ENDOCRINE SYSTEM

INTRODUCTON

The term endocrine is derived from the Greek word “endo”, meaning “within” and “crino” to
“separate”. This implies that cells of endocrine glands secrete chemical signals that influence
tissues that are separated from the endocrine glands by some distance.

The endocrine system is composed of glands that secrete chemical signals into the circulatory
system. In contrast, exocrine glands have ducts that carry their secretions to surfaces.

FUNCTION

1. Metabolism and tissue maturation: The endocrine system regulates the rate of
metabolism and influences the maturation of tissues such as those of the nervous system.
2. Water balance: The endocrine system regulates water balance by controlling the solute
concentration of the blood
3. Control blood glucose and other nutrients
4. Control of reproductive function
5. Uterine contractions and milk release
6. Iron regulation: The endocrine system regulates blood ph as well as calcium
concentration in the blood.

DIAGRAM

PITUITARY GLAND AND HYPOTHALAMUS

The pituitary gland or hypophysis secretes nine major hormones that regulate numerous body
functions and the secretory activity of several other endocrine glands.

The hypothalamus and pituitary gland are major sites where the nervous and endocrine systems
interact. The hypothalamus regulates the secretory activity of the pituitary gland

The pituitary gland is located inferiorly to the hypothalamus and it is connected to it by a stalk of
tissue called the infundibulum. The pituitary gland is divided into 2 parts:

 Posterior pituitary or neurohypophysis

 Anterior pituitary or adenohypophysis

Several major hormones are released from the hypothalamus. For instance

 Growth hormone – releasing hormone (GHRH)

 Growth hormone – inhibiting hormone (GHIH)
  Thyroid releasing hormone (TRH) that stimulates the secretion of thyroid stimulating
hormone from the anterior pituitary gland
 Corticotropin releasing hormone (CRH) that stimulates adrenocorticotropic hormone
from the anterior pituitary gland
 Gonadotropin releasing hormone (GnRH) the stimulates Luteinizing hormone (LH) and
Follicle stimulating hormone from the anterior pituitary gland
 Prolactin releasing hormone (PRH) and prolactin inhibiting hormone (PIH) regulates the
secretion of prolactin from the anterior pituitary gland

HORMONES OF THE HYPOTHALAMUS

Hormones Target tissues Response

Growth hormone releasing Anterior pituitary cells that Increase growth hormone
hormone (GHRH) secrete growth hormones secretion
Growth hormone inhibiting Anterior pituitary cells that Decrease growth hormone
hormone (GHIH) or secrete growth hormones secretion
somatostatin
Thyroid releasing hormone Anterior pituitary cells that Increased thyroid stimulating
(TRH) secrete thyroid stimulating hormone secretion
hormone
Corticotropin releasing anterior pituitary cells that Increase adrenocorticotropic
hormone (CRH) secrete adrenocorticotropic hormone secretion
hormone
Gonadotropin releasing Anterior pituitary cells that Increased secretion of LH and
hormone (GnRH) secrete luteinizing hormone FSH
and follicle stimulating
hormone
Prolactin inhibiting hormone Anterior pituitary cells that Decrease prolactin secretion
(PIH) secrete prolactin

Posterior Pituitary Hormones

The posterior pituitary stores and secretes two neuro – hormones called antidiuretic hormone and
oxytocin.

Anterior Pituitary Hormones

Releasing and inhibiting hormones that pass from the hypothalamus to the anterior pituitary
influence anterior pituitary secretion.

Hormones of the Pituitary Gland

Hormones Target tissue Response
Posterior pituitary

Antidiuretic hormone (ADH) Kidney Increased water reabsorption

(less water is lost in the form
of urine)
Oxytocin Uterus, mammary gland Increased uterine contractions;
increased milk expulsion from
mammary gland: unclear
function in male
Anterior pituitary

Growth hormone (GH) Most tissues Increased growth in tissues

somatotropin
Thyroid stimulating hormone Thyroid gland Increased thyroid hormone
(TSH) secretion
Adrenocorticotropic hormone Adrenal cortex Increased glucocorticoid
(ACTH) hormones secretion
Melanocyte stimulating Melanocyte in the skin Increased melanin production
hormone (MSH) to darken the skin colour
Luteinizing hormone (LH) Ovaries in females, testes in Ovulation and progesterone
males production in ovaries,
testosterone production and
support for sperm cells
production in the testes
Follicle stimulating hormone Follicles in ovaries in females, Follicle maturation and
(FSH) seminiferous tubes in males estrogen secretion in ovaries,
sperm cell production in males
Prolactin Ovaries and mammary glands Milk production in lactating
in females women, unclear function in
males.

Thyroid Gland
The thyroid gland is composed of two lobes connected by a narrow band of thyroid tissue called
the isthmus. It is one of the largest endocrine glands and it is highly vascular and appears more
red than the surrounding tissues.

The thyroid hormones include both triiodothyronine(T3) and tetraiodothyronine (T4) or

thyroxine and calcitonin

Hormones Target tissue Response

Triiodothyronine and Most cells of the body Increased metabolic rate;
tetraiodothyronine essential for normal process of
growth and maturation
Calcitonin Bone Decreased rate of breakdown
of bone by osteoclasts;
prevention of a large increase
in blood calcium level.

Parathyriod Gland
The parathyroid glands are usually embedded in the posterior part of each lobe of the thyroid
gland. Four parathyroid glands exist.

The parathyroid gland secretes parathyroid hormone (PTH) that is important in the regulation of
calcium level in body fluid. The bone, kidneys and the intestines are the major target tissues.

PTH stimulates osteoclast activity in bone and can cause the number of osteoclast to increase.
The increased osteoclast activity results in bone resorption and the release of calcium causing an
increase in blood calcium level.

