. Tingling
c. Tremor
5. Respiratory system:
a. Hyperreflexia
b. Positive Chvostek's or Trousseau's sign
c. Muscle cramps
d. Hoarseness
e. Laryngeal stridor
f. Edema
6. Dental defects
7. Eyes: Cataract and papilledema
DIAGNOSTIC EVALUATION
1. Assessment:
a. History: Head, neck or thyroid surgery; muscle cramps; convulsions; paresthesias,
malnutrition and alcohol abuse.
b. Physical examination: Findings related to hypocalcemia (positive Chvostek's sign, positive
Trousseau's sign, hyperactive deep tendon reflexes and convulsions).
2. Diagnostic tests:
a. Elevated phosphorus level in blood.
b. Decreased serum calcium level to a low level (7.5 mg/100 ml or less).
 c. Decreased magnesium level.
d. In chronic hypoparathyroidism, bone density may be increased as seen on radiography.
MANAGEMENT
MEDICAL MANAGEMENT
1. Calcium supplements: Oral calcium supplements for chronic management and calcium chloride or
calcium gluconate for emergency use in life threatening hypocalcemia.
2. Aluminium hydroxide gel or aluminium carbonate also administered after meals to bind phosphate
and promote its excretion through gastrointestinal tract.
3. Vitamin D (Calcitriol): It helps patient's body to absorb calcium and eliminate phosphorus.
NURSING MANAGEMENT
1. Provide patient with information on normal to parathyroid function and on hypoparathyroidism
(its causes, signs and symptoms, diagnosis and treatment).
2. Monitor vital signs.
3. Enquire patient about dietary habits, fluid intake.
4. Auscultate lung sounds.
5. Assess patient for respiratory distress in response to activity
6. Monitor serum calcium levels.
7. Ask patient for any sign of numbness and tingling around the mouth or in the finger tips or toes.
8. Discuss hypoparathyroidism action and side effects of medicines used to treat it.
9. Avoid straining during seizures.
10. Monitor level of anxiety by observing physical responses, repetitive movements, palpitation and
insomnia.
11. Reduce external stimuli, provide calm environment.
12. Administer anti-anxiety drugs as prescribed.
13. Encourage patient to eat and increase amount of meal.
14. Encourage patient to eat high-caloric food which are easily digested.
15. Provide calm environment and reduce bright light in room.
16. Encourage patient to verbalize his/her feelings.
17. Maintain intake and output chart.
18. Encourage patient for bed rest and restrict excessive activities.
19. Provide nutritional diet plan and review of nutrient needs.
20. Ask for regular medical follow-up to monitor
EFFECTIVENESS OF THERAPY AND FOR PREVENTION OF FATAL COMPLICATIONS
COMPLICATIONS
1. Seizures
2. Malformed teeth
3. Problems with kidney function.
4. Heart arrhythmias
NURSING CARE PLAN
NURSING ASSESSMENT
1. Monitor vital signs.
2. Enquire patient about dietary habits, fluid intake.
3. Do neuromuscular examination.
4. Assess behavioral changes such as anxiety, irritability.
5. Observe seizure activities.
6. Record analysis: ECG changes, serum Ca+ level.
NURSING DIAGNOSIS
1. Risk of injury related to tetany, seizures.
2. Anxiety related to disease, treatment.
3. Impaired nutrition pattern less than body requirement related to dysphagia.
4. Activity intolerance related to weakness, photophobia.
5. Knowledge deficient related to disease condition, treatment, self-care, prognosis and discharge
needs.
PLANNING
NURSING GOALS
1. To reduce risk of injury.
2. To relieve anxiety.
3. To maintain nutritional pattern.
4. To improve ability to participate in desired activities.
5. To enhance knowledge
NURSING INTERVENTIONS
REDUCE THE RISK OF INJURY
1. Monitor vital signs, to assess elevating temperature, tachycardia, respiratory distress.
2. Observe for nerve muscular irritability, e.g. numbness, paresthesias, twitching.
3. Avoid restraining during seizures.
4. Keep side rails raised and padded.
5. Monitor serum calcium level.
6. Administer anticonvulsants as prescribed to control the seizures activity.
RELIEVE ANXIETY
1. Monitor level of anxiety by observing physical responses, repetitive movements, palpitation,
insomnia.
2. Describe everything in brief statements by using simple words.
3. Reduce external stimuli, provide calm environment.
4. Provide diversional therapies, e.g. soft soothing music.
5. Administer anti anxiety drugs as prescribed by physician.
MAINTAIN STABLE WEIGHT BY REDUCING MALNUTRITION
1. Monitor food intake and body weight daily.
2. Encourage patient to eat and increase amount of meal.
3. Encourage to eat high-caloric foods that are easily digested.
4. Consult with dietitian to provide high caloric, protein, carbohydrate rich diet.
5. Maintain intake and output chart.
IMPROVE ABILITY TO PARTICIPATE IN DESIRED ACTIVITIES
1. Monitor vital signs and activity level of the patient.
2. Observe for tachypnea, dyspnea, pallor and cyanosis designs.
3. Provide calm environment and reduce bright light in room.
4. Encourage the patient for bed rest and restrict excessive activities.
5. Administer sedatives or anti anxiety agents as per prescription.
ENHANCE KNOWLEDGE
1. Assess patient's knowledge regarding disease and self-care.
2. Provide appropriate information regarding sign and symptoms of hypophora.
3. Provide knowledge including drug therapy and expected side-effects.
4. Provide nutritious diet plan and review of nutrient needs.
5. Ask for regular medical follow-up to monitor effectiveness of therapy and for prevention of fatal
complications.
PATIENT EDUCATION AND HEALTH MAINTENANCE
1. Educate patient and family regarding disease and self-care.
2. Instruct family members to maintain calm environment around the patient.
3. Encourage patient to eat high caloric foods that are easily digested.
4. Instruct patient to restrict excessive activities.
5. Encourage patient for bed rest.
EVALUATION: EXPECTED OUTCOMES
1. Risk of injury is reduced.
2. Anxiety is relieved.
3. Nutritional pattern is maintained.
4. Improved ability to participate in desired activities.
5. Knowledge is enhanced.
HYPERPARATHYROIDISM
Hyperparathyroidism is an excess of parathyroid hormone in the bloodstream due to over activity of
one or more of the body's four parathyroid glands.
CLASSIFICATION
1. Primary hyperparathyroidism: It occurs when normal regulatory relationship between serum
calcium level and PTH secretions is interrupted. It is2 to 4 times more common in women than in
males.
2. Secondary hyperparathyroidism: When glands are hyperplastic from malfunction of another
organ system is known as secondary hyperparathyroidism. It may be diagnosed at any age in the
renal patient.
3. Tertiary hyperparathyroidism: During this type of hyperparathyroidism, the parathyroid gland
becomes overactive and secretes an excessive amount of hormone despite the calcium proportions
being normal.
ETIOLOGY
PRIMARYHYPERPARTHYROIDISM
Non – cancerous growth on a gland
Hyperplasia of tow or more parathyroid glands
Malignant tumors
SECONDARY HYPERPARATHYROIDISM
Paget’s disease, multiple myeloma, carcinoma with bone metastasis.
Glands which are hyperplastic as a result of malfunction or another organ system, such as
kidney.
Severe calcium deficiency.
TERTIARY HYPERPARATHROIDISM
Autonomous hypersecretion of parathyroid hormone
Chronic secondary hyperparathyroidism
 After renal transplantation
RISK FACTORS
1. Women are more likely to get this condition than men.
2. Chronic renal failure.
3. History of neck exploration or thyroid surgery.
4. Previous radiation treatment for cancer that has exposed neck to radiation.
5. Severe, ongoing vitamin D or calcium deficiencies can trigger hyperparathyroidism.
PATHOPHYSIOLOGY
PRIMARY HYPERPARATHYROIDISM
1. Glands may be:
a. Adenomatous (about 80% of cases).
b. Hyperplastic (about 20% of cases).
c. Malignant (1% of cases).
2. Severity of hypercalcemia depends on the quantity of hyperfunctioning tissue
3. Excessive PTH stimulates transport of calcium into blood from intestine, kidneys and bone.
4. Nephrolithiasis occurs in 20 to 30% of patients with hyperthyroidism. It may be complicated by
pyelonephritis.
5. Bone changes include bone resorption related to hypercalcemia.
SECONDARY HYPERPARATHYROIDISM
1. A slight rise in serum phosphorus begins when glomerular filtration rate decreases. It causes serum
calcium level to fall and stimulate PTH secretion.
2. Increase PTH levels decrease renal tubular reabsorption of phosphorus.
3. As the glomerular filtration rate decreases, PTH is secreted in increased amount to decrease
tubular reabsorption of phosphorus and maintains serum phosphorus.
TERTIARY HYPERPARATHYROIDISM
It results from hyperplasia of the parathyroid gland.
CLINICAL MANIFESTATIONS
1. Nausea, vomiting or loss of appetite.
2. Neurosis to psychosis.
3. Depression, lethargy.
4. Demineralization of bone or bone tumors.
5. Tenderness on back and joints, arthritis.
6. Bone deformities causes pathological fracture.
a. Rickets
b. Osteoclastoma
7. Cardiac dysrhythmias.
8. Kidney stones, polydipsia and uremia.
9. Excessive urination.
10. Hypertension.
11. Bodyaches
12. Constipated bowels.
DIAGNOSTIC EVALUATION
1. ASSESSMENT:
a. History: Neck surgery, peptic ulcer disease, bone fractures with minimal trauma, polyuria,
polyphagia and kidney stones.
b. Physical examination: In addition to assessing for clinical manifestations and check for the
signs of hypertension.
2. Diagnostic tests:
a. CT scans: When ultrasonography fails to localize the parathyroid gland. It helps to locate
about 50 to 77% parathyroid tumors.
b. MRI: Used to observe detail parathyroid gland location on the film.
c. Urine test: Performed to determine creatinine clearance.
d. Radiographic examination:
i. Performed to determine bone resorption.
ii. Also helps to detect bone cysts with advanced disease, diffuse demineralization of
bones.
e. Ultrasonography: Used for pre-operative localization of parathyroid gland.
MANAGEMENT
MEDICAL MANAGEMENT
NON-PHARMACOLOGIC INTERVENTIONS
1. Primary hyperparathyroidism:Dietary management including a diet low in calcium or vitamin
D.
2. Secondary hyperparathyroidism: Calcium supplements and restriction of phosphorus.
PHARMACOLOGIC INTERVENTIONS
1. Hydration with saline solution helps to increase rapidly urinary excretion of calcium.
2. Antibiotic (plicamycin): It is a toxic antibiotic drug which inhibits bone resorption and lowers
serum
calcium.
3. Bisphosphonates: Recommended to prevent the loss of calcium from bones. It may lessen
osteoporosis which is caused by hyperparathyroidism.
SURGICAL MANAGEMENT
Surgery is the most common treatment for primary hyperparathyroidism and provides a cure in at
least 90% of all cases. A surgeon will remove only those glands that are enlarged or have a tumor
(adenoma). If all four glands are affected, a surgeon will likely remove only three glands and perhaps
a portion of the fourth leaving some functioning parathyroid tissue.

1. Surgery may be done as an outpatient procedure, allowing patient to go his/her home on the same
day.
2. In such cases, the surgery is done through very small incisions in the neck, and patient receives
only local anesthetics.
3. Complications from surgery are not common.
4. Risks include the following:
a. Damage to nerves controlling the vocal cords.
b. Long-term low calcium levels requiring the use of calcium and vitamin D supplements.
NURSING MANAGEMENT
1. A nurse should enquire patient about symptoms of hyperparathyroidism.
2. Assess the level of pain, its location, intensity, quality and duration.
3. Assess serum calcium level.
4. Monitor patient's vital signs.
5. Encourage patient to take a well-balanced diet.
6. Provide prescribed vitamin supplements.
7. Help patient to be as active as possible depending on the extent of bone disease.
8. Keep patient's bed in low position. to nod
9. Assist patient with ambulation as needed.
10. Provide small and frequent meals.
11. Instruct patient to maintain oral hygiene.
12. Maintain intake or output chart.
13. Provide diversional therapy.
14. Encourage patient to do Range of Motion (ROM) exercise as per tolerance.
15. Provide comfort measures such as pillow, cushion or heat therapy.
16. Encourage patient to do deep breathing exercise.
17. Provide steam inhalation, chest physiotherapy or incentive spirometry.
18. Instruct patient to take plenty of fluids.
19. Encourage patient to talk about his/her fears and ask questions.
20. Provide emotional and psychological support to patient or significant others.
COMPLICATIONS
1. Primary hyperparathyroidism:
a. Arthritic changes secondary to soft tissue calcification.
b. Pancreatitis
c. Severe hypertension
2. Secondary hyperparathyroidism:
a. Chronic renal failure necessitating.
b. Skeletal abnormalities associated with chronic renal failure.
NURSING CARE PLAN
NURSING ASSESSMENT
1. Monitor vital signs.
2. Enquire about symptoms of hyperparathyroidism.
3. Assess the dietary habits, alcohol consumption, smoking, use of over counter medicines, etc.
4. Do a thorough physical examination.
5. Assess the level of pain, quality, intensity, duration, aggravating factors.
NURSING DIAGNOSIS
PRE-OPERATIVE
1. Activity intolerance related to fatigue, weakness.
2. Impaired nutritional pattern less than body requirements related to nausea, vomiting.
3. Discomfort related to bone pain.
4. Disturbed sleeping pattern related to pain, psychosis.
POST-OPERATIVE
1. Ineffective airway clearance related to post anesthesia effect.
2. Ineffective gas exchange related to post-operative bed rest
3. Fluid volume deficit related to NPO status.
4. Risk of infection related to post surgery hospitalzation.
PLANNING
PRE-OPERATIVE NURSING GOALS
1. To promote activity level.
2. To maintain nutritional status.
3. To promote comfort level.
4. To promote sleep.
POST-OPERATIVE NURSING GOALS
1. To improve airway patent.
2. To improve breathing pattern.
3. To maintain fluid and electrolyte balance.
4. To prevent occurrence of infection.
NURSING INTERVENTIONS PRE-OPERATIVE
PROMOTE ACTIVITY LEVEL:
1. Assess the activity level of patient.
2. Plan nursing care along with patient.
3. Provide rest in between activities.
4. Encourage to take balanced diet.
5. Encourage to take plenty of fluids.
6. Provide prescribed vitamin supplements
MAINTAIN NUTRITIONAL STATUS:
1. Assess nutritional status of patient.
2. Enquire patient about his/her food likings and eating habits.
3. Provide small and frequent meal.
4. Encourage patient to maintain oral hygiene.
5. Encourage to take balanced diet.
6. Provide soft and bland diet.
7. Maintain intake/output chart.
PROMOTE COMFORT LEVEL:
1. Assess the pain level using pain scale.
2. Provide comfortable position.
3. Involve patient in his/her care plan.
4. Provide diversional therapy.
5. Encourage to do ROM as per tolerance.
6. Provide comfort measures such as pillow, cushion, heat therapy, etc.

