Related Anatomy and Physiology
Specitic Endocrinal Disorders and Nurses' Role
4.3.1 Diabetes
4.3.2 Thyroid Disorders
4.3.3 Adrenal Disorders
4.3.4 Pituitary Disorders
Nurses' Role in Pharn~acologicalManagement of Endocrine Disorders
Let Us Sum Up
Key Woi-ds
Answers to Check Your Progress
After completing this unit, you should be able to:
describe related anatomy and physiology of endocrinal system;
define various endocrinal disorders; and
explain causes, types, risk factors, pathophysiology, clinical manifestations,
diagnostic measures, complications, management strategies and nursing care
in specific endocrinal disorders.
The endocrine system integrates body functions by the synthesis and release of
hormones. Hormones an chemical substances that are shunted into blood by a
group of specialised cells so that they may exert a physiologic eft'ect at another
site. Honnones coxtract modulate to long distance. The cells or tissues that
response to a particular hormone are called target call or target tissues. The
endocrine system consists of Hypothalarnus, the nnterior and posterior pituitary.
thyroid, parathyroid, adrenal cortex and medulla, pancreas, gonads. pineal body
and thymus. Any abnormality in these glands leads to various disorders, which are
discussed in this unit in terms of nursing management.
Hypothalornus and Pituitary Gland
Hypothalamus consists ot' nervous tissue located belieat11 the central hemispheres
on each side of the 3rd ventricle. Pituitary gland is located in sellaturcia, an
indurtation of the sphenoid bone at the base of the brain. It is oval and of lcrn in
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diameter. It is has a larger anterior lobe or adinohypophysis and a smaller
postioner to be called numohypophysis.
Hypothalamus has endocrine and nonendocrine functions. Thc endocrine function
involves the production of regulatory hormones released into the blood stream and
travel through the pituitary stalk to the anterior pituitary, where they either
stimulate or inhibit the release of anterior pituitary hormones. The hormones
secreted are:
Thyrotropic: Releasing Hormone (TRH)
Gonadotropin: Releasing Hormone (GHRH)
Growth Hormone: Releasing Hormone (GHRH)
Growth Hormone: lilhibitiilg Hormone (Somatostatin) (GHIH)
Certicotrapin: Releasing Hormone (CRH)
Inhibiting Hormone (PIH)
Melanocyte: Inhibiting Hormone (MIH)
I Target Tissue
Interior Pituitary
TSH (thyroid-stimulating Thyroid
Adrenal cortex
Stimulates synthesis and release
of corticosteroids and adrenocortical
Stimulates ovulation and
progesterone secretion
1 Testes
FSH (follicle-stimulating
Stimulates synthesis and release
of thyroid hormone
1 Stimulates testosterone secretion 1
Stimulates estrogen secretion and
follicie maturation
1 Stimulates
I Testes
1 Prolactin
/ Mammary glands1 Stimulates breast milk production 1
Growth hormone
Bone and soft
Promotes growth through lipolysis,
protein anabolism, and insulin
Promotes pigmentation
ADH (antidiuretic
hormone, or
Promotes water reabsorption
Uterus and
Stimulates uterine contractions and
mammary glands ejection of breast milk
MSH (melanocytestimulating hormone)
Posterior Pituitary
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Pituitary. Gland
hormones are synthesized in the hypothalamus and are stored in the posterior
pituitary gland. They are transported from the hypothala the posterior pituitary
while bound to neurophysins.
Thyroid Gland
Located anteriorily in the neck directly below the cricoid cartilage. It has two
lobes joined by a thin isthmus, which lies on
: Increase blood glucose level of (glucogenesis)
: Promote synthesis and storage in carbohydrate proteins and
fat metabolism, Regulate blood glucose
Gonads and ovaries : Produce hormones related reproductive function
The thyroid is composed of folliular and parafollicular
cells. Follicular cells produce the thyroid hormonethyronis (T,) and tri-iodothyronine (T,), and parafollicular
cells produce and secrete thysocalcitonis. Functions of
thyroid hormons.