PTH induces calcium reabsorption within the kidneys so that less calcium leaves the body in
urine.

Adrenal Glands
The adrenal gland called suprarenal gland is near the superior poles of the kidneys.

Hormones secreted by the adrenal medulla are;

 Epinephrine (adrenaline)
 Norepinephrine (noradrenaline)

Hormones Target tissue Response

Adrenal medulla  Increased cardiac
output, increased blood
Epinephrine and Heart, blood vessels, liver, fat flow to skeletal
norepinephrine cells muscles and increased
blood flow to heart
 Increased blood flow
to the heart
 Increased release of
glucose and fatty acids
into blood
 Preparation for
physical activity
Adrenal cortex  Increased protein and
fat breakdown
Cortisol (glucocorticoids) Most tissues  Increased glucose
production
 Inhibition of immune
response

Aldosterone Kidney Increased sodium reabsorption

(mineralocorticoid) and potassium and hydrogen
secretion
Sex steroids (primary Many tissues  In females, it helps in
androgens) the development of
some secondary sexual
characteristics such as
axillary and pubic hair
 Sexual characteristics
in males

Pancreas
The pancreas lies behind the peritoneum between the greater curvature of the stomach and the
duodenum.

The pancreas is both an exocrine and an endocrine gland. The exocrine portion produces
pancreatic juice into the small intestines. The endocrine part which produces hormone that enter
the circulating system. The endocrine part secrets glucagon and insulin.

Pancreatic Hormones
Hormones Target tissue Response
Insulin Liver, skeletal muscle, fat Increase uptake and use of
tissue glucose
Glucagon Liver Increased breakdown of
glycogen
Release of glucose into the
circulatory system
Somatostatin Alpha and beta cells Inhibition of insulin and
glucagon secretion.

Hormones of the reproductive system

Reproductive hormones are secreted primarily from the ovaries, testes, placenta and pituitary
gland. The main endocrine glands of the male reproductive system are the testes. The function of
the testes depends on the secretion of FSH and LH from the anterior pituitary gland.
The main endocrine glands of the female reproductive system are the ovaries. Like the testes, the
function of the ovaries depend on the secretion of FSH and LH from the anterior pituitary gland.
The main hormones secreted by the ovaries are estrogen and progesterone.

Hormones of the Reproductive Organs

Hormones Target tissue Response
Testes  Aid in spermatogenesis
 Maintenance of
Testosterone Most cells functional reproductive
organs
 Secondary sex
characteristics
 Sexual behaviour
Ovaries  Uterine and mammary
gland development and
Estrogen Most cells function
 External genitalia
structures
 Secondary
characteristics
 Menstrual cycle
Progesterone Most cells Same as for estrogen
Relaxin Connective tissue cells Increased flexibility of
connective tissue in the pelvic
area especially the symphysis
pubis

ENDOCRINE DISORDERS
Introduction
The levels of many of the hormones in the body is regulated by negative feedback mechanisms.
Most endocrine disorders fall into one of the four categories:

 Too little hormone (hyposecretion)

 Hypersecretion
 Reduced response of the target cells (hyporesponsiveness)
 Hyperresponsiveness
PIYUITARY DISORDERS
1. Hypopituitarism:

Definition

It is a complex syndrome marked by metabolic dysfunction, sexual immaturity and growth

retardation. It results from a deficiency of the hormones secreted by the anterior pituitary gland.

Hormones produce at the anterior pituitary are corticotrophin, thyroid stimulating hormone,
luteinizing hormone, follicle stimulating hormone, growth hormone and prolactin.

Causes:

Primary hypopituitarism

 the most common cause is a tumor’

 congenital defects (hypoplasia of the pituitary gland)
 pituitary infarction ( most often from post partum haemorrhage)
 partial or total hypophysectomy
 radiation of chemical agents
 rarely, granulomatous diseases such as tuberculosis

Secondary hypopituitarism results from:

 deficiency of releasing hormones produced by the hypothalamus, the process maybe

idiopathic or may result from infection, trauma or tumor

Clinical manifestation:

For children:

 growth retardation
 delayed secondary tooth eruption
 delayed puberty
 wrinkles near the mouth and eyes of adults

For women

 amenorrhea
 dysparemia related to reduced vagina secretion
 infertility
 reduced libido
 breast atrophy
  absent axillary and pubic hair
 dry skin

For men

 weakness
 impotence
 reduced libido
 decreased muscle strength
 cold intolerance
 constipation
 increased or decreased menstrual flow
 nausea
 vomiting
 fatigue
 anorexia
 weight loss
 depigmentation of the skin and nipples
 absent postpartum lactation
 amenorrhea
 absent growth of pubic and axillary hair

Diagnostic test

 radioimmunoassay showing decreased plasma level of some or all pituitary glands

 gonadotropin releasing hormone administered intravenously can distinguish between
pituitary and hypothalamic causes of gonadotropin deficiency
 administering a dopamine antagonist such as metoclopramides evaluates prolactin
secretory reserve
 clomiphene, an estrogen antagonist, can also be used to diagnostic agents
 Diagnosis of dwarfism requires measurements of growth hormone levels in the blood
after administration of regular insulin to reduce hypoglycaemia or levodopa which causes
hypotension. These drugs should provoke increased growth hormone secretion.
Persistently low growth hormone levels despite provocative testing, confirming growth
hormone deficiency
 Computed tomography, scans and magnetic resonance imaging confirms the presence of
intracellular or extracellular tumours.

Medical management
 Replacement of hormones normally secreted by the target glands is the most effective
treatment for hypopituitarism.