PROMOTE SLEEP:
1. Assess the sleeping habits.
2. Provide conducive environment.
3. Maintain personal hygiene of patient.
4. Provide analgesics (prescribed) on regular schedule.
5. Encourage patient for book reading, meditation before going to bed.
POST-OPERATIVE
KEEP AIRWAY PATENT:
1. Assess the respiratory status, breathing sounds.
2. Provide fowler's position.
3. Do oral and endotracheal suctioning.
4. Check the pulse oxymetry.

IMPROVE BREATHING PATTERN:

1. Assess respiratory rate.
2. Provide fowler's position.
3. Encourage patient to do deep breathing exercise.
4. Provide steam inhalation, chest physiotherapy, incentive spirometery.
5. Provide plenty of fluids.
MAINTAIN FLUID AND ELECTROLYTE BALANCE:
1. Monitor vital signs.
2. Administer prescribed I/V fluids.
3. Strictly follow aseptic technique.
4. Set the fluid rate to prevent fluid overload.
5. Maintain intake/output chart.
PREVENT OCCURRENCE OF INFECTION:
1. Monitor vital signs.
2. Encourage for hand washing.
3. Follow aseptic technique.
4. Maintain personal hygiene.
5. Provide neat and clean environment.
6. Provide clean cotton clothes.
7. Provide plenty of fluids.
8. Administer prescribed antibiotics.
9. Monitor for complications.
PATIENT EDUCATION AND HEALTH MAINTENANCE EDUCATE PATIENT TO:
1. Maintain his/her oral hygiene.
2. Take balanced diet.
3. Perform ROM exercise as per his/her tolerance.
4. Take medicines exactly as ordered by physician.
5. Take plenty of fluids.
6. Contact health care provider, if symptoms get worse.
EVALUATION: EXPECTED OUTCOMES
PRE-OPERATIVE
1. Activity level is promoted.
2. Nutritional status is maintained.
3. Comfort level is promoted.
4. Sleep is promoted.
POST-OPERATIVE
1. Airway patent is improved.
2. Breathing pattern is improved.
3. Fluid and electrolyte balance is maintained.
4. Occurrence of infection is prevented.
 DIABETES MELLITUS
Diabetes mellitus is a chronic, progressive disorder which involves impaired glucose tolerance. It is a
group of metabolic disorders in which a person has high blood sugar either because:
1. Body does not produce enough insulin. placental
2. Cells do not respond to insulin, i.e., produced.
IT IS CHARACTERIZED BY CLASSICAL SYMPTOMS OF THE FOLLOWING:
1. Polyuria (frequent urination)
2. Polydipsia (increased thirst)
3. Polyphagia (increased hunger)
The incidence of diabetes mellitus increases with age because carbohydrate intolerances surface as
people age.
It is the 3rd leading cause of death in United States.
TYPES OF DIABETES MELLITUS
1. TYPE 1 [INSULIN DEPENDENT DIABETES MELLITUS (IDDM)]:
a. In this type of diabetes mellitus, insulin produces pancreatic beta cells that are destroyed by
to autoimmune process. It leads to absolute insulin deficiency.
b. It is characterized by the following:
i. Onset before 30 years of age.
ii. Rapid onset of hyperglycemia.
iii. Failure to respond to oral hypoglycemic agents.
c. This form of diabetes mellitus was previously referred to as "Insulin Dependent Diabetes
Mellitus" as "Juvenile Diabetes".
d. It is less common than type 2 diabetes mellitus.
2. TYPE 2 [NON-INSULIN DEPENDENT DIABETES MELLITUS (NIDDM)
a. It is characterized by the following:
i. Onset after age 30.
ii. Insidious onset
iii. Ability to produce some insulin.
iv. Minimal tendency towards ketosis.
v. Positive response to oral hypoglycemic agents.
 b. It can be prevented by the healthy lifestyle such as:
i. Healthy diet.
ii. Proper exercise.
iii. Maintaining healthy weight.
3. GESTATIONAL DIABETES MELLITUS (GDM): It occurs when pregnant women without a
previous diagnosis of diabetes develops a high blood glucose level. It may lead to type 2 diabetes
mellitus.
ETIOLOGY
1. Type 1 diabetes mellitus:
a. Beta cell destruction.
b. Relative or absolute lack of insulin.
c. Genetic predisposition to beta cell destruction.
d. Damage or removal of the pancreas.
e. Drugs and chemical toxins.
2. Type 2 diabetes mellitus:
a. Impaired insulin secretion.
b. Numbness and tingling due to neural tissue damage.
c. Heredity.
d. Obesity.
e. Lack of exercise which accentuates.
f. Insulin resistance.
g. High blood pressure
h. Pancreatic diseases.
i. Stress.
j. Sedentary lifestyle.
k. Unhealthy food.
3. Gestational diabetes mellitus: Some women tend to experience high level of blood glucose
during
pregnancy due to reduced sensitivity of insulin receptors.

RISK FACTORS
1. Type 1 diabetes mellitus:
a. Family history of the disease.
 b. Presence of certain genes indicates an increased risk of developing type 1 DM.
c. Type 1 usually develops in younger adults and children.
2. Type 2 diabetes mellitus:
a. Family history of the disease.
b. Being over 45 years of age.
c. Depression.
d. Having a baby that weights over 9 pounds at birth.
e. Polycystic ovary syndrome.
3. Gestational diabetes mellitus:
a. Obesity.
b. Lack of physical activity.
c. Polycystic ovary syndrome.
d. Previous gestational diabetes.
PATHOPHYSIOLOGY
Type 1 Diabetes Mellitus