T, and T, increase the basal metabotic rate which is associated with an increase
oxygen consumption and heat production. Sufficient dietary intake of protein and
iodine in essential for T, and T,.
Calcitomin partly regulate serum calcium leyel.
Porathyroid Glands
consists of four small glands located close of posterior surface of the thyroid
gland. The chief cells of parathyroid glands sythesize and secretes the parathyroid
hormone (PTH)
PTH .regulate calcium and phosphorus melabolism Adrenal glands
Adrenal Glands
Adrenal glands are retroperitoneal abdominal organs that cap the upper pole of
each kidney. Each gland consists of an outer adrenal cortex and ancinner adrenal
medulla. The adrenal cortex secretes three hormones, mineralocorticoids. Adrenal
Medulla secreads the catacholamins epinephrime and norepinephrines
(aldosterone), glucocorticoids (cortisol) and androgens.
Adrenal cortex hormones
Adrenal-medullary hormones-Table
4.2 and 4.3
Situated retroperitoneally behind the stomach and has both endocrine and exocrine
functions. The islets of langerhans composed of three distinct cell types. The alpha
cells which secretes glucagone, beta cells secretes insulin and delta cells secretes
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and proteins. The resulting hyperglycemia may causc acute or chronic
Carbohydrate metabolism involves active transport of glucose into cells and the
' inetabolism of glucose with release of enersy: storage of glucose not ~mnlediately
needed for energy as glycogen or fat; consersion of glycogen back t o glucose
whenever blood glucose drops; conversion of proteins to glucose whenever
, glycogen as well as glucose stores are depleted and energy is needed,
Insuln~deficiency either absolute or relative In the first type, pancreas either
produce no or very little insulin. In the latter, pancreas produce normal or even
excessive insulin but the body is unable to use it eff'ectively. This is known as '
insulin resistance. Insulin acts by lowering blood glucose by permitting entry of
glucose into cells of liver, muscle and other tissues where it is stored as glycogen
or burned for energy. It also promotes storage of fat in the adipose tissue.
indisposing Fuctors
Genetic surceptibility, obesity, Psychological stress, irecurrent intect in dietary
habits, prolonged use of cartain d r u g s , BP, Sedentary work.
Diabetes Mellitus is mainly classified into four types.
Type I: Insulin Dependent Diabetes Mellitus (IDDM)
This type of diabetes me!litus occurs either due to inefficient production or simply
the absence of insulin production by pancreas. Type I DM occurs below 30 yrs of
age. Type 1 DM is further classified into : Juvenile diabetes. Juvenile-onset
diabetes, Ketosis-prone diabetes. A patient with Type I DM is put on indefinite
insulin therapy.
/I: Non Insulin Dependent Diabetes Mellitus (NIDDM)
Unlike Type 1 DM, in Type 11, there is no indefinite requirement of insulin
therapy except for severe illness, pregnancy, etc. It can be controlled by diet and
exercise. Thls type of diabetes mellitus occurs mainly due to the inaFI1if: of body
to use insuli~leven though pancreas produce low, normal or high levels of ~nsu!~n.
It is classified into Adult - onset DM, Matunty onset DM, Ketosis--resistant DM.
Secondary DM
Diabetes Mellirus associated with other syndromes - Secondur). DM.
'These may result from some pancreatic discase. hormonal abnormalities. etc.
Grstatiorzai Diabetes Mellittis (C;D,bq
This type starts during the 2nd or 3rd trimester of pregnancy. It may disappear
after pregnancy.
7jpe I: Insulin Dependent Diabetes Mellitus (IDDM)
The blood ;?:.el of insulin is very low in the fully developed disease, and the
efyect of this can be ~redictedfrom known actions of insulin. In the liver, glucose
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formation is promoted, partly due to increased conversion of glycogen intn
glucose. but mainly by gluconeogenesis i.e. synthesis of glucose from noncarbohydrate sources chiefly amino acids derived from skeletal muscle. The uptake
of glucose by muscle and fat cells is reduced and the net effect is hyperglycemia.