Hormonal replacement includes cortisol, the most important drugs; thyroxine and androgens
or cyclic estrogen

Prolactin doesn’t need replacement. The patients of reproductive age may benefit from FSH
and human chorionic gonadotropin to boost fertility

Nursing intervention

 Until hormone replacement therapy is completed, monitor the results of all laboratory
tests for hormonal deficiencies
 Monitor patient for anorexia and encourage the patient to maintain adequate calories
intake
 Offer frequent small meals and keep accurate records of weight loss or gain
 Record vital signs every 4 to 8 hours and monitor intake and output
 Check eyelids, nail beds and skin for pallor which indicates anemia
 Provide meticulous skin care and use good hand washing techniques to prevent
infection
 Keep the patient warm if his body temperature is low. Provide extra clothing and
blanket and adjust room temperature if possible
 During insulin testing, monitor closely for signs of hypoglycaemia. Keep dextrose
available for IV administration to control hypoglycaemia rapidly
 To prevent postual hypotension, keep the patients supine during levodopa testing
 Institute safety precautions for patient with impaired visual acuity to decrease the risk
of injury
 Support the family in setting realistic goals for the child based on his age and abilities
 Provide strong emotional support for the patient who’s coping with changes in body
appearance and sexual functioning
 Encourage verbalization of feelings and discuss fear of rejection by others
 Provide a positive realistic assessment of the patient’s situation. Encourage him to
develop interests that support a positive self image
 Refer the family for psychological counselling or to appropriate community
resources. Emotional stress increases as the child becomes alder and more aware of
his condition.

Patients teaching

 Teach the patient and his family about the limitations imposed by the disease
 Review the treatment regimen with the patient and family especially long term hormonal
replacement therapy
  Discuss the importance of taking the medications as ordered and of keeping regular
follow up appointments for blood studies
 If the patient needs growth hormone replacement, teach him and his family how to
perform subcutaneous injection
 Teach the patient and his family measures to conserve the patient’s energy, manage
stressful situations and prevent infections. Stress the importance of adequate rest to avoid
fatigue, a balanced diet with adequate calories and fluids, good personal hygiene and
hand washing techniques
 Emphasize the importance of identifying and reporting emergency situations. If
necessary, teach the family to administer steroids parenterally

2. Diabetes Insipidus:

Definition

It refers to a deficiency of vasopressin (antidiuretic hormone) causing excessive thirst and the
production of large volume of urine.

Causes

The most common cause of diabetes insipidus is failure of vasopressin secretion in response to
normal physiological stimuli

A less common cause is failure of the kidneys to respond to vasopressin (congenital nephrogenic
diabetes insipidus).

Pathophysiology

Normally, vasopressin is synthesized in the hypothalamus and then stored by the posterior
pituitary gland. Once released into the general circulation, vasopressin acts on the distal and
collecting tubules of the kidneys, increasing their water permeability and causing reabsorption.
The absence of vasopressin in diabetes insipidus allows the filtered water to be excreted in urine
instead of being reabsorbed and results in the passage of large quantities of diluted fluid
throughout the body.

Types

They are two types of diabetes insipidus which are primary and secondary diabetes insipidus.

Primary pituitary diabetes insipidus is idiopathic in origin. The primary form may occur in
neonates as a result of congenital malformations of the central nervous system, infections,
trauma or tumour.
 Secondary pituitary diabetes insipidus results from intracranial neoplastic or metastatic
lesions, hypophysectory or other types of neurosurgery, a skull fracture or head trauma. It
may also result from infection.

A transient form of diabetes insipidus also occurs during pregnancy usually after the fifth or
sixth month of gestation. The condition usually spontaneously reverse after delivery.

Clinical manifestation

 Polyuria (4 to 16 liters/day)
 Extremely thirst
 Consumption of extraordinary large volumes of fluid
 Weight loss
 Dizziness
 Weakness
 Constipation
 Slight or moderate nocturia
 Fatigue from inadequate rest caused by frequent voiding and excessive thirst.

In children

 Sleep disturbance
 Irritability
 Anorexia
 Decreased weight gain
 Dehydration
 Fever
 Dyspnea
 Tarchy cardia
 Decreased muscle strength

Diagnostic test

 Urinalysis reveals almost colorless urine of low osmolarity

 Dehydration test
 Plasma or urinary vasopressin evaluation may be performed after fluid restriction

Medical management

Until the cause of the disease is identified and eliminated, administration of various forms of
vasopressin can control fluid balance and prevent dehydration.
  Aqueous vasopressin is a replacement agent administered by SC injection in dosed of 5 to
10 units. The duration of action is 3 to 6 hours
 Desmopressin acetate, a synthetic vasopressin analogue, affects prolonged antidiuretic
activity and has no pressor effects. It is given intranasal in doses of 10 to 25mg or
subcutaneously in doses of 1 to 2mg. Duration of action is 12 to 24 hours making it’s a
drug of choice
 Lypressin is a synthetic vasopressin replacement that gives as a short – acting nasal
spray. It has significant disadvantages including nasal congestion and irritations and
ulceration nasal passage

Nursing interventions

 Make sure that you keep accurate records of the patient’s hourly fluid intake and urine
output, vital sign and daily weight.
 Closely monitor the patient’s urine specific gravity. Also monitor his serum electrolyte
and blood urea nitrogen levels.
 During dehydration testing, watch the patient for signs of hypovolemic shock
 Monitor his vital signs and watch for changes in mental or neurologic status
 If the patient has any complains of dizziness or muscle weakness, institute safety
precautions to help prevent injury
 Make sure that the patient has easy access to the bathroom or bedpan
 Provide skin and mouth care. Use a soft toothbrush to avoid trauma to the oral mucosa. If
the patient has cracked lips, apply petroleum jelly
 Use caution when administering vasopressin to a patient with coronary artery disease
because the drug may cause coronary artery constriction
 Urge patient to verbalize his feelings and offer encouragement