Gestational Diabetes Mellitus

1. Gestational diabetes mellitus occurs when a woman previously not diagnosed with diabetes
mellitus
shows glucose intolerance during pregnancy.
2. Insulin resistance is caused by secretion of placental hormones. It leads to hyperglycemia.
3. After delivery, level of blood glucose returns to normal, in women with gestational diabetes
mellitus
and later on it develops type 2 diabetes mellitus.
CLINICAL MANIFESTATIONS
1. Onset is usually abrupt with type 1 diabetes mellitus and insidious with type 2 diabetes mellitus.
2. Chronic hyperglycemia often presents as disorders of altered tissue response evidenced by poor
wound healing and recurrent infections of the skin and genitourinary tract.
3. Polyuria (urinating frequently particularly at night).
4. Polydipsia (feeling very thirsty).
5. Weight loss and loss of muscle bulk.
6. Blurred vision.
7. Cuts or wounds that heal slowly.
8. Muscle cramps, irritability and emotional liability due to electrolyte imbalance.
9. Vision changes, such as blurring.
10. Numbness and tingling due to renal tissue damage.
11. Nausea, diarrhea or constipation due to dehydration and electrolyte imbalances or autonomic
neuropathy.
DIAGNOSTIC EVALUATION
1. History of risk factors for or clinical manifestations of diabetes mellitus, history of change in
alertness or vision.
2. Physical examination: Patient with more advanced diabetes mellitus may demonstrate any of the
following:
a. General findings: Obesity or lethargy.
b. Integumentary system: Evidence of poor healing, lipodystrophy or hypertrophy.
c. Neuromuscular system: Paresthesia of extremities
d. Cardiovascular system: Hypertension, bruits, cool extremities, orthostatic hypotension.
e. Gastrointestinal system: Hypoactive bowel sound, pain or rigidity.
3. Fasting Blood Glucose (FBG):
a. Drawn after at least 8 hour fast, to evaluate circulating amount of glucose.
b. It is diagnosed by measuring blood glucose levels.
c. Normally, it is less than 110 mg/dl. Patient is said to be diabetic, if the value is above 125
mg/dl. Critical value is 60 mg/dl to 500 mg/dl.
d. For this test, make sure that patient has maintained 8 hours fast overnight; sips of water are
allowed.
4. Random Blood Glucose (RBG):
a. Drawn at any time, without regard to the time of last caloric intake.
b. For this test, note the time and content of the last meal.
c. In this, elevated blood levels may occur after meals, after stressful event, etc.
d. Random blood sugar 200 mg/dl or higher or presence of classic symptom of diabetes.
e. It does not need to be repeated nor does the bus diagnosis need to be confirmed with
another test.
5. Fast Prandial Blood Glucose (FPBG):
a. Sample is taken 2 hours after standard meals, normally the blood glucose returns to fasting
levels within 2 hours.
b. Smoking and drinking coffee can increase the values.
c. Exercise can decrease values.
6. Glycated Hemoglobin (Glycohemoglobin, HbA1C, A1C):
a. It measures glycemic control over a period of 60 to 120 days by measuring the irreversible
reaction of glucose to hemoglobin through freely permeable erythrocytes during their 120 day
life cycle.
b. Currently, it is used to screen for diabetes as well as to monitor the control.
c. During this, no prior preparation such as fasting or withholding insulin or medications is
necessary.
d. Test results may be affected by the following:
i. Red blood cell disorders.
ii. Room temperature.
iii. Ionic charges.
iv. Ambient blood glucose values.
7. Glycosylated albumin:
a. Glucose is attached to the albumin.
b. Concentration of glycosylated albumin represents the average blood glucose level.
8. Oral Glucose Tolerance Test (OGTT):
a. It evaluates insulin response to glucose loading.
b. Fasting Blood Glucose (FBG) is obtained before the ingestion of a glucose load and blood
samples are drawn at timed intervals.
c. Patient needs a diet that offers 150 gms of CHO per day for three days. Then, fasting blood
glucose is taken.
d. Patient is given 75 gms of glucose to drink then therefore, the tolerance level of patient to
glucose is checked.
9. Ketonuria: In urine, presence of ketones indicates the body is using fat as a major source of
energy.
10. Proteinuria: In urine, presence of protein indicates that protein is being used as major source of
energy.
11. Fructosamine assay:
a. It may be advantageous in patients with hemoglobin variants which interfere with the
accuracy of glycated hemoglobin tests.
b. It should not be used as diagnostic test for diabetes mellitus.
c. For this, no special preparation or fasting is necessary.
12. C-Peptide Assay (Connecting Peptide Assay):
a. It acts as a maker for endogenous insulin production.
b. It can be performed after an overnight fast or after stimulation with the following:
 i. Sustacal.
ii. Intravenous (IV) glucose.
iii. 1 mg of glucagon subcutaneously.
MANAGEMENT
MEDICAL MANAGEMENT
GOALS OF MEDICAL MANAGEMENT
1. Control glycemia.
2. Prevent or minimize complications.
3. Educate patients on their lifelong responsibilities TAB regarding diabetic care.
NON-PHARMACOLOGIC INTERVENTIONS
1. DIET:
a. The goal of meal planning is to meet nutritional requirements essential for healthy growth
or development, control blood glucose and lipid levels diabetic diet.
b. Weight reduction is a primary treatment for type 2 diabetes mellitus.
2. EXERCISE:
a. It is important because it decreases cholesterol and triglyceride levels, lowers blood
pressure.
b. It helps the body to burn excess sugar.
c. Regularly scheduled; moderate exercise performed 30 to 60 minutes at least every other
day promotes the utilization of carbohydrates.
PHARMACOLOGIC INTERVENTIONS:
1. ORAL HYPOGLYCEMIC AGENTS: These drugs are not insulin; rather they stimulate the
pancreas to produce insulin. There are two major classes of such agents:
a. SULFONYLUREAS: Most commonly used agent. Duration of action is the most
significant difference.
SIDE EFFECTS: Easy bruising, unexplained bleeding, lethargy, mouth ulcers, etc.
b. BIGUANIDES: Derivation, metformin, decreased blood glucose in patients with type 2
diabetes by increasing the body's use of glucose. It may be used alone or in combination with
sulfonylureas to control hyperglycemia.
SIDE EFFECTS: Abdominal discomfort, anorexia, etc.
2. INSULIN THERAPY:
a. The key to successful insulin therapy is the rate of absorption from site of injection.
Intramuscular injections are absorbed faster than subcutaneous injections especially in thin
patients when subcutaneous injection is attempted by intramuscular injection is achieved.
b. Insulin works to decrease blood glucose by promoting the transport of glucose into cell and
inhibits the conversion of glycogen and amino acids to glucose.
 c. It is commonly prescribed three times and in insulin combination to achieve more
consistent glycemic control without major blood sugar fluctuations. Most often, short acting
insulin and intermediate acting insulin are combined
d. Self-injection of insulin.
3. ALPHA-GLUCOSIDASE inhibitors into simple sugar such as glucose and fructose, thereby
lowering post prandial and fasting glucose levels.
a. Contraindicated in inflammatory bowel disease and other conditions of the intestinal tract.
b. Abdominal pain, diarrhea and flatulence are common.
4. THIAZOLIDINEDIONE (TZD) DERIVATIVES:
a. Primarily, it decreases resistance to insulin in skeletal muscle and adipose tissue without
increasing insulin secretion.
b. Secondarily, it reduces hepatic glucose production.
c. It should be used cautiously in liver disease and heart failure.
d. Adverse reactions:
i. Edema
ii. Weight gain
iii. Anemia
iv. Increased incidence of bone fracture.
v. Elevation in serum transaminases.
5. BILE ACID SEQUESTRANT (COLESEVELAM):
a. Traditionally, it is a cholesterol lowering agent.
b. It is indicated for the Type-II DM treatment.
c. It may also work by reducing intestinal absorption of glucose.
d. Side effects:
i. Nausea
ii. Bloating
iii. Constipation
6. DOPAMINE AGONIST (BROMOCRIPTINE):
a. It acts to reduce levels by reducing the effects of insulin resistance on the central nervous
system.
b. Side effects:
7. GLP-1
i. Hypotension
ii. Syncope
7. GLP-1 INCRETIN MIMETICS (EXENATIDE AND LIRAGLUTIDE):
a. It lowers blood glucose by enhancing first-phase insulin secretion by the pancreas, slowing
gastric emptying and reducing appetite.
b. Liraglutide is injected once daily without regard to meals.
c. EXENATIDE: Injected twice daily within 1 to 60 minutes before breakfast and dinner.
d. They both are available in a disposable pen device.
SURGICAL MANAGEMENT
1. Pancreas transplantation.
2. Pancreas and kidney transplantation.
INDICATIONS
Patient having type-I diabetes mellitus receives pancreas transplants and anti-rejection medication
(cyclosporine is given to the patient). The patient's own pancreas is left intact and the new pancreas
is attached.
CONTRAINDICATIONS
1. Patient is having type-II D.M.
2. Patient is having type-I D.M. but having not properly functioning kidneys.
3. Patient is having well-functioning kidneys with type-I D.M. receives only pancreas
transplant but those having malfunctioning kidneys undergo kidney transplant first, then
pancreas transplant.
NURSING MANAGEMENT
1. Teach patient and family members about the cause, sign and symptoms and treatment of diabetes
mellitus.
2. Obtain a history of current problems, family history and general health history.
3. Perform a review of systems and physical examination to assess for signs and symptoms of
diabetes, general health of patient and presence of complications.
4. Assess intake and output chart which helps to identify hydration status.
5. Monitor patient's vital signs.
6. Assess blood sugar at insulin peaks as ordered or when the patient is symptomatic of
hypoglycemic.
7. Teaching about insulin:
a. Assist patient to reduce fear for injection by encouraging verbalization of fears regarding
insulin injection, conveying a sense of empathy and identifying supportive coping techniques.
b. Allow patient to handle insulin and syringe to become familiar with the equipment.
c. Teach self-injection to alleviate fear of pain from injection.
d. Educate patient about complications of insulin therapy.
 e. Administer IV insulin as ordered or monitor by finger stick blood sugar test every 30 to 60
minutes.
8. Improving activity tolerance:
a. Advice patient to assess blood glucose level before and after strenuous exercise.
b. Instruct patient to plan exercises on a regular basis each day.
c. Instruct patient to avoid exercise whenever blood glucose levels exceed 250 mg/day and
urine ketones are present.
9. Encourage patient to take fluids orally.
10. Administer medication as per doctor’s order which helps to maintain glucose level in the body.
11. Administer carbohydrate and protein rich diet. It helps to promote healing.
12. Refer patient to a dietitian, if dietary non-compliance contributed to hyperglycemia.
13. Provide knowledge regarding feet and nail care.
14. Maintain aseptic technique in invasive procedures such as infusion, catheter foley, etc.
15. Provide emotional and psychological support to patient and family members.
COMPLICATIONS
1. Neuropathy (nerve damage)
2. Retinopathy (eye damage)
3. Nephropathy (kidney damage)
4. Alzheimer's disease
5. Foot damage-diabetic foot
6. Diabetic dermatopathy
7. Infections
NURSING CARE PLAN
NURSING ASSESSMENT
1. Assessment of history of symptoms related to the diabetes.
2. Assess the patient's lifestyle, cultural, psychosocial, and economic factors, and effects of diabetes
on functional status should be performed.
3. Assess physical condition.
4. Assess the patient's blood pressure while sitting and standing to detect orthostatic changes.
5. Assess the body mass index and visual acuity of the patient.
NURSING DIAGNOSIS
1. Risk for unstable blood glucose related to stress, sedentary lifestyle or lack of adherence to
diabetes management.
2. Imbalanced nutrition: Less than body requirement related to increased metabolism rate and
increased appetite.
3. Fatigue related to decreased metabolic energy production.
4. Risk of impaired skin integrity related to decreased circulation and sensation caused by peripheral
neuropathy.
5. Risk for deficient fluid volume related to osmotic diuresis.
6. Deficient knowledge related to unfamiliarity with information.
PLANNING
NURSING GOALS
1. To normalize blood glucose level.
2. To maintain nutritional balance.
3. To maintain skin integrity.
5. To improve ability to participate in desired activities.
6. To enhance knowledge.
NURSING INTERVENTIONS
1. Assess blood glucose level before meals and at bedtime to get the baseline data regarding glucose
level.
2. Assess for signs of hyperglycemia.
3. Monitor for the signs of infection, i.e. redness, swelling or pain.
4. Check intake and output hourly.
5. Observe and document color and consistency of urine, stool and vomitus.
6. Monitor foot skin for blanching, erythema, warmth and size of lesion for early detection of
complications.
7. Perform active or passive ROM exercises and change the position at least every 2 hourly.
8. Encourage the patient to wear white cotton socks to prevent infection from moisture.
9. Administer or assist with oral hygiene after each meal and before bedtime.
10. Provide intravenous fluids to the patient to increase the hydration.
11. Provide frequent rest period.
12. Teach patient how to perform home glucose monitoring.
13. Instruct patient to avoid heating pads and always to wear shoes when walking.
14. Instruct the patient on the proper preparation, administration and storage of insulin.
15. Provide high protein, low carbohydrate and high sodium diet.
16. Provide a late morning snack, if needed in case the patient becomes hypoglycemic.
17. Provide well balanced diet to the patient.
18. Promote rest at night by warm bath or back massage at night.
19. Plan regular exercise for patient.
20. Provide diversional therapy and stress reduction technique, mental and physical stress greatly
contribute to sense of fatigue.
21. Teach patient to treat hypoglycemia, such as a carbohydrate snack.
22. Demonstrate the technique and timing of home monitoring of glucose and identify the need to
adjust the insulin doses.
23. Cut toe nails straight across after softening toe nails to prevent infection.
24. The patient should not walk barefoot to prevent ulceration and infection
25. Encourage the patient to drink and variation in fluid is helpful to increase intake.
PATIENT EDUCATION AND HEALTH MAINTENANCE
1. Ongoing education of patient includes advance, skills and rationales for treatment, prevention and
management of complications.
2. Encourage patient to eat full meals and take snacks as prescribed per diabetic habits, etc.
3. Administer medication or insulin as per doctor's order which helps to maintain glucose level in the
body.
4. Instruct patient to get plenty of rest and sleep.
5. Advice patient to take carbohydrate and protein rich diet. It promotes healing.
6. Instruct patient to drink plenty of fluids. 6 to 8 of fluid every hour is recommended, every third
hour the fluid should include sodium, i.e. broth.
7. Instruct patient to maintain skin integrity by protecting feet from breakdown.
a. Avoid applying drying agents to skin.
b. Apply skin moisturizers to prevent cracking and fissures.
8. Advice the patient to stop smoking or reduce, if possible, to reduce vasoconstriction and enhance
peripheral blood flow.
EVALUATION: EXPECTED OUTCOMES
1. Normal blood glucose level.
2. Nutritional balance is maintained.
3. Skin integrity is maintained.
4. Fluid level is maintained.
5. Ability to participate in desired activities is improved.
6. Knowledge is enhanced.
HYPOGLYCEMIA
When the blood glucose level falls less than 50-60 mg/dl, condition is termed as hypoglycemia.
EITOLOGY
1. To much insulin or oral hypoglycemic agents.
2. Too little food consumption.
3. Excessive physical activity or exercise.
4. Gastrointestinal tract disturbances.
RISK FACTORS
1. Older age.
2. Renal impairment.
3. Long duration of diabetes treatment.
4. Alcohol.
5. Recent moderate or intensive exercise.
6. Weight loss. pulse.
7. Skipping meals.
8. Antidepressants.
PATHOPHYSIOLOGY
1. Hypoglycemia causes the brain to receive an inadequate supply of blood glucose to function.
2. In patients with diabetes mellitus, the lack of glucose and epinephrine response to low blood sugar
levels aggravates the condition.
3. Reactive hypoglycemia: In reactive hypoglycemia, blood glucose falls 2-5 hours after eating.
4. Low levels will trigger the release of adrenaline to restore the blood sugar levels.
5. The release of adrenaline produces the symptoms of sweating, trembling and rapid heart rate.
CLINICAL MANIFESTATIONS
IN MILD HYPOGLYCEMIA
As the blood glucose level falls, the nervous system is stimulated. It causes:
1. Sweating, tachycardia
2. Palpitations
3. Nervousness
4. Air hunger
IN MODERATE HYPOGLYCEMIA
The decreased level of blood glucose deprives the brain cells of needed fuel for functioning. Signs of
impaired function of CNS includes:
1. Nervousness.
2. Inability to concentrate.
3. Headache.
4. Memory lapses.
5. Numbness of lips and tongue.
6. Emotional changes.
7. Irritational behavior.
8. Double vision
9. Drowsiness.
IN SEVERE HYPOGLYCEMIA
The nervous system is impaired to an extent that the patient needs the assistance of another person
for its treatment.
Symptoms include:
1. Disoriented behavior.
2. Seizures.
3. Difficulty in arousing from sleep.
4. Loss of consciousness.
DIAGNOSTIC EVALUATION.
1. Blood glucose level is monitored to check the range.
2. Autonomic neuropathy assessment is done.
3. Vision checkups or visual examination is done for the patient.
MANAGEMENT
MEDICAL MANAGEMENT
1. For immediate treatment, patient must be given 10-15gms of fast acting simple glucose. It is
important for diabetic patient especially those receiving insulin to carry some form of simple sugar
all the times.
2. Patients are encouraged to avoid high calorie, high fat, dessert foods, e.g. cookies, cakes, ice-
creams, etc.
3. For patient who are unconscious and can't swallow sugar, an injection of glucagon 1 mg can be
administered S/C or I/M. It stimulates the liver to release glucose.
4. 50% dextrose solution is administered I/V, 25-50 ml only. the patient
NURSING MANAGEMENT
1. Patient teaching is must to prevent hypoglycemia by 10 consistent pattern of eating, administration
of insulin and exercising.
2. Between meals and bed time, snacks may be needed to counter the maximum insulin effect.
3. Routine blood glucose examination should be performed so as to adjust the changing insulin
requirement and to adjust dose.
4. Family members should be taught about symptoms of hypoglycemia such as change in behavior,
anger, and irrational behavior.
COMPLICATIONS
If hypoglycemia left untreated, it can lead to any of the following:
1. Seizures
2. Unconsciousness
3. Death
HYPERGLYCEMIA OR DIABETIC KETOACIDOSIS
Diabetic Ketoacidosis (DKA) is a life-threatening complication of diabetes mellitus. DKA is
caused by an absence or markedly inadequate amount of insulin. This results in disorders in the
metabolism of carbohydrate, protein and fat. It is an emergency condition needs to be treated
immediately.
ETIOLOGY
1. Hyperglycemia, due to decreased use of glucose by the cells and increased production of glucose
by the liver. It promotes healing.
2. Dehydration and electrolyte loss, resulting from polyuria, with a loss upto 65 L of water and upto
400 to 500 mEq each of sodium potassium and chloride over 24 hours.
3. Acidosis, due to excess breakdown of fat to fatty acids and production of ketone bodies, which are
also acids.
THREE MAIN CAUSES OF DKA ARE:
1. Decreased or missed dose of insulin.
2. Illness or infection
3. Initial manifestation of undiagnosed or untreated diabetes.
RISK FACTORS
1. Type 1 diabetes that has not been diagnosed.
2. Stomach illness with a lot of vomiting.
3. Heart disease, such as heart attack.
4. Pregnancy.
5. Medications, such as steroids and antipsychotic drugs.
6. Recreational drug use, such as cocaine.
7. Blood clots to the lungs.
CLINICAL MANIFESTATIONS
1. Polyuria and polydipsia (increase thirst).
2. Blurred vision, weakness and headache.
3. Orthostatic hypotension in patient with volume depletion.
4. Weak rapid pulse.
5. Decreased blood pressure.
6. Gastrointestinal symptoms such as anorexia, nausea/vomiting and abdominal pain (may be
severe).
7. Acetone breath (fruity odor).
8. Kussmaul's breathing (air hunger)-hyperventilation with very deep but labored respiration.
9. Mental status varies widely from patient to patient (alert/lethargic/comatose).
DIAGNOSTIC EVALUATION
CRITERIA FOR DKA INCLUDE:
1. Blood glucose level > 300 mg/dl. no slug
2. Low blood pH < 7.30.
3. Hyponatremia.
4. Hypokalemia or hyperkalemia.
5. Elevated creatinine, blood urea.
6. Nitrogen and hematocrit values may be seen with dehydration.
7. After rehydration, continued elevation in serum creatinine and BUN level suggest underlying renal
insufficiency.
8. Urinalysis: Presence of glucose and acetone.
MANAGEMENT
MEDICAL MANAGEMENT
The aim of medical management is:
1. To restore normal hemodynamic status.
2. To treat dehydration.
3. To maintain electrolyte balance. and
4. To treat acidosis.
FLUID THERAPY
1. 0.9% saline IV given in a dose of 0.5 to 1 L/h in first hour after diagnosis. Saline should be
continued till signs of severe dehydration disappear.
2. Infusion of maintenance fluid should be continued over 24 to 36 hours.
3. Blood glucose level should be monitored hourly and when blood glucose level falls to 300 mg/dl
or less, 5% dextrose should be added to prevent a precipitous decline in the blood glucose level.
RESTORING ELECTROLYTE
The major electrolyte of concern during treatment of DKA is potassium. A major potassium shift
takes place from extracellular to intracellular component during treatment due to insulin effect,
hydration and correction of acidosis. Thus, potassium replacement is important to be done. Before
starting potassium replacement, ensure adequacy of urine output.
REVERSING ACIDOSIS
Acidosis of DKA is reversed with insulin which inhibits the breakdown of fat is regularly is infused
at a slow continuous rate (5 U/hr).
NURSING MANAGEMENT
1. Monitor patient's vital signs and level of consciousness.
2. Monitor fluid balance: Prescribed fluids should be administered and monitor patient for the signs
of complications related to fluid overload, dehydration and electrolyte imbalance.
3. Insulin therapy should be administered as prescribed.
4. Regular monitoring of capillary blood glucose and ketones.
5. Monitor metabolic acidosis and electrolytes.
6. Provide psychological support to patient and family.
This includes keeping the patient and family fully informed about the patient's clinical condition and
the care given.
COMPLICATIONS
1. Fluid overload
2. Pulmonary edema
3.Heart failure
4. Hypokalemia
5. Hyperglycemia
6. Ketoacidosis
7. Cerebral edema
8. Hypoglycemia
PREVENTION OF HYPERGLYCEMIA
Drinking fluids every hour is important to prevent dehydration.
Blood glucose and urine ketones must be assessed every 3-4 hours.
Frequent but small portions of carbohydrates should be given.
Diabetes self-management including insulin administration blood glucose testing should be taught to
the patient.
DIABETIC NEPHROPATHY
Nephropathy or renal disease is a secondary complication which occurs due to change in the kidney
after diabetic micro vascular changes.
ETIOLOGY
1. High cholesterol and triglyceride level.
2. High blood pressure.
3. Smoking.
RISK FACTORS
1. High blood cholesterol.
2. Smoking.
3. Family history of diabetes and kidney disease.
4. Hyperglycemia which is not well controlled.
5. Hypertension which is not controlled.
CLINICAL MANIFESTATIONS
1. Renal failure
2. Hypoglycemia episodes
3. Foot ulcerations
4. Congestive heart failure
5. Nocturnal diarrhea
DIAGNOSTIC EVALUATION
1. Urine examination for the presence of albumin, blood urea nitrogen (BUN), etc.
2. Small amount of protein leakage from kidney in urine may occur.
3. Hypertension may also develop.
MANAGEMENT
MEDICAL MANAGEMENT
Maintain the normal blood glucose levels carefully.
Manage the following things:
1. Hypertension
2. UTI
3. Nephrotoxin substances
NURSING MANAGEMENT
1. Monitor patient's vital signs.
2. Check laboratory tests for BUN.
3. Ensure patient eats a low protein diet.
4. Teach patient how to monitor blood glucose at home.
5. Encourage patient for exercise.
6. Urge the patient not to smoke or use drugs that affect the kidneys.
7. Teach patient about options for dialysis.
8. Instruct patient to contact health care provider, if following occurs:
a. Fever
b. Dyspnea
c. High blood pressure
COMPLICATIONS
1. Anemia
2. Hyperkalemia (rise in potassium levels in the blood)
3. Diabetic retinopathy
4. End-stage kidney disease.
Prevention to avoid kidney damage from diabetic nephropathy Low potassium food and limit
the amount of protein.
Quitting smoking
Maintaining a healthy weight.
Keeping blood sugar levels within the target range.
Keeping blood pressure under control with medicine, diet and exercise
DIABETIC FOOT
Three diabetic complications contribute to the risk of foot infection:
1. NEUROPATHY: It leads to loss of pain and pressure sensation causing dryness and fissuring of
the skin.
2. PERIPHERAL VASCULAR DISEASE (Micro-vascular changes) poor circulation of lower
extremities causes poor wound healing and development of gangrene.
3. IMMUNOCOMPROMISE: Hyperglycemia impairs the ability of WBCs to destroy bacteria, so
there is lowered resistance to certain infections.
a. This sequence of events leads to the development of diabetic foot ulcers which begins with
soft tissue injury of the foot.
b. Formation of a fissure between toes or in any dry skin area.
c. Formation of callus (tough area):
i. Injuries are not felt by the patient. It may be thermal, chemical or traumatic. Thorough
inspection of patient on daily basis is very important.
ii. Drainage, swelling, redness of leg or gangrene is the first sign of foot problem.
ETIOLOGY
1. Poor circulation
2. High blood sugar
3. Nerve damage
4. Irritated or wounded feet
RISK FACTORS
1. Diabetes for > 10 years
2. Anatomic foot deformity
3. Previous history of foot ulcer
4. Tobacco use
5. Peripheral neuropathy
CLINICAL MANIFESTATIONS
1. Ulcers or blisters
2. Redness on feet
3. Warm or swollen feet
4. Itching
5. Dryness
6. Sore feet
MANAGEMENT
1. Bed rest
2. Antibiotics
3. Wound debridement
4. Controlling glucose levels may promote wound healing.
5. In patient with peripheral vascular disease, foot ulcers may not heal because of decreased ability of
O2, nutrients and antibiotics to reach the injured tissue.
6. Amputation may be necessary to prevent spread of infection.
NURSING MANAGEMENT
FOOT CARE TIPS
To take care of feet of diabetic patient:
1. Patients should be taught to keep their blood glucose level within a normal range.
2. Ask the patients to look at their feet every day for cuts, blisters, red spots and swelling.
3. Use the mirror to check the bottom of feet or ask a family member for help, if patient has trouble
in seeing.
4. Wash feet every day in warm, not hot water.
5. Do not soak feet.
6. Dry feet well. Be sure to dry between the toes.
7. Keep the skin soft and smooth by keeping a thin coat of skin lotion over the top and bottom of
feet, but not between toes.
8. Smooth corns and calluses gently using a pumice stone to smooth corns and calluses.
9. Trim toe nails straight across and file the edges with every board and nail file.
10. Never walk bare footed.
11. Wear comfortable shoes that fit well and protect feet.
12. Protect feet from hot and cold by wearing shoes and socks.
13. Keep the blood flowing to feet by keeping them up while sitting.
14. Wiggle toes and move ankles up and down for 5 minutes, 2 or 3 times a day.
15. Do not cross legs for long periods of time.
16. Contact doctor if a cut, sore, blister on the foot does not begin to heal after one day.
17. Follow doctor's advice about foot care.
COMPLICATIONS
1. Abscess
2. Skin and bone infections
3. Gangrene
4. Deformities
5. Amputation