Following a carbohydrate meal, the blood glucose level rises even higher, because
in the absence of insulin, storage of glycogen in the liver is inhibited. Glycosuria
results when the renal threshold is exceeded; this causes an osmotic diuresis with
loss of water and electrolytes. The patient becomes dehydrated and thirsty.
In the absence of insulin, the neutral fats in adipose tissue are broken down; the
released fatty acids pass in to the blood and are taken up by the liver to form
acetyl coenzyme A. Normally this enters the kreb's cycle and is metabolized but
in severe diabetes, when there is an increase in the ratio of glucagons to insulin,
acetyl coenzyme A is converted into ketone bodies. In the presence of low blood
insulin levels, the uptake of ketone bodies by the peripheral tissues is inhibited.
The elid result of the biochemical derangements is therefore hyper glycemia with
glyosuria, ketosis with ketonuria and a severe metabolic acidosis. In this type of
diabetes mellitus, the body's mechanism 1s geared to the maintenance of a high
blood glucose level, even though this exceeds the renal threshold. The body
literally starves In the mldst of plenty as fats and proteins are converted into
glucose only to be passed in the urine and lost from the body. Loss of weight,
muscle wasting and hunger are therefore characteristic.
@pe II Non Insulin Dependent Diabetes Mellitus(N1DDM)
Insulin resistance is the main factor in Type I t DM. Normally, insulin binds to
specific receptors on cell surfaces. As a result of insulin bind~ngto these
receptors, a series of reactions involved In glucose metabolism occurs within the
cell. The insulin resistance of Type II diabetes is 'associated with a decrease in this
intracellular reaction. The insulin thus becomes less effective In stimulating
glucose uptake by the tissues.
In order to overcome insulin resistance and to prevent building of glucose in
blood there nlust be increased secretion of insulin. If beta cells are unable to nieet
the demand, Type 11 DM develops.
Clinirul Munifesstations
Thc classical clinical manifestations of diabetes mellitus are increased frequency
of urination- polqul-ia. Increased thirst: polydipsia. Increased hunger- polyphagia.
Other symp:oms include. Lethargy. sleepiness. fatigue, non-healing wound.
repeated ~ntection,visual disturbar~ces,pruritis. In diabetic ketoacidos~scondition,
patlent rnay ha\c Fruity odour of breath. nausea, vomiting, abdo~ninalpain and
' lx!vc~it~lation
Diagnostic tests include Physical examination, medical history alla laboratory tests.
Clinical manifestations suggest the presence of diabetes, but lab tests are needed
to make a definitive diagnosis viz. Fasting Blood GIucose, Random Blood
glucose. Post pra~dralBlood Glucose, Glycosylated Haemoglobin, Oral Glucose
Tolerance Test, Ketonuria. Proteinuria.
Common acute con~pl~cations
include- Hypoglycemia, Diabetic ketoacidosis, Hyper
osmolar Non-Ketotic Syndrome, Osmotic diuresis 1.e. loss of H,O & electrolytes.
C:hron~ccomplications include Cerebrovascular disease. ~ o r o l ~ aartery
Fertphzral vascular disease. Diabetic Foot, Retinopathy, Neuropathy and
Nephro pathy.
The main goal of treatment of diabetes is .to try to normalize insulin activity and
blood glucose levels tb reduce the development of vascular and neuropatbic
complications. Five components of diabetes management are:
Dietary Management
Diet and weight control constitute the foundation of diabetes management. Meal
Planning involves planning of calorie requirements on the basis of age, sex. body
weight and degree of activity. The goal of a diabetic diet is to emphasize on
intake of complex Carbohydrates, which are absorbed more gradually from GIT
causing less of a blood glucose rise.
Complex carbohydrates include starches like bread, cereal, rice and pasta. Dietary
fibres are very important for a diabetic as they lower cholesterol levels. There are
insoluble fibres such as whole grain bread. cereals etc. of soluble fibres such as
legumes, oats, etc.
Alcohol-Ingestion of alcohol by diabetes is not completely restricted but high
intake may cause hypoglycen~ia.