Patient teaching

 Before the dehydration test, tell the patient to take nothing by mouth until the test is over
and explain the need for hourly urine tests, vital signs and weight check
 Educate the patient on the signs of severe dehydration
 Educate patient to record his weight daily and also how to monitor intake and output
 Encourage the patient to maintain fluid intake during the day to prevent severe
dehydration but limits fluid in the evening to prevent nocturia
 Educate patient and family about long term replacements therapy
 Educate patient to take medication as prescribed and to avoid abrupt discontinuation
without the doctor’s order. Teach them how to give SC or IM injections and how to use
nasal applications

3. Hyperpituitarism
 Definition
It is a chronic, progressive disease marked by hormonal dysfunction and skeletal
overgrowth

Causes
 Tumors of the anterior pituitary gland
 Genetically hyperpituitarism can also occur

Clinical manifestation

 Hypertrophy of the face and extremities

 Diaphoresis
 Fatigue
 Heat intolerance
 Weight gain
 Headache
 Decreased vision
 Decreased libido
 Impotence
 Oligomenorrhea
 Infertility
 Joint pain
 Sleep disturbance

Diagnostic test

 Growth hormone radioimmunoassay shows increased plasma growth hormone levels

 Glucose suppression test offers more reliable information. Glucose normally suppreses
growth hormone secretion. Therefore, a glucose infusion that fails to supress the
hormone level to below the accepted norm of 5mg suggests hyperpituitarism
 Skull x – ray, computed tomography scan and magnetic resonance imaging may help
locate the pituitary tumor
 Bone x – ray show a thickening of the cranium and of the long bone
Medical management

The aim of the treatment is to stop over production of growth hormones by removing the
underlying tumor

Nursing intervention

 Provide emotional support to help the patient cope with an altered body image
 Encourage him to verbalize his feelings and discuss fear of rejection by others
 Provide a positive but realistic assessment of his situation
 Encourage him to develop other interest that support a positive self image
 Be sensitive to any mood changes that patient may experience. Reassure him and his
family that these changes result from hormonal imbalances caused by the disease and can
be lessened with treatments
 Administer analgesics in case of arthritis of the hand or osteoarthritis of the spine
 Evaluate muscle weakness
 Provide adequate skin care
 Monitor glucose level and observe for signs of hyperglycaemia.

THYROID DISORDERS

1. Hypothyroidism
Definition
It refers to a deficiency of the thyroid hormones T3 or T4. It is classified as primary or
secondary. Primary hypothyroidism stems from a disorder of the thyroid gland itself.
Secondary hypothyroidism is caused by a failure to stimulate normal thyroid function or
by a failure of target tissues to respond to normal blood levels of thyroid hormone
Causes
It results from a variety of abnormalities that lead to insufficient synthesis of thyroid
hormones.
 Thyroid gland surgery (thyroidectomy)
 Chronic autoimmune thyroiditis
  Inflammatory conditions such as sarcoidosis ( it is chronic disorders f unknown
cause in which the lymph nodes in many parts of the body are enlarged and
granulomas develop in the lungs, liver and spleen)
 Failure from the pituitary to produce thyroid stimulating hormone
 Failure of the hypothalamus to produce thyroid releasing hormone
 Inborn errors of thyroid hormone synthesis
 Inability to synthesize thyroid hormones because of iodine deficiency
 The use of antithyroid medications such as propylthiouracil.

Clinical manifestation

 Fatigue
 Forgetfulness
 Sensitive to cold
 Unexplained weight gain
 Anorexia
 Decreased libido
 Joint stiffness
 Muscle cramping
 Dry skin
 Puffy face, hands and feet
 Hair loss
 Weak pulse
 Brady cardia
 Muscle weakness
 Hypotension’
 Abdominal distension

Diagnostic test

 Radioimmunoassay with radioactive iodine shows low serum levels of thyroid hormones.
  Serum TSH levels determine the primary or secondary nature of the disorders. An
increase serum TSH level with thpothyriodism is due to thyroid insufficiency; a
decreased TSH level is due to hypothalamic or pituitary insufficiency
 Serum antithyriod antibodies are elevated in autoimmune thyroiditis
 Radioisotope scanning of the thyroid tissues identifies ectopic thyroid tissue
 Skull x – ray, CT scan and MRI helps locate pituitary or hypothalamic lesions that may
be the underlying cause of hypothyroidism.

Treatment or medical management

The recommended treatment consist of gradual thyroid hormone replacement with synthetic
hormone. Synthetic hormone includes leuothyrioxine (T4), liothyronine (T3), liotrix ( T3 and
T4) and thyroglobulin (T3 and T4). Treatment begins slowly especially in the elderly patients to
avoid adverse cardiovascular effects. The dosage increases every 2 to 3 weeks until the desire
response is obtained.