DISORDERS OF ADRENAL GLAND

CUSHING'S SYNDROME (HYPERCORTISOLISM)
Cushing's syndrome is a cluster of clinical abnormalities caused by excessive adrenocortical
hormones or related corticosteroids and the lesser extent, androgens and aldosterone. Cushing's
disease is a specific type of Cushing's syndrome that results from excessive pituitary ACTH secretion
from a pituitary tumor.
CLASSIFICATION
ACTH-DEPENDENT
1. Pituitary-dependent bilateral adrenal hyperplasia, i.e., Cushing’s disease.
2. Ectopic ACTH syndrome, e.g., bronchial carcinoid, small cell lung carcinoma and pancreatic
carcinoma.
3. Iatrogenic (ACTH therapy).
NON-ACTH-DEPENDENT
1. Iatrogenic (chronic glucocorticoid therapy, e.g., for asthma).
2. Adrenal adenoma.
3. Adrenal carcinoma.
Pseudo-Cushing's Syndrome, i.e. Cortisol Excess as Part of Another Illness
1. Alcohol excess (biochemical and clinical features).
2. Major depressive illness.
3. Primary obesity (mild biochemical features, some clinical overlap.
ETIOLOGY
1. Excessive secretion of ACTH/cortisol.
2. Familial Cushing's syndrome.
3. Autonomous, ectopic ACTH secretion by a tumor outside the pituitary.
4. Excessive intake of corticosteroid medications, e.g. prednisone, prednisolone.
RISK FACTORS
1. Adrenal tumors.
2. Administration of exogenous steroids.
3. Pituitary tumors especially in Cushing's disease.
PATHOPHYSIOLOGY
1. The excess cortisol results in anti-inflammatory effects and excessive catabolism of protein and
peripheral fat to support hepatic glucose production.
2. The mechanism may be ACTH dependent.
a. Elevated plasma ACTH levels stimulate the adrenal cortex to produce excess cortisol.
b. ACTH independent in which excess cortisol is produced by the adrenal cortex.
3. It suppresses the hypothalamic pituitary adrenal axis and also present in ectopic ACTH secreting
tumors.
CLINICAL MANIFESTATIONS
1. Diabetes mellitus with decreased glucose tolerance fasting hyperglycemia and glycosuria due to
cortisol induced insulin resistance and increased glycogenolysis and glycogenesis in liver.
2. Peptic ulcer due to increased gastric secretions and pepsin production and decreased gastric
mucus.
3. Ecchymosis (bruises) and striae (lines) develop Thin, fragile skin acne.
4. Multiple weaknesses: Proximal myopathy, secondary to hypokalemia and protein tissue wasting.
5. Poor wound healing.
6. Osteoporosis due to matrix wasting can cause pathologic fractures.
7. Muscle weakness.
8. Hypertension:
 • Edema of lower extremities.
9. Pancreatitis
10. Decreased libido, amenorrhea, oligomenorrhea, virilism in women and impotence or
feminization in men.
11. Truncal obesity, thin extremities obesity.
12. Round moon face and fat deposits on the back of neck and on shoulders
13. Others:
a. Glycosuria, kidney stone
b. Hypokalemia
c. Hypoglycemia
d. Dyslipidemia
e. Irritability
f. Hypomania, depression
DIAGNOSTIC EVALUATION
1. History: Recent onset of weakness, increase in weight or abdominal girth, roundness of face or
acne, impaired wound healing, more frequent infections, depression, mania or psychosis,
osteoporosis, polydipsia and polyuria and impotence and decreased libido.
2. Physical examination: Check for signs of clinical manifestations.
3. MRI view of pituitary to localize the tumor.
4. CT scan of pituitary gland and adrenal gland to localize the tumor.
5. Urinary free cortisol levels more than 150 μg/24 hours,
6. Blood levels of corticotrophin-releasing hormone, ACTH and different glucocorticoids to diagnose
and localize cause to pituitary or adrenal gland.
MANAGEMENT
MEDICAL MANAGEMENT
GOALS OF MEDICAL MANAGEMENT
1. Eradicate the tumor.
2. Avoid permanent hormone deficiency.
3. Correct electrolyte balance.
NON-PHARMACOLOGIC INTERVENTIONS
1. Diet with decreased calories and carbohydrates low amount of sodium and high amount of
potassium.
2. As a palliative measure to treat the tumor or residual tumor, radiation may be applied externally or
internally to pituitary gland.
PHARMACOLOGIC INTERVENTIONS
Drugs such as mitotane (lysodren) or aminoglutethimide (cytadren), to block steroid synthesis for
inoperable tumor.