Exercise lowers blood sugar and reduces cardiovascular risk factors.
SMBG--self monitoring of blood glucose.
Two methods are used; Use of dip strips and Blood glucose monitors, eg.
Acuchek 111 meter allows for double-checking of results. One touch I1 aanitor
does not require removal of blood from strip used. Urine can be tested fix
Insulin therapy--Insulin preparations vary according to time course of action,
concentration source etc.
Time course- Short Acting Insulin, internlediate acting insulin. !ong acting insulin.
Insulin Rrgzmens
May vary from 1-4 injectionslday. Usually it is a combination of a long acting
and a short acting insulin.
Surgical lManagcrnent
Transplantation of pancreas is done in severe cases. lt may be done along with
kidneys. 311ring any surgery, complicatioils of hypoglycemia can be present.
Hence, good and pre- post operative management is necessary. Continuous
observation is needed.
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Nursing manageittent involves:
Nfirsing Assessment
Obtain a history of current problems, family history, general health history.
Has patient experienced polyuria, polydipsia, polyphagia and other
~ b m b e rof years since diagnosis of diabetes.
Family members diagnosed with diabetes, their subsequent treatment and
Perform a review of systems and physical examination to assess for signs
and symptoms of diabetes, general health and presence of complications.
weight loss or gain, increased fatigue, tiredness, anxiety.
Skin--Lesions, infections, dehydration, evidence of poor wound healing.
Eyes--changes in vision, floaters, halo, blurred vision, dry or burning
eyes, cataracts. glaucoma.
Mouth--gingivitis, periodontal disease.
Cardiovascular--orthostatic hypotension, cold extremities. weak pedal
pulses. leg claudication.
Gastrointestinal--Diarrhoea, constipation, early satiety, bloating,
increased flatulence, thirst.
Genito urinary--increased urination, nocturia, impotence, vaginal
Neurologic--Numbness and tingling of extremities, decreased pain and
and Nursing Interventions
AItered nutrition more than body requirement related to excessive intake of
Assess current timing and content of meals.
Ad\ice patient on the importance of an individualized meal plan in
meeting weight loss goals.
Discuss goal of dietaq- therapy with patient.
Assist patient to identify problems that may have an impact on dietary
ad!lerance and possible solutions to these problems.
Explain the importance of exercise in maintaining /reducing body weight
calorie expenditure for energy in exercise.
E:lhance metabolic and efficient food utilization.
Ass~stpatient to establish goals for weekly weight 10:s~and incentives to
assist in achieving them.
Strategise with the patient to address the potential social pitfalls of
weight reduction.
Fear related to insulin injection:
Assist patient to reduce fear of injection by encouraging verbalization of
fears regarding insulin injection, conveying a sense of empathy, and
identifying supportive coping techniques.
Demonstrate and explain thoroughly the procedure for insulin selfinjection.
Help patient to master technique by taking step-by-step approach.
Allow patient time to handle insulin and syringe to become familiar
with the equipment
Teach self-injection first to alleviate fear of pain from injection.
Instruct patient in filling syringe when he or she expresses confidence in
selti'injection procedure.
Review dosage and time of injections in relation to meals, activity ar,d
bedtime based on patient's, individualized insulin regimen.
k s k for injury (hypoglycemia) related to effects of insulin, inability to eat.
Closely monitor blood glucose levels to detect hypoglycemia.
Instruct patient in the importance of accuracy of insulin preparation and
meal timing to avoid hypoglycemia.
Treat hypoglycemia promptly with 10-15 g of fast acting carbohydrate.
Encourage patients to carry a portable treatment for hypoglycemia a: all
Assess patient for cognitive or physical impairment that may interfere
with the ability to accurately administer insulin.
Between meal snacks as well as extra food taken before exercise should
be encouraged to prevent hypoglycemia.
Encourage patient to wear an identification bracelet or card that may
assist prompt treatment in a hypoglycaemic emergency.
Activity intolerance related to poor glucose control.