Rapid treatment may be necessary for patients to undergo emergency surgery (because of
sensitivity to CNS depression)

In underdeveloped areas, prophylactic iodine supplement have successfully decreased the

incidence of iodine deficient goiter

Nursing intervention

 Routinely monitor and keep accurate records of the patient’s vital signs, fluid intake,
urine output and daily weight.
 Monitor patient’s cardiovascular status
 Watch closely for chest pain or dyspnea
 Provide rest periods and gradually increase activity to avoid fatigue and to decrease
myocardial oxygen demand
 Encourage the patient to cough and breath deeply to prevent pulmonary complications
 Maintain fluid restriction and low salt diet
 Check for abdominal distension and monitor the frequency of bowel movement
  Provide the patient with a high bulk, low calorie diet and encourage activity to combat
constipation and promote weight loss.
 Monitor mental and neurologic status. Observe the patient for disorientation, decreased
level of consciousness and hearing loss
 Provide meticulous skin care
 Turn and reposition the patient every 2hours if he/she is on extended bed rest
 Provide extra clothing and blankets for a patient with decreased cold tolerance. Also
adjust room temperature if possible
 During thyroid replacement therapy, watch for symptoms of hyperthyroidism such as
restlessness, sweating and excessive weight loss
 Encourage patient to verbalize his feelings and fears about changes in body image and
possible rejection by others

Patient teaching

 Help the patient and his family understand the patient’s physical and mental changes
 Stress the importance of obtaining prompt medical care for respiratory problems and
chest pain
 Teach the patient and family about long term hormone replacement therapy. Emphasize
that the patient needs lifelong administration and that she should take as prescribed
 Advise the patient and family to keep accurate records of daily weight
 Educate the patient to eat well balanced diet that is high in fibre and fluids to prevent
constipation, to restrict sodium to prevent fluid retention and to limit calories to minimize
weight loss
 Educate the patient to schedule activity to avoid fatigue and to get adequate rest.
2. Hyperthyroidism

Definition

It refers to the over production of thyroid hormone resulting from metabolic imbalances. It is
also called thyrotoxicosis.

Causes
  In Grave’s disease, thyroid stimulating antibodies bind to and then stimulate the
thyroid stimulating hormone receptors of the thyroid gland

Many experts believe that Grave’s disease is the result of genetic and immunologic factors. The
disease increases incidence among monozygotic twins points to an inherited factor, probably
with a polygenic inheritance pattern.

Clinical manifestations

The patient’s history may disclose that the onset of symptoms followed a period of acute
physical or emotional stress.

 Nervousness
 Heat intolerance
 Weight loss despite increased appetite
 Excessive sweating
 Diarrhoea
 Tremors and palpitation
 Difficulty concentrating
 Trouble climbing stairs
 Dyspnea
 Anorexia
 Nausea and vomiting
 Menstrual abnormalities
 Hair loss
 Mood swings
 Muscle atrophy
 Conjunctiva and cornea appear reddened
 Strabismus
 The thyroid gland may feel asymmetrical
 Enlarged thyroid gland
 Enlarge liver or hepatomegaly
  Tachycardia
 Increase bowel sounds

Diagnostic tests

 Radioimmunoassay shows increased serum T3 and T4 concentrations

 Thyroid scan reveals increased uptake of radioactive iodine (131I). This test is
contraindicated to pregnant women
 Thyrotropin releasing hormone (TRH) stimulation test helps confirm a diagnosis of
hyperthyroidism if the TSH level fails to rise within 30mins after administration of TRH

Medical management

Treatment of hyperthyroidism consist of drugs, radioiodine and surgery

Antithyriod drugs therapy is used for children, young adults, pregnant women and patients who
refuse surgery or radioiodine treatments. Thyroid hormone antagonist include propylthiouracil
(PTU) and methimazole which blocks thyroid hormone synthesis.

Treatment with iodine (131I) consist of a single oral dose and is the treatment of choice for women
past reproductive age or men and women not planning to have children. Patients of reproductive
age must give informed consent for this treatment because small amounts of iodine concentration
in the gonads. During treatment, the thyroid gland picks up the radioactive elements as it would
regulate iodine. Subsequently, the radioactivity destroys some of the cells that normally
concentrate iodine and produce thyroxine, thus decreasing thyroid hormone production and
normalizing thyroid size and function.

Thyroidectomy is indicated for patients under age 40 who have very large goiter and whose
hyperthyroidism has repeated relapsed drug therapy. This surgery removes parts of the thyroid
gland, decreases its size and capacity for hormone production.

Nursing management.

 Keep accurate records of vital signs, weight, fluid intake and urine output
 Measure neck circumference daily to check for progression of thyroid enlargement
  Monitor serum electrolytes level and check for hyperglycaemia and glycosuria
 Monitor signs of heart failure such as dyspnea, jugular vein distension and peripheral
edema
 Minimize physical and emotional stress. Try to balance rest and activity periods. Keep
patient’s room cold and quiet and the lights dim
 Encourage patient to eat a well balanced diet with adequate calories and flluids. Offer
small frequent meals
 Monitor the frequency and characteristics of stool and give antidiarrheal preparations as
ordered
 Provide meticulous skin care to minimize skin breakdown
 Reassure the patient and his family that mood swings and nervousness will probably
subside with treatments
 Encourage patient to verbalize feelings about changes in body image. Help him identify
and develop coping strategies
 Offer emotional support and refer him and his family to a mental health counsellor if
necessary.
 If iodide is part of the treatment, mix it with milk, juice or water to prevent GI distress
and give it through a straw to prevent tooth discoloration
 Monitor the patient taking propranolol for signs of hypertension
 If the patient is taking PTU or methimazole, monitor complete blood counts to detect
leukopenia, thrombocytopenia and agranulocytosis
 Avoid excessive palpation of the thyroid for this can precipitate thyroid storm.

After thyroidectomy

 Check often for respiratory distress and keep a tracheotomy tray at the bedside
 Check the dressings for spots of blood which may indicate haemorrhage into the neck.
Change dressings and perform wound care as ordered. Also check the back of the
dressing for drainage. keep the patient in a semi – fowler position and support his head
and neck with sang bags to ease tension on the incision
 Check for dysphagia or hoarseness from possible laryngeal nerve injury
  Watch for signs of hypocalcaemia, a complication that results from accidental removal of
the parathyroid glands during surgery.