SURGICAL MANAGEMENT
Adrenalectomy and lifelong hydrocortisone replacement are indicated for all adrenal forms of
cushing's syndrome.
NURSING MANAGEMENT
1. Assess patient and laboratory studies for hypokalemia, hypernatremia and hypercortisolism that
may contribute to weakness.
2. Assess patient for improved ambulation and increased tolerance for activity.
3. Monitor vital signs.
4. Assess patient for actual and potential infection sites.
5. Change patient's position every 2 hours.
6. Provide ambulatory assistance as needed.
7. Use sterile technique when caring for areas of impaired skin integrity.
8. Provide an atmosphere, i.e. calm, safe and supportive.
9. Prevent emotionally upsetting scenarios.
10. Encourage patient for mental catharsis.
11. Encourage patient to do range of motion exercises.
12. Plan care with patient and anticipate needs.
13. Reassure the patient.
14. Encourage patient to discuss his/her feelings.
15. Provide antibiotic therapy as ordered.
COMPLICATION
1. Congestive heart failure.
2. Hypertension.
3. Pathologic fractures.
4. Masking of infections.
NURSING CARE PLAN
NURSING ASSESSMENT
Do thorough history taking and physical examination:
1. Monitor vital signs, blood glucose.
2. Monitor intake and output chart.
3. Monitor abdominal girth, BMI.
4. Observe patient for typical symptoms of cushing's Syndrome such as moon like face, buffalo
hump in neck, central obesity, etc.
5. Enquire about dietary habits.
6. Enquire about rise of ACTH drugs.
7. Assess the sleeping pattern.
8. Observe changes in mood, mental activity.
NURSING DIAGNOSIS
1. Fluid volume excess related to sodium and H₂O retention.
2. Altered nutritional pattern related to disease condition.
3. Disturbed body image related to central obesity, moon face and buffalo hump.
4. Discomfort related to backache.
5. Anxiety related to disturbed body, treatment.
6. Altered sleeping pattern related to disease condition.
7. Risk of infection related to disease.
PLANNING
NURSING GOALS
1. To maintain fluid and electrolyte balance.
2. To maintain nutritional needs.
3. To improve self-body image and self-esteem.
4. To promote comfort.
5. To relieve anxiety.
6. To improve sleeping pattern.
7. To improve health/prevent infection occurrence.
NURSING INTERVENTIONS
MAINTAIN FLUID AND ELECTROLYTE BALANCE
1. Monitor vital signs.
2. Record body weight.
3. Check intake/output chart.
4. Administer prescribed medicines.
MEET NUTRITIONAL NEEDS
1. Assess nutritional status.
2. Ask about patient's likings and disliking’s about food.
3. Provide small and frequent diet.
4. Serve meal in attractive way.
5. Serve high fibre, high-potassium and calcium rich diet.
6. Maintain intake/output chart.
IMPROVE SELF BODY IMAGE AND SELF ESTEEM
1. Ask patient about his/her perception about himself/herself and disease.
2. Enquire about his/her coping strategies.
3. Encourage to ventilate his/her feelings.
4. Reassure the patient.
5. Educate him/her about disease condition.
6. Teach the family members about patient's symptoms.
7. Use gentle approach.
8. Make patient optimist.
PROMOTE COMFORT
1. Assess level of discomfort.
2. Enquire about coping strategies.
3. Provide comfortable position.
4. Involve patient in daily activities.
5. Provide analgesics before doing activities.
6. Provide comfort devices such as pillow, cushion.
7. Encourage to do range of motion exercises.
RELIEVE ANXIETY
1. Assess anxiety level of patient.
2. Encourage for mental catharsis.
3. Listen actively to patient.
4. Clarify his/her doubts, concerns about disease process.
5. Use optimistic approach.
6. Try to meet patient with self help group.
7. Involve family members in care of patient.
IMPROVE SLEEP
1. Assess sleeping pattern of patient.
2. Provide conducive environment to sleep.
3. Avoid nap during day time.
4. Involve patient in daily activities during day time,
5. Maintain hygiene of patient.
6. Advice to take shower before falling sleep.
7. Read book, do prayer/meditation before going to bed.
IMPROVE HEALTH/PREVENT INFECTION OCCURRENCE
1.Monitor vital signs.
2. Maintain personal hygiene of patient.
3. Provide neat and clean, ventilated room.
4. Provide clean cotton clothes and change it daily.
5. Follow aseptic technique during invasive procedures.
6. Follow hand washing before and after medication.
7. Take well balanced diet.
8. Follow exercise schedules
PATIENT EDUCATION AND HEALTH MAINTENANCE
1.Encourage patient to manage his/her blood sugar levels.
2. Advice patient to eat heart healthy food that help to protect the heart, including plenty of fruits and
vegetables, nuts and sources of fibres
3. Encourage patient to weight himself/herself at the same time every morning after he/she urinate,
but before he/she eat.
4. Advice patient to do deep breathing exercise.
5. Instruct patient to maintain personal hygiene.
6. Advice patient to take shower before falling sleep.
7. Instruct patient to follow hand washing before and after medication.
8. Instruct patient and family members to contact health care provider, if any of these occur:
a. Increase in weight.
b. Pain is worse.
c. Symptoms get worse.
d. Blurred or double vision.
e. Severe headache.
EVALUATION: EXPECTED OUTCOMES
1. Fluid and electrolyte balance is maintained.
2. Nutritional needs are maintained.
3. Self-body image and self-esteem is improved.
4. Comfort is promoted.
5. Anxiety is relieved.
6. Sleeping pattern is improved.
7. Health/prevented infection occurrence.
ADDISON'S DISEASE
Addison's disease is a syndrome resulting from insufficient secretion of cortisol by the adrenal glands
due to destruction or dysfunction.
TYPES OF ADDISON'S DISEASE
1. PRIMARY ADDISON'S DISEASE: It is a hypofunction of the adrenal gland that originates in
the adrenal gland.
2. SECONDARY ADDISON'S DISEASE: It is a hypofunction of the pituitary hypothalamic unit.
Etiology
1. PRIMARY ADDISON'S DISEASE:
a. Tuberculosis accounts for approximately 20% of cases.
b. Autoimmune induced insufficiency may be idiopathic.
c. Bilateral adrenalectomy.
d. Neoplasm's.
e. Family history of autoimmune disease.
2. SECONDARY ADDISON'S DISEASE:
a. Bilateral adrenalectomy.
b. Hemorrhagic infarction and necrosis of adrenal glands.
c. Pituitary tumors.
d. Pituitary infarction.
e. Irradiation of pituitary.
RISK FACTORS
1. Infectious processes, e.g., Tuberculosis and histoplasmosis.
2. acquired immunodeficiency syndrome.
3. Large doses of corticosteroids, which suppress the hypothalamic pituitary adrenal axis and cause
atrophy of adrenal glands.
4. History of other endocrine disorders.
5. Adrenalectomy.
CLINICAL MANIFESTATIONS
1. Anorexia.
2. Nausea and vomiting.
3. Hypotension (postural).
4. Hyponatremia.
5. Acidosis.
6. Hyperpigmentation.
7. Slow, sluggish movements.
8. Addisonian crisis: A life threatening response to acute adrenal insufficiency.
a. Sudden high fever.
b. Weakness
c. Severe penetrating pain in abdomen, lower back and legs.
d. Severe vomiting and diarrhea
e. Hypotension
f. Circulatory collapse
g. Shock
h. Coma
DIAGNOSTIC EVALUATION
1. Radiographs, CT scan, MRI view of adrenal glands and pituitary gland to identify location and
size of glands and thus identify tuberculous changes.
2. Decreased plasma cortisol level and also decreased urinary 17-ketosteroids.
3. Decreased serum sodium and fasting blood glucose level and increased potassium level. 22982A I
4. Decreased hematocrit, increased lymphocyte and eosinophil counts
5. Increased Blood Urea Nitrogen (BUN).
MANAGEMENT
MEDICAL MANAGEMENT
1. The main aim of medical management includes:
a. Prevent morbidity and mortality associated with addisonian crisis.
b. Correct electrolyte imbalance
c. Correct hypotension
2. Pharmacologic interventions are listed
NURSING MANAGEMENT
1. Assess patient for sources and signs of infection and other stressors.
2. Assess laboratory values related to stressor.
3. Assess skin turgor and mucous membrane.
4. Evaluate patient for signs and symptoms of hypercalcemia and hyponatremia.
5. Encourage frequent hand washing to decrease bacterial and viral infections.
6. Evaluate serum cortisol level.
7. Administer IV fluids and vasopressors as ordered.
8. Reassure the patient.
9. Correct hyponatremia with intravenous fluids.
10. Encourage patient for oral fluids as tolerated.
11. Instruct patient to ingest salt additives in condition of excess heat or humidity.
12. Provide high protein, low carbohydrate and high sodium diet.
13. Encourage for small frequent meals to maintain adequate blood glucose level.
14. Encourage rest periods after eating to facilitate digestion.
15. Demonstrate the procedure of self-administration of medication.
COMPLICATIONS
1. Diabetes
2. Hashimoto's thyroiditis
3. Pernicious anemia
4. Thyrotoxicosis
5. Ovarian hypofunction or testicular failure.
NURSING CARE PLAN
NURSING ASSESSMENT
Complete history taking and physical examination.
1. Monitor vital signs.
2. Monitor daily intake and output chart.
3. Assess the sleeping pattern.
4. Monitor weight of the patient.
5. Observe patient for typical symptoms of Addison's disease.
NURSING DIAGNOSIS
1. Risk for fluid volume deficit related to increase in sodium and water excretion with potassium
retention.
2. Risk for imbalanced nutrition related to decreased gastrointestinal enzymes, decreased gastric acid
production.
3. Risk for decreased cardiac output related to any situation that increased corticosteroids (i.e. stress,
infection, GI-upsets) may lead to shock or vascular collapse.
4. Knowledge deficit related to self-administration of steroid medication.
PLANNING
NURSING GOALS
1. To maintain fluid and electrolyte balance.
2. To maintain nutritional needs.
3. To maintain adequate cardiac output.
4. To improve knowledge.
NURSING INTERVENTIONS
MAINTAIN FLUID AND ELECTROLYTE BALANCE
1. Assess skin turgor and mucous membranes for signs of dehydration.
2. Monitor vital signs, especially blood pressure and heart rate for orthostatic changes.
3. Assess color, concentration and amount of urine.
4. Observe patient for petechiae.
5. Encourage the patient for oral fluids as tolerated.
6. Instruct the patient to ingest salt additives in condition of excess heat or humidity.
7. Administer parenteral fluids as prescribed.
MAINTAIN NUTRITIONAL NEEDS
1. Assess nutritional status and monitor weight of the by patient.
2. Monitor serum glucose levels.
3. Provide high-protein, low-carbohydrates, high sodium diet.
4. Encourage for small frequent meals to maintain adequate blood glucose level.
5. Encourage rest period after eating to facilitate digestion.
MAINTAIN ADEQUATE CARDIAC OUTPUT
1. Monitor vital signs, especially blood pressure.
2. Assess skin warmth and peripheral pulses.
3. Monitor for dysrhythmias.
4. Monitor urine output.
5. Monitor oxygen saturation through pulse oximetry, as appropriate.
6. Minimize stressful situations and promote a quiet environment.
7. Provide proper rest.
8. Administer IV fluids rapidly, if hypotension develops with decreased cardiac output.
9. Administer glucocorticoids (IV) as prescribed.
IMPROVE KNOWLEDGE REGARDING SELF ADMINISTRATION OF STEROID
MEDICATIONS
1. Provide information appropriate to individual situation.
2. Discuss drug therapy, including actions of prescribed steroid hormones.
3. Discuss importance, principles, signs of over and under dosage.
4. Teach the patient for an intramuscular self-injection kit to be available at all time.
5. Demonstrate the procedure of self-administration of medication.
PATIENT EDUCATION AND HEALTH MAINTENANCE
1. Educate patient and family about the causes and management of Addison's disease.
2. Educate patient that maintaining an adequate circulating blood volume is a priority.
3. Advice patient to take oral fluids
4. Advice patient to take high protein, low carbohydrate and high sodium diet
5. Instruct patient to get plenty of rest and sleep.
6. Teach the effects of illness and treatment.
7. Teaching about self-administration of steroids, increasing oral fluid intake, diet and side effects of
medications.
8. Instruct patient to contact health care provider, if symptoms get worse.
EVALUATION: EXPECTED OUTCOMES
1. Fluid and electrolyte balance is maintained.
2. Nutritional needs are maintained.
3. Adequate cardiac output is maintained.
4. Knowledge is improved.
PHEOCHROMOCYTOMA ADRENOMEDULLARY DISORDER
A catecholamine which secretes neoplasm associated with hyperfunction of the adrenal
medulla is known as pheochromocytoma. It may appear wherever chromaffin cells are located;
however, most are found in the adrenal medulla. Approximately, 0.1 to 0.2% of patient with diastolic
hypertension have a pheochromocytoma. Tumors are found in both sexes equally. They occur in
patients of any age. Most commonly, it is diagnosed during the 4th decade of life.
ETIOLOGY
Usually, cause is unknown.
1. Pheochromocytoma occurs wherever chromaffin tissue is found.
2. Chromaffin cell tumor, usually found in the adrenal medulla.
3. It causes excessive secretion of epinephrine and norepinephrine.

RISK FACTORS
1. Smoking
2. Micturition: It can trigger the paroxysm of hypertension.
3. Pregnancy
4. Drugs which may increase catecholamine release such as histamines, some anesthetics, atropine,
chlorpromazine, steroids and glucagon.
5. Genetic conditions such as Multiple Endocrine Neoplasia, type 2 (MEN2), Von Hippel—Lindau
disease and Neurofibromatosis 1 (NF1)
PATHOPHYSIOLOGY
1. Pheochromocytoma synthesizes and hyper secrete catecholamine into the circulatory system
which triggers a paroxysm related to excess of those hormones.
2. These catecholamines are converted by catechol-methyltransferase into metanephrines and
normet-anephrines which are inactive metabolites.
3. Paroxysm usually begins with a sensation of something deep in the chest.
4. Symptoms associated with pheochromocytoma are related to tumor hypersecretion of
catecholamines and increases stimulation of o and ẞ adrenergic receptors.
5. Patient notes a pounding or forceful heartbeat from B receptors-mediated increase in cardiac
output, Throbbing spread to trunk or head causing headache.
6. Intense a receptor-mediated peripheral vasoconstriction causes cool, moist hands and feet.
7. Increase in cardiac output and vasoconstriction causes marked elevation of systolic and diastolic
blood pressure when catecholamines are released.
8. Tachycardia results from epinephrine hypersecretion.
9. Decrease heart loss and increase metabolism may cause a rise in temperature or flushing and
diaphoresis.
10. Extra-adrenal pheochromocytoma: It arises in paraganglion chromaffin tissue of autonomic
nervous system.
11. Familial pheochromocytoma: It tends to be small tumors with low levels of catecholamine
release.
12. Malignant pheochromocytoma: They are associated with local invasion or distant metastasis. In
certain patients, such as SDH B gene mutation carriers, pheochromocytoma is more likely to be
malignant.
CLINICAL MANIFESTATIONS
1. Symptoms of pheochromocytoma vary in intensity and frequency and last minutes to hours,
depending on the pheochromocytoma paroxysmal release of catecholamines.
2. Headache is reported in 80 to 90% of paroxysms.
3. Hypertension may be paroxysmal (intermittent) or persistent (chronic).
a. Chronic form mimics essential hypertension, however, antihypertensives are not effective.
b. Headache and vision disturbances are common.
4. Rapid heart rate.
5. Emotional changes including psychotic behavior may occur.
6. Other commonly reported symptoms are:
a. Diaphoresis
b. Tremor
c. Nausea or vomiting.
d. Dizziness with position changes.
DIAGNOSTIC EVALUATION
1. Medical history or physical examination.
2. Blood and urine test:
a. Elevated plasma levels of catecholamines epinephrine and norepinephrine.
b. Increased vanillylmandelic acid found in 24 hours urine collection as a result of increased
excretion of catecholamines.
c.Arteriography usually reserved for cases in which CT scan fails to reveal the adrenal gland
adequately.
d. CT scans and MRI of adrenal glands or of the entire abdomen is done to identify tumor.
e. Position emission tomography: Performed to detect radioactive compounds taken up by
tumor.
MANAGEMENT
MEDICAL MANAGEMENT
GOALS OF MEDICAL MANAGEMENT
1. To reduce blood pressure.
2. To reduce incidence of complications.
3. Prepare patient for surgery.
PHARMACOLOGIC INTERVENTIONS.
1. Adrenergic antagonists: They are prescribed for a few days to 2 weeks before surgery to decrease
symptoms, reduce blood pressure and eliminate paroxysms.
2. Phenoxybenzamine is the drug of choice for frequent paroxysms or persistent hypertension,
prazosin for blood pressure control, a-blockers as a competitive antagonist to norepinephrine.
3. Patients who are not able to undergo surgery may be managed pharmacologically for prolonged
periods.
4. Successful treatment of malignant tumors involves chemotherapeutic agent and radiation therapy
in addition to palliative treatment.