Advice patient to assess blood glucose level before strenuous exercise.
lrlstruct patient to plan exercises on a regular basis.
Encourage patient to eat a carbohydrate snack before exercising to avoid
Advice patient that prolonged strenuous exercise may require increased
food at bedtime to avoid nocturnal hypoglycemia.
Instruct patient to avoid exercise when blood glucose levels exceed 250
mgldl urine ketones are present.
Counsel patient to inject insulin into the abdominal site on days when
anns or legs are exercised.
Know!edge deficit rit use of oral hypoglycemic agents.
I c l e n t i ~a n j barriers to Izarnilig such as ~isual,hearing lo\\ l~rtex~c:~.
distractive environment.
Encourage active participation of' patkn! a?!d fhmily i!? etlucaric~~~al
Teach the action. use and side effects ot' Drugs
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Risk for impaired skin integrity related to decreased sensation of circulation
to lower extremities.
Assess feet and leg for skin temperature, sensation, soft tissue injuries,
callous, dryness, hammer etc.
Maintain .skin integrity by protecting feet from breakdown.
Instruct patient in foot care guidelines.
Advice patient to stop smoking.
lneffecti\e coping related to chronic disease of complex self care regimens.
Discuss with the patient, the perceived effects of diabetes on lifestyle,
finances, family and occupation.
Explore previous coping strategies and skills that have had positive
Encowage patient and family participatioii in diabetes self-carc regimen
to foster confidence.
Identify available support groups to assist in lifestyle adaptation.
Assist family in providing emotional support.
i s ! L ~ ~ f tEii:/catio?z
Fdrgeted to the newly diagnosed or those undergoing stressful
circumstances that preclude more in-depth education.
Educational focus-skills management to include-insulirnoral agents,
hypoglycaemic treatment, blood glucose monitoring of basic dietary
Lifestyle Management Skills
Ongoing education of patient to include advanced skills rationale for
treatment, management.
Education focus-Lifestyle management issues, to include sick day
management and dietary consideration for dining out.
Evaluation of Care
Evaluation of care can be done on parameters like:
maintenance of ideal body weight by patient
Patient demonstrates self-injection of insulin with minimal fear,
Hypoglycemia ideptified or treated appropriately
Patient tolerates activity without compromise in glycemic control
Patient verbalizes appropriate use and action of oral hypsglymemic agents,
No skin breakdown
Patient verbalizes initial strategies for coping with diabetes.
Diabetes Insipidus (Posterior lobe Hyposecretion)
It is a deficiency of AD11 that results in inability to conserve water.
Risk Fuctors
Head injury
Neuro surgery
Tumors of hypothalmus and pituitary
Centrally acting drug
Brain infection
Clinical Manvestations
Genito urinary-polyuria, nocturia: Gastro intestinal-weight loss, polydipsia;
Integumentary-dry skin and mucous membranes; Neurologic-mentation changes as
electrolyte imbalance and hypotension worsen. Diagnostic evaluation involves
History Taking, Physical Examination, Integumentary and cardiovascular changes,
Laboratory tests, etc.
Medical management involves IV' Fluids, ADH replacement with Vasopressin.
Surgical management involves Hypophysectomy to remove posterior pituitary
tumor. Nursing Management includes monitoring intake and output, assessing
serum and urine values. Client and family teaching and preventing complications
like Electrolyte imbalance, Hypovolemia, Hypotension, Shock, etc.
Thyroid Disorders
Thyroid gland is one of the important endocrine glands. The disorders will be
discussed in detail in the following text.
Related Terminology
Euthyroid; is indicative of normal fknctioning of the thyroid gland.
Hypothyroidism; involves a decrease in normal thyroid gland activity.
Myxedema; a complication of hypothyroidism characterized by a generalized
hypometabolic state.
Hyperthyroidism; is increased glandular functioning.
The role of thyroid hormone (L-triiodothyronine, T,; L-tetraiodothyronine, T,) in
the regulation of diverse cellular activities, including normal growth and
development, and general metabolism is well established.