Patient teaching

 Stress the importance of regular medical follow up, visits after discharge because
hypothyroidism may develop 2 to 4 weeks postoperatively and after iodine therapy.
 Tell the patient who had iodine therapy not to cough freely because his saliva is
radioactive for 24 hours
 Educate patient taking PTU or methimazole to take these drugs with meals to minimize
GI distress and to avoid over – the – counter cough preparations because many contain
iodine
 Educate patient taking propranolol to rise slowly after sitting or lying down to prevent a
feeling of faintness
 Educate patient on antithyroid drugs to identify and reports symptoms of hypothyroidism.

3. Simple goiter

Definition

It refers to an enlargement of the thyroid gland not caused by inflammation or neoplasm.

It is classified as endemic or sporadic. Endemic goiter usually results from geographically related
nutritional factors such as iodine – depleted soil or iodine deficiency that accompanies
malnutrition.

Sporadic goiter follows ingestion of certain drugs or foods.

Simple goiter is most common in females especially during adolescence, pregnancy and
menopause, when the demand on the body for thyroid hormone increases.

Causes

Simple goiter occurs when the thyroid gland cannot secret enough thyroid hormone to meet
metabolic requirements. As a result, the thyroid mass increases to compensate for inadequate
hormone synthesis.
Endemic goiter usually results from inadequate dietary intake of iodine which leads to
inadequate secretion of thyroid hormone

Sporadic goiter commonly results from ingestion of large amount of goitrogenic food or use of
goitrogenic drugs. Goitrogenic foods contain agents that decrease T4 production. Such foods
include cabbage, pear, soya beans, peanuts, strawberries and spinach. Goitrogenic drugs include
prophylthiouracils, phenylbutazone, cobalt and lithium.

Inherited defects may cause insufficient T4 synthesis or impaired iodine metabolism. Because
families tend to live in one geographic area, this familiar factor may contribute to endemic and
sporadic goiters.

Clinical manifestation

 Respiratory distress
 Dysphagia
 Dizziness
 Enlargement of the thyroid glands at the anterior neck
 Tracheal compression as auscultation

Diagnostic test

 Serum thyroid hormone levels are usually normal. Abnormalities in T3, T4 and TSH
levels rule out this diagnosis
 Thyroid antibody titers are usually normal. Increases indicates chronic thyroiditis
 Iodine uptake is usually normal but may increase in the presence of iodine deficiency
 Urinalysis may show low urinary excretion of iodine
 Radioisotope scanning identifies thyroid neoplasm

Medical management

The goal of treatment is to reduce thyroid hyperplasia.

Exogenous thyroid hormone replacement with leuothyroxine and liothyronine is the treatment of
choice because it inhibits TSH secretion and allows the gland to rest
Small amount of iodide often relieve goiter that results from iodine deficiency.

Sporadic goiter requires avoidance of known goitrogenic drugs and foods

In rare cases of a large goiter unresponsive to treatment, a subtotal thyroidectomy may be

performed to relieve pressures on surrounding structures.

Nursing management

 Measure the patient’s neck circumference daily to check for progressive thyroid gland
enlargement
 Check for the development of hard nodules in the gland which may indicate cancer
 Monitor respiratory status. Help the patient find a position that facilitates breathing and
tell her not to lie supine
 Elevate the head of the bed 90 degrees during meal time and 30mins afterward to
decrease the risk of aspiration. Keep suction equipment available.
 Educate patient to eat soft food which are easy to swallow and ensure that the patient
takes adequate calories
 Provide frequent mouth care and lubricate the patient’s lips to prevent cracks.
 Encourage the patients to verbalize feelings and fears about changes in body image. Offer
emotional support.

Patient teaching

 To maintain constant hormone levels, instruct the patient to take her prescribed thyroid
hormone preparations at the same time each day
 Educate patient and family to identify and report signs of thyroitoxicosis such as
increased pulse rate, palpitation, nausea, vomiting, diarrhea, sweating and shortness of
breath
 Educate the patient with endemic goiter to use iodized salt
 Educate patient who is at risk of simple goiter to avoid goitrogenic foods.

4. Thyroiditis
Definition
It refers to the inflammation of the thyroid gland.

Types of thyroiditis
Hashimoto’s thyroiditis is a common chronic inflammatory disease of the thyroid gland
in which autoimmune factors play a prominent role. It occurs most often in middle aged
women and is the most common cause of sporadic goiter in children.
Subacute thyroiditis is a transient inflammation of the thyroid gland.
Chronic thyroiditis with transient thyrotoxicosis also called silent or painless thyroiditis,
it is self limiting episode of thyrotoxicosis associated with chronic lymphatic thyroiditis.
Pyogenic thyroiditis usually follows pyogenic infection and its relatively uncommon.

Causes
The causes are associated to the different types.
Hashimoto’s thyroiditis is result from lymphocytic infiltration of the thyroid gland and
formation of antibodies to thyroid antigens in the blood.
Subacute thyroiditis is viral and may follow mumps, influenza and adenovirus infections.
The cause of chronic thyroiditis is not known.
Pyogenic thyroiditis results from bacterial invasion of the thyroid gland. The most
common causative microorganisms are staphylococcus aureus, streptococcus hemolyticus
and pneumococcus.

Clinical manifestations
 Fatigue
 Weight gain then weight loss
 Sensitive to cold
 Pain
 Nervousness
 Enlarged thyroid gland
 Reddened skin over the thyroid gland.
Diagnostic test

Precise diagnosis depends on the type of thyroiditis.

 In Hashimoto’s thyroiditis, thyroid failure is evident by a rise in thyroid stimulating

hormone. Histologic confirmation by fine needle biopsy is usually performed.
 In subacute thyroiditis, thyroid hormone levels may be elevated, suppressed or normal
depending on the phase of the disorder.
 In chronic thyroiditis, elevated T3 and T4, decreased iodine uptake, low serum thyroid
antibodies and slightly elevated erythrocyte sedimentation rate are present.