SURGICAL MANAGEMENT
1. UNILATERAL OR BILATERAL ADRENALECTOMY:
a. Surgical removal of one or both adrenal gland is to the primary treatment for
pheochromocytoma depending on whether tumor is unilateral gas bilateral.
b. It is indicated as soon as the blood pressure is decreased and paroxysms are eliminated.
2. Surgical removal of adrenal gland can cure the patient, provided the growth is discovered before
cardiovascular damage becomes permanent.
3. Highest of post-operative care include monitoring blood pressure. It is common for blood pressure
fall to 90/60 mmHg. Total lack of decline in blood pressure may indicate residual tumor tissue
pressure therapy is usually not indicated.
4. Laparoscopic surgery: It is used more often for tumors smaller than 6 cm but for larger tumors.
NURSING MANAGEMENT
1. Monitor vital signs, especially blood pressure changes: Severe hypertension can precipitate a
cerebrovascular accident and sudden blindness.
2. Pre-administer antihypertensive medications as orders.
3. Promote rest and decrease stressful stimuli, acute attacks may be precipitated by emotional stress,
physical exertion and change in position. bas
4. Monitor urine test for glucose and acetone-patients with pheochromocytoma may present with
manifestations of diabetes mellitus.
5. Instruct to avoid doing vigorous and prolonged exercise, at least two days prior to and day of urine
collection.
6. Provide high-calorie, well balanced diet.
7. Instruct patient to avoid smoking and stimulants like coffee and tea, chocolate, bananas and vanilla
food 2 days prior.
8. Inform patient that there is possibility to continue steroid therapy throughout life.
PRE-OPERATIVE CARE
1. Take measures to reduce the blood pressure and prevent intraoperative hypertensive crisis.
2. A non-relative alpha blocker such as phenoxybenzamine is prescribed to normalize blood pressure
POST-OPERATIVE CARE
1. After surgery, patient is at risk of hypotension from venous dilation, patient may need IV fluids,
colloids, and vasopressors.
2. Surgery causes significant blood loss and hypo-volemia. Bleeding should be controlled.
3. Biochemical assay is done to ensure that all cells have been removed.
4. For patient with an adrenalectomy observe for blood pressure changes as they are at a risk for
shock due to a drastic drop in catecholamine levels.
COMPLICATIONS
1. Myocarditis.
2. Hypertensive retinopathy.
3. Cerebral vascular accident.
4. Congestive heart failure.
5. Death due to myocardial infarction.
NURSING CARE PLAN
NURSING ASSESSMENT
1. Monitor vital signs of patient.
2. Assess patient's level of consciousness.
3. Auscultate breathe sounds of patient.
4. Monitor oxygen saturation.
5. Assess the level of pain, its location, intensity and severity.
NURSING DIAGNOSIS
1. Decreased cardiac output related to increased vascular resistance.
2. Risk of ineffective tissue perfusion (cardiopulmonary and renal) related to hypertension.
3. Pain related to increased cerebral vascular pressure.
4. Anxiety related to increased catecholamine.
5. Disturbed sleep pattern related to high level of circulating catecholamine.
6. Activity intolerance related to body weakness.
PLANNING
NURSING GOALS
1. To maintain adequate cardiac output.
2. To increase tissue perfusion.
3. To reduce pain.
4. To reduce anxiety level.
5. To improve sleeping pattern.
6. To increase activity tolerance.
NURSING INTERVENTIONS
1. Assess the level of consciousness.
2. Assess the vital signs.
3. Assess the central and peripheral pulses and capillary refill.
4. Provide oxygen therapy as indicated.
5. Discuss with the patient about intensity, severity,
tolerance and precipitating factors of pain. bas
6. Encourage the patient to verbalize his/her problem. It helps to identify all contributing factors for
anxiety.
7. Monitor the activity level of the patient. It provides baseline data for planning of activities.
8. Restrict fluids and sodium as ordered, if increased preload becomes a problem.
9. Administer oxygen as prescribed.
10. Provide calm and quite environment.
11. Provide ROM exercises at least every 4 hourly.
12. Use non-invasive pain relief techniques such as progressive relaxation, guided imagery or
rhythmic breathing.
13. Encourage family members to stay with patient.
14. Place the patient in preferred sleeping position, support position with pillows. It promotes the
patient's comfort and follows the patient's usual routine.
15. Assist the patient in self-care activities.
16. Encourage progressive activity and increased self-care as tolerated.
17. Involve the patient in the planning of the activities.
18. Administer IV fluids as ordered.
19. Administer medications as prescribed.
20. Apply hot or cold application according to what the patient states provides best pain relief.
PATIENT EDUCATION AND HEALTH MAINTENANCE
EDUCATE PATIENT AND FAMILY ABOUT THE FOLLOWING:
1. How and when to take medications.
2. How to measure patient's blood pressure.
3. Avoid the following:
a. Smoking
b. Coffee
 c. Tea
4. Get good nutrition and eat a variety of healthy food such as fruits, vegetables, milk and cheese.
5. Get plenty of rest and sleep
6. Contact health care provider, if they notice any of the following:
a. Nausea or vomiting.
b. Pain is worse and does not go away even after taking pain relievers.
c. Fever
d. Blurred or double vision.
e. Trouble breathing or fast heartbeat.
EVALUATION: EXPECTED OUTCOMES
1. Adequate cardiac output is maintained.
2. Increased tissue perfusion.
3. Pain is reduced.
4. Anxiety level is reduced.
5. Sleeping pattern is improved.
6. Increased activity tolerance.
DISORDERS OF PITUITARY GLAND
DIABETES INSIPIDUS (DI)
Diabetes Insipidus (DI) is a disorder of the posterior pituitary gland related to water metabolism. It
results from the deficiency of Antidiuretic Hormone (ADH) circulating vasopressin. It is
characterized by polydipsia or polyuria.In uncomplicated diabetes insipidus, prognosis is good with
adequate water replacement and patient's usually lead normal lives.
TYPES OF DIABETES INSIPIDUS
1. Neurogenic (central) diabetes insipidus:
a. Localized or generalized edema secondary to head trauma or vascular lesions.
b. Central nervous system infections or inflammation.
c. Vasopressin inhibiting drugs such as:
i. Glucocorticoids
ii. Ethanol
iii. Adrenergic agents
iv. Phenytoin
d. Tumors of the hypothalamus or pituitary glands accounts for 25 percent of central diabetes
insipidus
2. Complete diabetes insipidus: Complete absence of vasopressin disrupts the hypophyseal tract. It
causes 80% degeneration of the supraoptic and paraventricular nuclei.
3. Nephrogenic diabetes insipidus: In the renal, deficiency of vasopressin receptors collecting ducts
results from a rare hereditary disorder or is acquired secondary to the following:
a. Pyelonephritis
b. Obstructive uropathy
c. Hypocalcemia
4. Dipsogenic diabetes insipidus: It causes extreme thirst which creates an increased fluid intake.

ETIOLOGY
1. Health injury, brain tumor.
2. X-linked recessive trait or end stage renal failure (nephrogenic diabetes insipidus, less common).
3. Failure of renal tubules to respond to ADH.
4. Certain drugs such as:
a. Lithium (Duralith)
b. Phenytoin (Dilantin)
c. Alcohol (Transient diabetes insipidus)
RISK FACTORS
1. Pregnancy
2. Head tumors
3. Sickle cell disease
4. Pituitary disorders
PATHOPHYSIOLOGY
1. Diabetes insipidus is related to an insufficiency of ADH leads to polyuria or polydipsia.
2. In healthy individuals, when bodily fluids are depleted, ADH is released from pituitary gland. It
prevents the excretion of fluids from the body in form of urine.
3. Neurogenic or central diabetes insipidus:
a. An inadequate response of ADH to plasma osmolarity due to disruption of hypothalamus or
occurs pituitary gland.
b. Many organic lesions which can cause diabetes
It man insipidus include:
i. Brain tumor
ii. Hypophysectomy aneurysms
 iii. Thrombosis
iv. Infections and immunologic disorders.
c. It has an acute onset.
d. A three-phase syndrome can also occur. It involves:
i. Normal diuresis
ii. Progressive loss of nerve tissue and increased diuresis.
4. Nephrogenic diabetes insipidus:
a. It is caused by an inadequate renal response to ADH.
b. Generally, it is related to disorders and drugs which damage the renal tubules.
i. Causative disorders include pyelonephritis, amyloidosis, destructive uropathies,
polycystic disease and intrinsic renal disease.
ii. Drugs such as lithium carbonate (eskalith), general anesthetics, such as
methoxyflurane and demeclocycline (declomycin).
c. Care genetic form of nephrogenic diabetes insipidus is an X-linked recessive trait.
5. Complete diabetes insipidus: It includes complete absence of vasopressin which disrupts the
hypophyseal tract.
6. Dispogenic diabetes insipidus: It is an uncommonly recognized disorder. It occurs as a result of
hypothalamic disease or trauma.
CLINICAL MANIFESTATIONS:
1. Genitourinary:
a. Polyuria (a few litres to 18 L/day).
b. Clear urine
c. Frequent urination
d. Nocturia
2. Gastrointestinal:
a. Weight loss
b. Polydipsia
3. Integumentary: Dry skin and mucous membrane.
4. Polydipsia (intense thirst): Drink 4 to 5 L daily; has craving for cold water.
5. High serum osmolality, i.e. above 295 mOsm and high serum sodium level, i.e. greater than 145
mEq/L.
DIAGNOSTIC EVALUATION
1. Urinalysis: Showing almost colorless urine of low osmolality (50 to 200 mOsm/kg, less than that
of plasma) and low specific gravity less than 1.055.
2. Water deprivation test: It helps to identify vasopressin deficiency, resulting in renal inability to
concentrate urine
3. Measurements of serum and urine ADH-decreased or absent.
4. MRI: It helps to observe abnormalities in or near the pituitary gland.
5. Blood test: It measures the amount of electrolytes and glucose in blood.
MANAGEMENT
MEDICAL MANAGEMENT
GOALS OF MEDICAL MANAGEMENT
1. To identify the cause of diabetes insipidus
2. To prevent complications such as dehydration, electrolyte imbalance.
3. To correct the cause.
NON-PHARMACOLOGIC INTERVENTIONS
Increase oral fluids, especially water.
PHARMACOLOGIC INTERVENTIONS
1. Diuretics are used because they have some action of vasopressin. Hypoglycemic agents are also
given.
2. Vasopressin replacement: It is performed by synthetic vasopressin, i.e. desmopressin. It is
administered intranasally or intramuscularly.
3. Pitressin tannate in oil may be given intramuscularly daily.
4. Chlorpropamide may stimulate ADH release and helps to reduce symptoms.
5. Mild salt depletion and prostaglandin inhibitors: They are used to treat nephrogenic form of
diabetes insipidus.
NURSING MANAGEMENT
1. Teach patient and significant others about the disease, its symptoms and treatment.
2. Monitor urine output and urine specific gravity.
3. Assess patient's anxiety level.
4. Obtain patient's weight daily.
5. Obtain complete health history of patient to determine possible cause of DI.
6. Always be gentle, polite and follow optimist approach.
7. Involve family members in patient's care
8. Encourage patient to maintain personal hygiene.
9. Observe for the signs of dehydration.
10. Administer prescribed medications as ordered by physician.
11. Encourage hydration and provide easy access to fluids, administer IV fluids, if necessary.
12. Instruct patient to avoid food or liquid which produce diuresis.
13. Provide specific verbal and written instructions, show patient how to administer the medication
and observe return demonstrations as appropriate.
14. Instruct patient to wear Medic Alert bracelet
15. Provide emotional and psychological support to patient.
16. Teach patient for follow-up and monitor signs of complications.
COMPLICATIONS
1. Electrolyte imbalance
2. Dehydration
3. If untreated, may result in death.
NURSING CARE PLAN
NURSING ASSESSMENT
1. Assess the vital signs of the patient.
2. Measure and record total intake and output every shift:
a. Check intake and output hourly.
b. Observe and document color and consistency of urine, stool and vomitus.
c. Check urine specific gravity every 4 hourly.
3. Assess for the signs of infection, i.e. redness, swelling or pain.
NURSING DIAGNOSIS
1. Deficit fluid volume related to compromised endocrine system, hypopituitarism.
2. Risk for impaired skin integrity related to urinary frequency with high volume output and the
potential for incontinence.
3. Anxiety related to stress or threat.
PLANNING
NURSING GOALS
1. To maintain fluid level.
2. To maintain skin integrity.
3. To reduce anxiety.
NURSING INTERVENTIONS
1. Monitor for the signs of infection, i.e., redness, swelling or pain.
2. Assess for continence or incontinence.
3. Monitor skin surface for blanching, erythema, warmth and size of lesion for early detection of
complications.
4. Explain all procedures and rationale for procedures to patient helps to increase patient cooperation.
5. Encourage the patient to drink and variation in fluid is helpful to increase intake.
6. Administer or assist with oral hygiene after each meal and before bedtime.
7. Provide intravenous fluids to the patient to increase the hydration.
8. Weight patient daily at specified time each day.
9. Perform active or passive ROM exercises.
10. Change the position at least every 2 hourly.
11. Provide well balanced diet to the patient.
12. Provide back massage and wound care to the patient.
13. Encourage the patient to verbalize his/her problem.
14. Help the patient to practice coping strategies, such as Plat progressive muscle relaxation.
15. Provide calm and non-threatening environment helps to relax the patient.
PATIENT EDUCATION AND HEALTH MAINTENANCE
1. Inform patient and significant others that metabolic status must be monitored on a long-term basis
because of the severity of diabetes insipidus changes from time to time.
2. Instruct patient to wear Medic Alert bracelet.
3. Encourage family involvement for successful home management.
4. Teach patient to be alert for the signs of dehydration.
5. Tell patient to consider eliminating coffee and tea from diet. It may have an exaggerated diuretic
effect.
6. Instruct patient to call health care provider, if any of the following occurs:
a. Dry mouth or cracked lips.
b. More tired than usual.
c. New headaches.
d. Vision changes.
EVALUATION: EXPECTED OUTCOME.
1. Fluid level is maintained. of Image
2. Skin integrity is maintained.
3. Anxiety is reduced.

HYPOPITUITARISM
 Hypopituitarism is a complex syndrome marked by metabolic dysfunction, sexual immaturity
and growth retardation. The main cause of hypopituitarism is the deficiency of hormones secreted by
anterior pituitary gland.
Hypopituitarism is also known as dwarfism when it occurs in childhood. It results in related
growth in children, sexual immaturity and metabolic dysfunctions.
It may be primary or secondary, depending on its cause.
1. PRIMARY HYPOPITUITARISM: It is caused by disorders that affect the pituitary gland.
2. SECONDARY HYPOPITUITARISM: It is caused by disorders of the hypothalamus.
3. PANHYPOPITUITARISM: It is caused when both the anterior and posterior lobes fail to secrete
hormones.