Diseases of the thyroid are among the most common endocrine disorders in
clinical practice. These disease are typically detected and managed based oil the
results of thyroid function tests, the diversity and multiplicity of which car) be
conhsing to some clinicians.
Hypothyroidism is a deficiency of thyroid hormone resulting in slc~wedbody
metabolism and heat production due to decrease'd (1 consumption by the tissues:
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under-activity of the thyroid; and pronounced personality changes. It slows the
develcpment and functioning of ulmost body system. Prevalance rates are greater
in elderly women (10%) than in elderly men (2.3%). Eventhough highest
lncldence is in adults b/w 30-65 yrs. it is seen in newborn also.
It is caused by congenital defects of the thyroid (cretinism), Defective hormone
synthesis, Iodine deficiency (pre and post natal), Antithyroid drugs. Surgery or
radioactive therapy for hype'ithyroidism. Following chronic inflammatory
(autoirn~ntme)diseases such as llashiinoto's disease, arnyloidos~s,and sarcaidosis.
It invoives Cretinism, Iodine tleficiency d~sorders,l'lashimoto's thyroiditis. etc.,
Failure of hypothalamus and pituitary to secrete the thyroid related hannunrs may
occur due tc? head injury, tumor etc.
Its cabsed by thyroiJ horrnolie deficie~icresduring feisl or early neonatal life. It
can he ataszd by maternal iodine depriva~arcongenital thyroid abnormalities.
lot-line drliciency (prenatal and post natal)
Iodine is ueczssaq for TI1 secretion. [:)dine deficiency may result from certain
iatrogenic drugs (which block TH synthesis); lithium carbonate whict: is used to
s e a t tna~iic-depressivemental disorders and antitl~yroidd n g s are examples.
Soyabeans inay also block TI-+synthesis if consumci in sufficient quantities.
i-Iowevcr. the use of iodized salt has reduced this risk in the United States.
In this disease, classified as an autoimmune disorder, antibodies develop that
tfestrny thyroid tissue. Functional thyro~dtissue is replaced with fibrous tissue and
TH levels decrease. In addititm, decreasiug levels of TH prompt the gland to
enlarge to compensate, causing a goiter. This disorder 1s more common in women
2nd has a familial link.
it can bc inadveno:~tl.i caused in the process of tlr,at~il&hqpertllyroidi5nl. Infact,
~ h cmost common cause of hypothyroidism tocia:, is radiodctive lodlnc. Trl.eat~:?cnt
!i,r Grave's disease (hyperthyroidism) where radiation'therapy results in o.ier*~:c,truction of thyroid tissue.
En~lemicgoiter- is caused principalIy by nutritional iodine deficiency. It tends to
in goiter 'belts', geographical areas characterized by soil and water that are
deficieni in iodine. Endemic goiter typically occurs in winter months and is thrice
a i prevaler-it In women as in men. Also, because the need for TH is particularly
?::cat during growth spurts, pregnancy, and lactation goiter cornlllonly develops in
rldolcscents, pregnant women and nursing mothers living in iodine - deficient
goiter: Major causes include Genetic defects resulting in faulty iodine
*i:eti?bolism. Ingestion of large amounts of nutritional goitrogens (.goiter-producing
:!>?ilk that inhibit thyroxine (T,) production) like cabbage, soyabeans, peanuts.
. . .,l!zs,
pcas, strawberries, spiqach, and radishes, all of which contain goitr-ogenic.
::.iob;lcs, 1ngestio;l of inedicinal goitrogens I'or eg. .4dreucrgic antagor:ists,
.. z:icocr~rticoids,
dopamine. methiniazole. lithium, retiimpin, carbanxizepine,
I-iiopylthiouracil(PTU). and thicrcarbamides (aminothiazonate).
Antithyroid Drugs
A variety of drugs, especially antithyroid drugs, if given over a sufficient perioci
of tirne and in large doses, can impair the func!ioa of the thyroid and result in
hypothyroidism. These drugs deplete the thyrc;~dof its hormone stores.