Medical management

Appropriate treatment varies with the type of thyroiditis.

Drug therapy includes leuothyroxine, analgesics and anti – inflammatory drugs for mild subacute
granulomatous thyroiditis.

Propranolol for transient hyperthyroidism and steroids for severe episodes of acute illness

A partial thyroidectomy maybe necessary to relieve tracheal or oesophageal compression

Nursing intervention

 Monitor vital signs, especially respiratory status and help the patient find a position that
facilitates breathing and educate him to avoid lying supine
 Educate patient on nutritious food high in calories especially those the patient can
swallow easily and elevate the head of the bed to 90 degrees during meal tome and for
30minutes afterward to decrease risk of aspiration
 Provide mouth care and lubricate the patient’s lips to prevent cracks
 Keep accurate records of fluid intake and output
 Measure the patient’s neck circumference daily and record progressive enlargement
 If the patient has fever, provide comfort measures and administer antipyretics as ordered
 Encourage the patient to drink plenty of fluid
  Encourage the patient to verbalize his feelings and fears about body image changes and
offer emotional support.

Patient teaching

 Teach the patient and family to identify and report signs of respiratory distress,
hyperthyroidism and hypothyroidism.
 Educate the patient that lifelong hormone replacements therapy is necessary after
thyroidectomy.

PARATHYROID DISORDERS.
1. Hypoparathyroidism

Definition

It refers to a deficiency in parathyroid hormones (PTH) secretion by the parathyroid glands or a

decreased action of PTH in the periphery causes hypoparathyroidism.

Hypoparathyroidism may be acute or chronic and is classified as idiopathic, acquired or

reversible. The idiopathic and reversible forms are common in children and can be corrected by
replacement therapy while the acquired form which is irreversible is most common in older
patients who have undergone thyroid gland surgery.

Causes

Idiopathic hypoparathyroidism may result from an autoimmune genetic disorder or the

congenital absence of the parathyroid glands.

Acquired hypoparathyroidism results from accidental removal or injury to one or more

parathyroid gland during thyroidectomy or other neck surgery

The reversible form amy result from hypomagnesaemia – induced impairment of hormone
secretion, from suppression of normal gland function due to hypocalcaemia or from delayed
maturation of parathyroid gland.

Clinical manifestation
  Tingling in the fingertips, mouth and feet
 Muscle spams
 Pain
 Throat constriction
 Dysphagia
 Difficulty in walking
 Fall easily
 Nausea
 Vomiting
 Abdominal pain
 Constipation or diarrhoea
 Anxiety
 Depression
 Dry skin
 Alopecia
 Brittle hair
 Loss of eyelashes and fingernails
 Decayed teeth from weaken enamel
 Chvostek’s sign
 Trousseau’s sign

Diagnostic test

 Radioimmunoassay for parathyroid hormone shows diminished serum PTH concentration

 Blood and urine tests reveals decreased serum and urine calcium levels, increased serum
phosphate levels (more than 5.4 mg/dl) and reduced urine creatinine levels.
 X – rays indicates greater bone density and malformation

Medical management
Because calcium absorption from the small intestines depends on the presence of activated
vitamin D, treatment initially includes vitamin D with or without supplemental calcium and it’s
usually a lifelong therapy.

If the patient can’t tolerant the pure form of vitamin D, alternatives include dihydrotachysterol if
renal function is adequate and calcitriol if renal function is severely compromised. These
alternatives will only be effective if the patient has adequate PTH.

In the acute form, IV administration of 10% calcium gluconate, 10% calcium chloride to raise
serum calcium level.

Sedative and anticonvulsant may control muscle spams until calcium levels rise

Oral calcium supplements can be given to a patient with the chronic hypoparathyroidsm

Nursing intervention

 Monitor and record vital signs

 Maintain the patient’s IV line including IV calcium gluconate and calcium chloride and
assess the site for irritation
 Monitor serum calcium and phosphorus levels
 Closely monitor the patient receiving both digitalis and calcium because calcium
potentiates the effects of digitalis. Signs of digitalis toxicity include arrhythmias, nausea,
fatigue and visual changes.
 Provide skin care
 Institute safety precautions to minimize the risk of injury from falls. Provide support for
walking
 Encourage patient to verbalize his feelings about body image changes and rejection by
others and offer emotional support.

Patient teaching

 Stress the importance of long term management and follow up care especially periodic
checks of serum calcium levels
 Advise the patient that long term replacement therapy will be necessary
 Educate patient to take medication as ordered and to discontinue its abruptly.
2. Hyperparathyroidism

Definition

It refers to an excessive secretion of parathyroid hormone (PTH)

Causes

It is classified as primary and secondary.

In primary hyperparathyroidism, one or more of the parathyroid gland is enlarges increasing

PTH secretion and elevating serum calcium level. The most common cause is adenoma.
Other causes include a genetic disorder or multiple endocrine neoplasia.

In secondary hyperparathyroidism, there is excessive compensatory production of PTH

stems from a hypocalcaemia - producing abnormalities outside the parathyroid gland which
causes a resistance to the metabolic action of PTH. Some hypocalcaemia – producing
abnormalities are vitamin D deficiency, chronic renal failure or osteomalacia.

Clinical manifestation

 Polyuria
 Chronic low back pain
 Bone tenderness
 Leg pain
 Nausea
 Vomiting
 Anorexia
 Constipation
 Weight loss
 Drowsiness
 Lethargy (mental and physical sluggishness)
 Loss of memory
  Alteration in level of consciousness
 Hypertension.