ETIOLOGY
1. Infections or inflammation of the brain and tissues that support the brain.
2. Invasion: Pituitary tumors, CNS tumors and carotid aneurysm.
3. Infarction: Postpartum necrosis.
4. Immunological: Lymphocytic hypophysitis.
5. Idiopathic: Familial
6. Isolated: Deficiency of anterior pituitary hormones.
RISK FACTORS
1. Type 1 diabetes mellitus
2. Sickle cell anemia
3. Pituitary tumor
4. Hypothalamic disease
5. Severe loss of blood
6. Pituitary apoplexy
PATHOPHYSIOLOGY
1. Hypopituitarism describes the low secretion of anterior pituitary hormone and panhypopituitarism
describes the low secretion of all anterior pituitary hormones.
2. They both can results from malfunction of pituitary gland or hypothalamus
3. Partial or complete forms of hypopituitarism affect adults and children. In children, it may cause
dwarfism and delayed puberty.
4. Primary hypopituitarism: It results from damage to or destruct of anterior pituitary as a result of
the following:
a. Chemical agents.
 b. Postpartum hemorrhage that causes pituitary necrosis.
c. Radiation of head and neck.
d. Head trauma that produces injury to pituitary.
e. Invasive neoplasms from primary or metastatic cancer of breast, lung or gastrointestinal
tract.
5. Secondary hypopituitarism: It results from damage to pituitary's ability to produce hormones
needed to stimulate or inhibit hypothalamic activity (TSH and ACTH) as a result of the following:
a. Tuberculosis and Syphilis
b. Head trauma

CLINICAL MANIFESTATIONS
1. Deficiency of ACTH causing weakness, fatigue, weight loss, fasting hypoglycemia and altered
mental function due to hypocortisolism, loss of axillary and pubic hair due to androgen deficiency in
females, orthostatic hypotension and hyponatremia due to aldosterone deficiency.
2. Deficiency of TSH causing secondary hypothyroidism (usually less severe than primary thyroid
failure).
3. Deficiency of GH causing dwarfism in children and hypoglycemia in all ages.
4. Deficiency of LH and FSH causing hypogonadism. It includes amenorrhea, breast atrophy and
decreased vaginal secretions in women and decreased libido, impotence, reduce muscle strength and
testicular atrophy in men.
5. Deficiency of prolactin causing lactation dysfunction or gynecomastia.
6. Others:
a. Integumentary: Hypothermia and wrinkled, waxy, smooth skin.
b. Musculoskeletal: Loss of muscle tone.
c. Cardiovascular: Bradycardia and hypotension.
d. Neurologic: Hypoactive reflexes.
e. Reproductive: Poorly developed, secondary sexual characteristics.
f. Hematologic: Anemia related to thyroid and androgen deficiency.
DIAGNOSTIC EVALUATION
1. Hormonal deficiency of tropic and target organ hormones affected, chosen after evaluation of
clinical picture.
2. CT and MRI of pituitary and target glands: It shows destruction of anterior pituitary or atrophy of
target gland.
3. Blood tests: It helps to identify low levels of thyroid, adrenal or sex hormones.
4. Vision test: Performed to determine, if growth of pituitary tumor has impaired patient's sight and
visual fields.
MANAGEMENT
MEDICAL MANAGEMENT
1. Deficiency of ACTH: Glucocorticoid’s support.
2. Deficiency of TSH (Secondary hypothyroidism):
Thyroxine supplement.
3. LH and FSH deficiency cause hypogonadism:
a. Men: Testosterone replacement to restore libido and patency and secondary sexual characteristics
and chorionic gonadotropin, menotropins or both to relieve spermatogenesis.
b. Women: Estrogen and progesterones to maintain secondary sexual characteristics, clomiphene
citrate to promote ovulation and small doses of long-acting androgens to improve diminished libido.
4. Deficiency of GH: Exogenous hormone replacement for children.
5. Deficiency of prolactin: Bromocriptine is recommended.

NURSING MANAGEMENT
1. Provide knowledge about disease, its causes, sign and symptoms, treatment to patient and family
members.
2. Monitor vital signs, i.e., blood pressure, heart rate and rhythm every 2 hours.
3. Watch for chest pain or dyspnea because hypo-thyroidism can develop chronic arteriosclerosis.
4. Monitor intake and output to ensure balance is equal due to hormone regulation.
5. Instruct patient to elevate his/her head while sleeping which helps to reduce trauma to eye.
6. Observe patient's eyelids, nail beds and skin pallor which indicate anemia.
7. Keep emergency equipment’s available in case of respiratory distress.
8. Help patient to increase self-esteem by supporting all actions, hopes and desires of the patient.
9. Teach relaxation techniques to patient which helps to reduce anxiety.
10. Teach patient how to perform regular skin care every day.
11. Instruct patient to avoid scratching the skin.
12. Encourage patient to take plenty of fluids.
13. Encourage patient to use the moisturizing lotion.
14. Fluid electrolyte balance should be maintained in case of low blood pressure as the low blood
pressure is one of symptoms of hypopituitarism.
15. Range of motion exercises should be advised to patient to reduce joint stiffness and to reduce the
unintentional weight gain
COMPLICATIONS
1. Adrenal crisis is the most acute complication which can arise in the treatment of patient with
hypopitularism
2. Side effects of drug therapy can develop. In severe illness, failing to take extra corticosteroids can
be life threatening
NURSING CARE PLAN
NURSING ASSESSMENT
1. Assess the vital signs of the patient.
2. Monitor for the signs of infection, i.e. redness, swelling or pain.
3. Assess patient's feelings about his/her changed and coping mechanism.
4. Encourage the patient to verbalize his/her problem.
NURSING DIAGNOSIS
1. Disturbed body image related to changes in body structure and function of the body due to
deficiency of gonadotropin and growth hormone deficiency.
2. Risk for impaired skin integrity related to declining hormonal levels.
3. Self-care deficit related to the decrease in muscle strength.
4. Anxiety related to threat or change in health status.
PLANNING
NURSING GOALS
1. To improve body image
2. To maintain skin integrity.
3. To maintain muscle strength.
4. To reduce anxiety.
NURSING INTERVENTIONS
1. Assess patient's feelings about his/her changed appearance and coping mechanism. The patient
may withdraw from social interaction.
2. Reassure the patient that the physical changes are the result of elevated hormone levels and most
will resolve when those levels return to normal.
3. Encourage the patient to verbalize feelings about the body image changes.
4. Reduce pressure on affected skin surface by using air mattress or comfort devices. Pressure
predisposes tissue breakdown.
5. Perform active or passive ROM exercises and change the position at least every 2 hourly.
6. Provide well-balanced diet to the patient.
7. Provide back massage and wound care to the patient.
8. Provide positive reinforcement for all activities attempted positive reinforcement may promote
ongoing efforts.
9. Educate family to intervene if the patient becomes tired, not capable of carrying out task of daily
activities to support the patient.
10. Plan activities with the rest periods to save energy and decrease fatigue which will improve
patient's capability to perform the tasks for daily living.
11. Encourage the patient to verbalize his/her problem. It helps to identify all contributing factors for
anxiety.
12. Provide calm and non-threatening environment that helps to relax the patient.
13. Assist the patient to learn to recognize and identify the symptoms of anxiety.
14. Encourage the family members to stay with patient.
15. Administer anti-anxiety medications as ordered.
MEDICATION HELPS TO REDUCE ANXIETY.
PATIENT EDUCATION AND HEALTH MAINTENANCE EDUCATE PATIENT TO:
1. Take medications as directed by physician. It may help to balance the hormone level.
2. Weight himself/herself daily.
3. Wear a Medic Alert bracelet.
4. Take plenty of fluids.
5. Eat well balanced diet.
6. Perform Range of Motion (ROM) exercises which helps to reduce joint stiffness.
7. Get plenty of rest and sleep.
8. Contact health care provider, if he/she notice any of the following:
a. Menstrual period stops or become irregular.
b. Sudden weight gain or loss.
c. Chest pain or shortness of breath.
EVALUATION: EXPECTED OUTCOMES
1. Body image is improved.
2. Skin integrity is maintained.
3. Muscle strength is maintained.
4. Anxiety is reduced.
HYPERPITUITARISM
Over secretion of hormones from the anterior pituitary is known as hyperpituitarism. Usually, a
combination of hormones is hypersecreted rather than single hormone.
TYPES OF HYPERPITUITARISM
1. Gigantism
2. Acromegaly
GIGANTISM
Gigantism is abnormally large growth due to an excess of growth hormone during childhood, before
the bone growth plates have closed. It results in increased growth of bones, cartilage and other
tissues as well as increase catabolism of carbohydrate and protein synthesis.
In gigantism, a proportional overgrowth of all body tissue starts before epiphyseal closure.
TYPES OF GIGANTISM
1. Pituitary gland gigantism (located at the base of brain).
2. Mammary gigantism (always occur in humans).
3. Cerebral/sotos syndrome gigantism (a genetic disorder occurs rarely, during 2 to 3 years of life
manifested by excessive physical growth).
4. Local gigantism (enlargement of certain body parts).

ETIOLOGY
1. The most common cause of excessive growth hormone release is a non-cancerous (benign) tumor
of the pituitary gland.
2. Others:
a. McCune-Albright Syndrome (MAS): Abnormal growth in bone tissue, gland abnormalities.
b. Carney complex: non-cancerous tumors on connective tissue, spots of darker skin,
cancerous or non-cancerous endocrine tumors.
c. Multiple Endocrine Neoplasia Type 1 (MEN-1): On Tumor in the pituitary gland, pancreas
or to parathyroid gland.
d. Neurofibromatosis: Tumors in nervous system.
RISK FACTORS
1. Gigantism decrease in normal span of person's life.
2. Pituitary gland tumor.
3. Parent or sibling with gigantism.
CLINICAL MANIFESTATIONS
1. Abnormal growth: Increased height, enlarged hands and feet.
2. Depression
3. Headache
4. Visual field impairment
5. Osteoarthritis
6. Peripheral neuropathies
7. Endocrinopathies
8. Delayed puberty
9. Irregular menstrual periods in teens.
DIAGNOSTIC EVALUATION
1. CT scan or MRI: Performed to determine size and location of tumor.
2. Oral glucose tolerance test: It is used to confirm the diagnosis of gigantism.
3. Blood test: Helps to measure the level of growth hormone and insulin like growth factor 1 (GF-1).
It is a hormone produced by liver.
4. X-rays of skull or jaw: Performed to detect the bone thickness.
MANAGEMENT
MEDICAL MANAGEMENT
1. Growth hormone release growth hormone antagonist, pegvisomant (Somavert) which blocks the
effects of growth hormone.
2. Somatostatin analogs, such as octreotide helps to reduce GH release.
3. Radiation therapy has also been used to bring growth hormone levels to normal. However, it can
take 5-10 years for the full effects to be seen and this almost always leads to low level of other
pituitary hormones.
SURGICAL MANAGEMENT
1. Surgery is the first recommended treatment for gigantism.
2. Surgery is performed as a planned hospital admission.
3. Its main purpose is to remove or reduce the size of tumor of lower growth hormone levels and also
reduce pressure on optic nerve.
NURSING MANAGEMENT
1. Educate patient and family members that gigantism cannot be prevented. Early treatment may
prevent the disease from getting worse or help to avoid complications.
2. Monitor patient's vital signs.
3. Assess the level of patient's anxiety.
4. Provide emotional support to patient or significant others
5. Encourage patient to share a sense of helplessness, shame or fear associated with disease
manifestations.
6. Encourage patient to socialize with his/her surroundings.
7. Administer medications as ordered by physician.
8. Keep accurate assessment of height and weight.
9. Emphasize importance of regular follow-up with endocrinologist.
10. Instruct family members to call health care provider, if patient has signs of excessive growth.
COMPLICATIONS
1. Adrenal insufficiency
2. Hypogonadism
3. Diabetes insipidus (rarely)
4. Hypothyroidism
ACROMEGALY
Acromegaly is a rare hormonal disease of excessive bone and soft tissue growth due to elevated
levels of growth hormone. Usually, it affects middle aged adults.
ETIOLOGY
1. Cause of increased growth hormone release is usually a non-cancerous (benign) tumor of the
pituitary gland.
2. Pituitary gland (located just below the brain): It controls the production and release of several
different hormones including growth hormone.
RISK FACTORS
1. Hereditary
2. Lung cancer
3. Adrenal tumors
PATHOPHYSIOLOGY
1. Acidophilic, growth hormone secreting tumor creates an unpredictable growth hormone secretes
pattern which replaces the usual peaks that occur 1 to 4 hours after onset of sleep.
2. Increased amount of growth hormone leads to rapid growth in all body tissue.
3. Excess growth hormone increases bone density and width and proliferation of connective and soft
tissue.
4. Increased growth leads to acromegaly, if it occurs after epiphyseal closure.
5. As the tumor continues to grow, it results in destruction of entire pituitary gland.
6. Tumor mass itself may induce optic nerve, cranial nerve palsies, hydrocephalus and hypopituitary.
7. Patients with acromegaly may also be at increased risk for the following:
a. Cardiac hypertrophy
b. Arthritis
c. Sleep apnea
d. Development of other neoplastic lesions.
CLINICAL MANIFESTATIONS
1. Enlarged hands or feet.
2. Coarse oily, thickened skin.
3. Deepened, husky voice due to enlarged vocal cords and sinuses.
4. Joint pain.
5. Large glands in the skin (sebaceous glands).
6. Widely spread teeth.
7. Excessive sweating.
8. Large jaw (prognathism) and tongue.
9. Headache
10. Women: Irregular menstrual cycle.
11. Men: Impotence.
DIAGNOSTIC EVALUATION
1. High growth hormone level.
2. GH and 1GF-1 measurement: Blood sample is taken to measure the level of GH and 1 GF.
Elevated levels suggest acromegaly.
3. Spine X-rays: It helps to detect abnormal bone growth.
4. Pituitary MRI: Detects a pituitary tumor.
5. Echocardiogram: It may show an enlarged heart, leaky mitral valve or leaky aortic valve.
MANAGEMENT
MEDICAL MANAGEMENT
1. Bromocriptine (Parlodel): It may be given before surgery which helps to shrink tumors.
2. Pegvisomant: It is prescribed to patient who is not responding to other forms of treatment.
3. Octreotide (Sandostatin) and Lanreotide (Soma-tuline depot): Recommended to reduce excess
growth hormone secretion.
4. Cabergoline: Helps to lower hormone level.
5. Radiation therapy:
a. It is recommended when tumor cells remain after surgery.
b. It helps to destroy any lingering tumor cells and slowly reduces the level of growth
hormone.
SURGICAL MANAGEMENT
ENDOSCOPIC TRANSNASAL TRANSSPHENOIDAL:
1. In most cases, it is preferred to treat the acromegaly.
2. It is performed to remove most of the pituitary tumors.
3. Removal of tumor can normalize the growth hormone production and also eliminate pressure on
issues surrounding pituitary gland to relieve associated sign and symptoms.
NURSING MANAGEMENT
1. Provide knowledge about acromegaly to patient and family members.
2. Monitor vital signs and weight as well as neurologic status.
3. Assess patient's level of consciousness.
4. Assess body changes of the patient.
5. A nurse must provide patient and significant others with emotional support and comfort
throughout the perioperative period.
6. Notify physician, if urine output is greater than 200mL/hr with specific gravity of less than 1.005.
7. Educate patient about the symptoms of growth hormone excess and recent advances in the
treatment.
8. Instruct patient not to brush his/her teeth for two weeks after surgery.
9. Instruct patient to avoid sneezing, coughing and bending over from the waist to avoid disrupting
the
graft.
10. Reassure the patient that treatment reverses some of the physical deformities.
11. Elevate patient's head to facilitate breathing and fluid drainage.
12. Instruct patient to avoid activities which can increase intracranial pressure for upto 2 months after
surgery.
13. Administer IV fluids, if ordered.
14. Provide oral fluids to the patient.
15. Instruct patient to report increased nasal drainage.
COMPLICATIONS
1. Hypertension
2. Diabetes mellitus
3. Osteoarthritis
4. Goiter
5. Vision loss
NURSING CARE PLAN OF GIGANTISM AND ACROMEGALY
NURSING ASSESSMENT
1. Encourage the patient to verbalize his/her problem. It helps to identify all contributing factors for
anxiety.
2. Measure and record total intake and output every shift:
 a. Check intake and output hourly.
b. Observe and document color and consistency of urine, stool and vomitus.
c. Check urine specific gravity every 4 hourly.
3. Assess the sleeping pattern of the patient.
4. Monitor vital signs.
5. Assess patient's anxiety level.
NURSING DIAGNOSIS
1. Disturbed body image related to anxiety over thickened skin and enlargement of face, hands, and
feet.
2. Ineffective coping related to change in appearance.
3. Disturbed sleeping pattern related to soft tissue swelling.
4. Fluid volume deficit related to abnormal losses through the skin and decrease in intake of fluid.
5. Anxiety related to changes in body appearance as evidenced by restlessness.