Risk Factors
History of neck injury. Ingestion of large amounts of medical goitrogens. ba~nily
history of thyroid disease. Iodine-deficient areas, Ingestion of large amounts 01'
nutritional goitrogens. Pregnant women, Lactating mother, Adolescents wlth
decreased thyroid hormones. Elderly clients. Clients with autoimmut~edibease.
Elderly men receiving aminoglute thiade ( 1000 mglday or greater) for prostrate
cancer. Increased serum cholesterol. I-fistory of treatment with lithium. amiod3ro1ic
or iodme.
Although there are many causes of hypothyroidism, tine effects on the patlent
resulting from deficiencies of the thyroid horniones are the satne sy!nptoms may
begin at any age and usually occur insidiously over many rnonths to years. The
severity of the symptoms will be dependent upon the degree and duration of
thyroid hormone deficiency.
Changes in Fluid and Electrol~vteDjwumics
A decrease in thyroid hormone will alter the fluid and electrolyte dynamics, with
total body water and extracellular fluid being increased whiie plasrt-rla vc>lurnc i b
decreased. Capillary permeability is also increased causing tilt: accun~ulat~on
mucoprotein deposits in tissues. This leads to fluid retention and resutts in
thickened. edematous, puffy skin most noticeable in the eyeliils, hands, and feet.
It's a nonpitting type of edema. There may be sticky secretions on 'ihe eyelids.
The fluid retention also causes ihtl tongue to enlarge and speech t~ be thick and
slurred. The speech is deliberate and slow as a r e s ~ ~ iSwelling
uf the vocal cords
gives the voice a hoarse tone. The patient may experience ai-i overall weight gain
attributable to the fluid changes as well as the acqilisition of fat. I~lypotl~yroi~l
patients tend to drink small alnounts of water and to have diminished urinary
output. The decrease in renal filnctior? cdrrelates with the decrease in cnrdiac
output. Certain deviations from normal renal function correlates will1 the decreasi.
in cardiac output. Certain deviations from normal renal function are revcaled by
laboratory tests. Minimal amounts of protein may be seen in the urine, which
could be due to the increased capillary permeability typical of hypothyroidism,
Hypothyroidism decreases formation and absorplion of bone, yet the serum Ca &
Phosphorus cone. usually remain normal. Calcium in the urine is reduced. Recent
research studies reveal that an increased secretion of parath!rotd hormone occur%
in hypothyroidism. apparently as a homeostatic nlcchanlsm to kecp !he serum ('a
level normal in spite of the slowed bone metabolism.
A decrease in thyroid hormone will also affect cell growth and pro!iferation. This
hormone is not only essential for nornlai growth and development, hut also affects
both inale and female reproductive systems. I n :hi: felnale, excessive and ir-regular
menstrual bleeding results from endometriai pr~~!ii'ei.xiul;.This proh!c!n pcrsists
because of decrease i l l progesieroqe sccret;cin. In bzth sexes. libiciii is usudlli.
decreased. Like wise, reduced fertility is also seen in both sexes, women who dv
become pregnant often aboi-t.
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Associated with hypothyroidism is an obergrowth of the horny layer of the
epidennis known as hyperkeratosis. This causes the skin to become unusually dry
and rough and decreases the activity of the sweat glands. The skin may show fine
wrinkling and scaling, Hyperkeratosis also affects the appendages of the skin. The
hair becomes dry, coarse, and brittle and often lacks luster; its growth is retarded.
and it tends to fall out. The eyebrows are often sparse, especially in the temporal
areas. The nail becomes thin and brittle with longitudinal and transverse grooves.
Another change indicating cellular growth and proliferation is increased
subcutaneous fat with definite fat pads being formed, especially above the
clavicle. 111 addition. the hands and feet may have a broad appearance because of
the thickening of subcutaneous tissue.
Metabolic CThange.s Hypothyr-oidism
It has especially profound effects OE metabolism. In fact, perhap., the most
common physiological deviation in health status is lowering of the metabolic rate.