Diagnostic test

 Serum PTH, ionized calcium and calcium phosphorus determinations are the tests used to
detect hyperparathyroidism
 Radioimmunoassay confirms diagnosis by showing increased concentration of PTH
 X – ray spectrophotometry or other microscopic examinations of the bone demonstrate
increased bone turnover
 CT scan and MRI can help locate parathyroid lesions
 Supportive laboratory test reveal decreased serum phosphorus level and elevated urine
calcium and serum chloride.

Medical management

Primary hyperparathyroidism may be treated by surgical removal of the adenoma.

If surgery is not necessary, other treatments can decrease calcium level and it includes forcing
fluids, limiting dietary intake of calcium, promoting sodium and calcium excretion using
diuresis.

To prevent postoperative magnesium and phosphate deficiencies, the patient receives IV

magnesium and phosphate

Treatment of secondary hyperparathyroidism aims to correct the underlying cause of

hypertrophy and it includes vitamin D therapy. The patient with renal failure requires dialysis.

Nursing intervention

 Record intake and output during hydration to reduce serum calcium level
 Before treatments, obtain baseline serum potassium, calcium, phosphate and magnesium
levels because these values may change abruptly during treatment
 Auscultate the lungs regularly, listening for signs of pulmonary edema in the patient
receiving large amounts of sodium chloride solution
  Take safety precautions to minimize the risk of injury from a fall
 Schedule care to allow the patient with muscle weakness as much rest as possible
 Provide comfort measures to alleviate bone pain
 Monitor signs of peptic ulcer and administer antacids

Patients teaching

 Teach patient and her family to identify and report signs of respiratory distress
 Emphasize the need for periodic blood tests

ADRENAL DISORDERS
1. Adrenal hypofunction

Definition

It refers to a deficiency in the production of adrenal hormones and it is also called adrenal
insufficiency.

It is classified as primary and secondary. Primary adrenal hypofunction originates within the
adrenal gland itself and it’s characterized by decreased mineralocorticoid, glucocorticoid and
androgen secretion.

Secondary adrenal hypofunction originates out of the adrenal gland such as pituitary tumor

Causes

 Massive destruction of the adrenal gland that usually results from an autoimmune process
in which circulating antibodies react specifically against the adrenal tissue
 Other causes include tuberculosis, bilateral adrenalectomy, haemorrhage into the adrenal
gland, neoplasms and infections such as HIV, meningococcal and pneumonia
 Secondary adrenal hypofunction results from glucocorticoid deficiency that stem from
hypopituitarism which can cause decreased corticotrophin secretion.
Clinical manifestation

 Muscle weakness
 Fatigue
 Light headedness
 Weight loss
 Nausea
 Vomiting
 Anorexia
 Chronic diarrhoea
 Anxiety
 Irritability
 Confusion
 Dehydration
 Decreased libido resulting from reduced androgen production
 Amenorrhea
 Decreased axillary and pubic hair
 Abnormal colouration

Diagnostic test

 Plasma and urine steroid testing determine baseline levels

 Measurement of corticotrophin levels allows the classification of the disease as primary
or secondary
 Reduced serum sodium levels
 Increased serum potassium, serum calcium and blood urea nitrogen levels

Medical management

Treatment includes lifelong corticosteroid replacement for primary and secondary adrenal
hypofunction

In general cortisone or hydrocortisone are given

Testosterone injection is given to women with Addison’s disease who have muscle weakness and
decreased libido

Treatment for adrenal crisis is prompt IV administration of 100mg of hydrocortisone followed by

hydrocortisone diluted with dextrose in 0.9% sodium chloride solution given IV

Nursing intervention

 Monitor vital signs carefully especially for hypotension and signs of shock
 Monitor level of consciousness and input and output
 If the patient has diabetes mellitus, check blood glucose levels periodically because
steroid replacement may necessitate adjustment of insulin dosage
 Provide good skin care
 Use protective measures to minimize the risk of infection
 Educate patient to eat food high in protein and carbohydrates
 For women receiving testosterone injections, watch for and report facial hair growth and
other signs of masculinization
2. Cushing syndrome

Definition

It refers to the excess production of mineralocorticoid and androgen

It is classified as primary and secondary

Causes

it results from excess production of corticotrophin and consequent hyperplasia of the

adrenal cortex. Corticotrophin over production may stem from pituitary hyper secretion

Clinical manifestation

 Adiposity of the face, neck and trunk

 Purple striae on the skin
 Fatigue
 Muscle weakness
  Sleep disturbance
 Water retention
 Amenorrhea
 Decreased libido
 Irritability
 Acne
 Thin extremities from muscle wasting
 Swollen ankles

Diagnostic tests

 Initial screening consist of a 24 hour urine test to determine free cortisol excretion rate
and a low dose dexamethasone test. Failure to suppress plasma and urine cortisol levels
confirms the diagnosis of Cushing’s syndrome.
 A low dose dexamethasone suppression test can determine if Cushing’s syndrome results
from pituitary dysfunction. In these diagnostic tests, dexamethasone suppresses plasma
cortisol levels. Failure to supress these levels indicates that the syndrome results from an
adrenal tumor

Medical management

Management include radiation, drug therapy or surgery

Drug therapy include the use of drugs like mitotane, metgrapone or aminoglutethimide

Bilateral adrenalectomy mandates lifelong steroid replacement therapy to correct hormonal

deficiencies

Nursing intervention

 Keep accurate records of vital signs, fluid intake, urine output and weight
 Educate patient to eat food high in protein and potassium but low in calories and sodium
 Use protective measures to reduce the risk of infection
 Schedule activities around the patient’s rest periods to avoid fatigue
 Institute safety precautions to minimize the risk of injury from falls
 Help the bed ridden patient turn and reposition herself every 2 hours
 Encourage the patient to verbalize her feelings about body image changes and offer
emotional support