PLANNING
NURSING GOALS:
1. To improve body image.
2. To enhance coping.
3. To maintain sleeping pattern.
4. To maintain fluid volume.
5. To reduce anxiety.
NURSING INTERVENTIONS
1. Monitor skin turgor, electrolytes, blood urea nitrogen and hematocrit level.
2. Explain all procedures and rationale for procedures to patient which helps to increase his/her
cooperation.
3. Assist the patient to learn to recognize and identify the symptoms of anxiety.
4. Provide thorough teaching and complete aftercare instructions for the patient.
5. Teach relaxation exercises as needed it decreases sympathetic response and decreases stress.
6. Encourage use of cognitive behavioral relaxation (e.g., music therapy, guided imagery).
7. Provide intravenous fluids to the patient to increase the hydration.
8. Administer anti-anxiety medications as ordered.
9. Be realistic and positive during treatments, in health teaching, and in setting goals within
limitations.
10. Encourage patient to make choices and participate in planning of care.
11. Provide calm and non-threatening environment helps to relax the patient.
12. Help the patient to practice coping strategies such as progressive muscle relaxation technique,
meditation or guided imagery.
13. Assist the patient to eat and drink as necessary.
14. Administer required medication, e.g., analgesics or sedative and promotes relaxation.
15. Provide warm, non-caffeinated fluids after 6 pm, limit fluids after 8:00 pm.
16. Increase exercise and activity during day as appropriate for the patient's condition.
17. Administer or assist with oral hygiene after each meal and before bedtime.
18. Encourage the family members to stay with patient.
19. When appropriate, discuss reasons for sleep pattern disturbances.
20. Assist the patient to bathroom or bedside commode.
21. Place the patient in preferred sleeping position, support position with pillows.
PATIENT EDUCATION AND HEALTH MAINTENANCE
1. Educate family members about sign and symptoms of gigantism and acromegaly.
2. Instruct patient to meet with other patients who have gigantism or acromegaly.
3. Instruct patent to avoid activities which increase intracranial pressure, such as coughing, sneezing
and blowing.
4. Instruct family members to give emotional or psychological support to patient.
5. Administer medicines as ordered by physician.
6. Instruct patient to maintain oral hygiene.
EVALUATION: EXPECTED OUTCOMES
1. Body image is improved.
2. Coping is enhanced.
3. Sleeping pattern is maintained.
4. Fluid volume is maintained.
5. Anxiety is reduced.
PITUITARY TUMOR (PT)
Pituitary Tumor (PT) is a non-cancerous abnormal growth that develops in the pituitary
gland. It is located at the base of the brain which secretes an excess amount of ACTH, which in turn
stimulates the adrenal glands to make more cortisol. Some pituitary tumors cause excessive
production of hormones that regulate important functions of the body. Other pituitary tumors restrict
normal functions of pituitary gland causing it to produce lower levels of hormones.
 Pituitary tumors represent various cell types symptoms reflect tumor effects on target tissue
or on local structures surrounding the pituitary gland. Almost, all pituitary tumors are benign
glandular tumors called pituitary adenomas.
Stages of Pituitary Tumors
Stage 0: Pituitary gland appears normal in this stage.
Stage 1: Microadenoma enclosed with Sella turcica.
Stage 2: Macroadenoma enclosed with Sella turcica.
Stage 3: Tumor invades into Sella turcica locally in one place.
Stage 4: Tumor invades into Sella turcica. It diffuses in more than one phase.
TYPES OF PITUITARY TUMORS
1. Growth hormone-secreting tumors: Acromegaly is a rare disorder which is caused by a non-
cancerous tumor in the pituitary gland. This condition often requires surgery as the first line of
treatment.
2. Adrenocorticotropic hormone-secreting tumors: Cushing's syndrome is caused when the
pituitary gland produces too much adrenocorticotropic hormone. The pituitary gland can cause this
condition.
3. Prolactinoma: The most common secretory tumor is prolactinoma. It produces too much
prolactin. It can be treated with medications.
4. Non-secreting tumors: These tumors do not secrete hormones but can cause health problems
because of their size and location.

ETIOLOGY
1. As with most brain tumors, the cause of pituitary tumors is unknown.
2. Some conditions may make person more likely to get pituitary tumors such as:
a. Isolated familial acromegaly.
b. Familial isolated pituitary adenoma.
c. Multiple endocrine neoplasia type 1 and type 2.
RISK FACTORS
Family history of hereditary conditions such as:
1. Families with MEN type 1 have increased risk of pituitary tumor.
2. Familial acromegaly.
3. Carney complex: It is a rare genetic condition which can increase the risk of pituitary tumor.
PATHOPHYSIOLOGY
1. Pituitary tumors are benign tumors arise from one of the five cell types which comprise the
anterior pituitary, i.e.:
 a. Lactotrophs
b. Gonadotrophs
c. Corticotrophs
2. Malignancy is rare in pituitary tumors. 99% of pituitary tumors are benign.
3. Pituitary tumors development is monoclonal process with several contributing factors. Monoclonal
nature of most pituitary tumors suggests that they arise from mutate pituitary cells.
4. Pituitary tumor may hypersecrete hormones or may be non-functional.
5. They are characterized by size and by what hormones, if any are secreted.
a. Size:
i. Microadenoma: Less than 10 mm wide.
ii. Macroadenoma: Greater than 10 mm wide.
b. Functional status:
i. Hormone secreting: Exaggerated hormone activity may secrete multiple hormones.
ii. Non-secreting: Usually, diminished hormone activity.
6. Pituitary tumors are usually macroadenomas with self secreting TSH.
7. It can occur in every age group but its incidence tends to increase with age.
8. Pituitary Transforming Gene-1 (PTTG-1) is a newly disordered oncogene. It serves as a marker of
malignancy grades in several endocrine malignancies. It is known to regulate the cellular mitosis
process.

CLINICAL MANIFESTATIONS
Manifestations of pituitary tumors are caused either by direct pressure from the tumor itself or by a
change in the normal hormone levels. As the tumor grows, it puts pressure on the optic nerve and this
often causes headaches and sight problems.
1. Mass effects:
a. Headache
b. Nausea and vomiting (in some cases).
c. Impairment of cranial nerves II, III, V and VI on testing.
2. ACTH-secreting tumors: Over production of ACTH can produce a number of symptoms
including:
a. Fat accumulation around midsection and upper back.
b. Thinning of arms and legs with muscle weakness.
c. Bone weakening.
d. Increased facial hair in women and mental changes, such as depression.
3. Growth hormones-secreting tumors:
 a. Excess production of growth hormones can cause
a condition known as gigantism.
b. Enlargement of hands and feet
c. Joint pain.
d. Increased body hairs
e. Misaligned teeth
f. Heart problems.
4. Prolactin secreting tumors:
a. In women:
i. Irregular menstrual periods.
ii. Lack of menstrual periods.
iii. Milky discharge from breasts.
b. In men:
i. Breast growth
ii. Loss of sex drive.
iii. Lowered sperm count.
5. Thyroid stimulating hormone-secreting tumors:
a. Frequent bowel movements.
b. Excessive sweating.
c. Weight loss.
d. Rapid or irregular heartbeat.
6. Anterior pituitary tumors: Tumors which secrete FSH and LH are very rare and are likely to
cause Infertility.
7. Posterior pituitary tumors:
a. In posterior pituitary, tumors are very rare.
b. Disturbance in this area is more likely to be caused by pressure being applied to the area
from the surrounding tissues.
c. Diabetes insipidus is the most common problem of the posterior pituitary tumors.
DIAGNOSTIC EVALUATION
1. Medical history or physical examination.
2. Blood and urine test: Performed to determine overproduction or deficiency of hormones.
3. Neurological examination: It helps to determine how brain, spinal cord and nerves are working.
4. CT and MRI: Helps to observe the location and size of pituitary tumors.
5. Vision testing: This test can determine if a pituitary tumor has impaired patient's sight or
peripheral vision.
MANAGEMENT
MEDICAL MANAGEMENT
Prolactin Secreting Tumors: Some prolactin secreting tumors can be treated with a drug treatment,
such as cabergoline and parlodel.
1. It helps to decrease prolactin secretion.
2. It also reduces the size of tumor.
ACTH-Secreting Tumors: Mifepristone is recommended to patient with Cushing's syndrome who
has type 2 diabetes mellitus or glucose tolerance.
Growth Hormone-Secreting Tumors: Octreotide (sandostatin) and lanreotide (somatuline depot).
1. It causes a decrease in growth production.
2. It may also shrink the tumor.
Radiotherapy
1. It uses a high energy X-rays to destroy abnormal cells.
2. It is an effective and safe form of treatment.
SURGICAL MANAGEMENT
CRANIOTOMY (TRANSCRANIAL APPROACH)
1. During this surgical procedure, incision is made into patient's scalp.
2. Pituitary tumor is removed through patient's upper part of the skull.
3. This procedure is helpful to reach large or more complicated tumors.
1. In this procedure, pituitary tumor is removed through nose and sinuses without an external
incision.
2. It is not useful to remove large sized tumors especially, if a tumor has invaded nearby nerves or
brain tissue.
3. Generally, it is very well tolerated procedure because of its minimally invasive characteristics, few
side effects and quick patient recovery.
NURSING MANAGEMENT
1. A nurse should teach patient the nature of hormonal deficiencies after treatment and the purpose of
replacement therapy.
2. Instruct patient or significant others about the early signs and symptoms of cortisol or thyroid
hormone deficiency or excess and the need to report them.
3. Assess the level of pain, its location and intensity.
4. Perform thorough neurologic examination and general physical examination to identify signs of
hormone deficiency or excess.
5. Prepare patient for surgery or other treatment by describing nursing care thoroughly.
6. Importance of skin care should be explained to patient or his/her family members.
7. Provide emotional support through diagnostic process and answer questions about treatment
options.
8. Caring for a patient after resection of pituitary tumor:
a. Continually, assess patient's neurological status.
b. Monitor and record vital signs.
c. Monitor ICP and cerebral perfusion pressure.
d. Administer mannitol as ordered.
9. Observe patient for frequent swallowing and ask if he/she has a salty task in mouth.
10. If patients urine output is greater than 250 ml/hour for three consecutive hours, notify the
physician.
11. Encourage patient for oral fluids and prevent I/V fluids also.
12. Maintain a calm and clean environment around the patient.
13. Encourage patient in assuming active role in self-care through information seeking and problem
solving.
14. Teach patient about the need for frequent initial follow-up visits.
COMPLICATIONS
1. Menstruation ceases and infertility occurs almost always after total or nearly total ablation.
2. Hypothyroidism and adrenocortical insufficiency after ablation.
NURSING CARE PLAN
NURSING ASSESSMENT
1. Monitor vital signs.
2. Monitor for pain at least every 2 hourly and ask the
3. Assess the thinking process (Determine orientation to patient to rank pain on scale of 0-10 at
episode of pain, place, person, or time) to get the information regarding the extent of interference
with sensory processing.
NURSING DIAGNOSIS
1. Acute pain related to biological injuries.
2. Risk for injury related to sensory dysfunction.
3. Risk of disturbed thought process related to physiological changes, such as CNS stimulation.
4. Anxiety related to changes in health status and a threat to self-concept.
PLANNING
NURSING GOALS
1. To reduce pain.
2. To reduce risk of injury.
3. To reduce risk of disturbed thought process.
4. To reduce anxiety.
NURSING INTERVENTIONS
1. Monitor for pain at least every 2 hourly and ask the patient to rank pain on scale of 0-10 at episode
of pain.
2. Discuss with the patient about intensity, severity, tolerance and precipitating factors of pain.
3. Promotes relaxation by decreasing the sensory stimuli.
4. Provide calm and quite environment.
5. Monitor sleep-rest pattern.
6. Promote rest period during day and at least 8 hours sleep each night.
7. Provide ROM exercises at least every 4 hourly.
8. Administer pain medication as ordered to reduce pain response.
9. Keep side rails raised and padded, bed in a low position, and airway at the bedside to reduce the
potential for injury, if seizures occur.
10. Assess the level of anxiety as it may alter thought processes.
11. Reorient to person, place, or time as indicated to maintain awareness of reality and environment.
12. Encourage visits by family and relatives for maintaining socialization and orientation.
13. Administer medication as prescribed to promote relaxation and reduces CNS hyperactivity.
14. Encourage the patient to verbalize his/her problem.
15. Assist the patient to learn to recognize and identify the symptoms of anxiety. bed ads to
16. Help the patient to practice coping strategies such as progressive muscle relaxation technique,
meditation or guided imagery. These methods are successful to decrease anxiety.
17. Administer anti-anxiety medications as ordered. Medication helps to reduce anxiety.
18. Provide emotional and psychological support to patient
19. Provide calm and non-threatening environment.
20. Encourage patient's family members to stay with patient.
PATIENT EDUCATION AND HEALTH MAINTENANCE
1. Instruct patient to avoid smoking and drinking excessive amount of alcohol.
2. Encourage patient to get plenty of sleep and relax often to prevent fatigue.
3. Instruct patient to eat slowly at frequent intervals.
4. Advice patient to drink a glass of warm water 30 mins before breakfast and gently massage lower
abdomen which reduces the risk of constipation.
5. Avoid activities that may cause increase in intracranial pressure particularly during the first month
after surgery.
6. If applicable, advice patient about the need for post-surgery radiation therapy.
7. Help patient to identify sources of information and support available in the community.
8. Advice patient to wear Medic Alert Bracelet.
9. Teach patient about the need for frequent initial follow-up visits and lifelong medical management
when on hormonal therapy.
10. Teach patient to notify health care provider, if signs of thyroid or cortisol imbalance become
evident.
EVALUATION: EXPECTED OUTCOMES
1. Pain is reduced.
2. Risk of injury is reduced.
3. Risk of disturbed thought process is reduced.
4. Anxiety is reduced.