In gastrointestinal tract there are not only decreases in gastric hydrochloric acid
secretion, but generalized decrease in peristalsis and slowed absorption. A lowered
food requirement and decreased peristaltic activity combine to make the patient
feel anorexic with frequent conlplaints of constipation and fecal impaction. The
overall decrease in metabolic rate leads to a reduction in body temperature and
intolerance to cold. Protein synthesis is slowed; this is complicated by the
diffusion of albumin through capillary walls into the tissues, leaving loss of
protein available for growth and body healing The lowered metabolic rate slows
cholesterol metabolism and increases the levels of cholesterol in the blood.
Another of the metabolic effects of hypothyroidisin is a decrease in the conversion
of carotene to vitamin 'A' in the liver. This leads to increased serum carotene and
accounts for the slight yellowish colouring of the skin.
Adrenal steroid metabolism slams to accommodate the reduced needs of the
hypothyroid patient. Under stress, however, the plasma cort~solconcentration is
normal and sutXcient to respond to the needs of the pt.
Changes in /3,\ygenation
The effects of hypothyroidism on oxygenation arc also widespread. The
generalized decrease in the body's metabolism decreases 0, consumption by the
:ells. The body compensates for the lessened deinand for oxygen by decreasing
&adiac output and increasing peripheral resistance. The decrease in cardiac output
aesults in slowing of the heart rate (bradycardia). a decrease in blood pressure.
and a narrowing of the pulse pressure. These combine to slow peripheral
circulation time allowing more complete extraction of oxygen, I-iowever, in the
presence of peripheral vasoconstriction the skin becomes cool and pale and further
mcreases the patient's tendency to cold intolerance. The body further compensates
fbr the decreased need for oxygen by decreas:ng the r3Umbcr ~ j fRRCs, That IS.
hypothyroidism causes diminished blood cell formation. probably a\ a response to
the decreased oxygen demand. The resultant normocytic, normochromic aneinia
may be complicated by other factors. Excess~vemenstrual bleeding arld decreased
iron absorption because of lack of H('1 can superimpose an lron deficiency arcernla
on the already existing condition. S~milarly.diminished intrinsic factor in the
stomach can interfere w ~ t hthe normal absorption rrf V,t. R , ? deficiencj, whicii
results from. an mderlying progresswe gastritis brought on by an auloimmunc
phenoinenon. Decreases in circiiilatics~lthroughout the body can create systemic
effects. For eg: the decrease in renal blood flow !es.ens the gloirienllar filtration
rate and tubular reabsorption. This impairs excretion of the body's watitzr and
farther complicates excretion of the body's water and farther complicates the fluid
retention and electrolyte balance. The changes in circulation also affect the body's
ability to fight infection and heal itself. Capillary permeability also increases in
hypothyroidism. In severe cases, its probably the cause of pericardial effusion
which can develop. In addition, capillary fragility is increased and may cause the
patient to bruise more easily.
Changes in Perception and Co-ordination
Perception and coordination are also affected in hypothyroid individual. The
patient's movement tends to be slow and clumsy with muscle weakness. stiffness,
cramps, and transient pain. These symptoms are though to be due to mucoprotein
edema, which causes a separation of the muscle fibers. Slowed muscle contraction
and relaxation times compound the muscle weakness and pain. This is especially
evident in the relaxation time of the ankle jerk (Achilles tendon), although these
findings may be within the normal range.
Sensory changes often involves numbness and tingling of the fingers due to
compression of the median nerves by mucoprotein deposits. Night blindness
occurs due to a deficiency in Vit. A. An adequate supply of \'it. A is necessary to
maintain levels of retrieve, the pigment required for dark adaptation. Conversion
of carotene to Vit. A is decreased in the hypothyroid individual. Deafness is also a
very characteristic and troublesome symptom. This can be due to VIIth nerve
damage from pressure by mucoprotein deposits, conduction problems, or a
combination of these.
In addition, perception and co-ordination are affected by a decrease in cerebral
blood flow, which often leads to cerebral hypoxia. Consequently, there is a general
slowing of all intellectual junctions. The patient may experience memory defects,
lethargy, somnolence, and in more severe cases, coma.
When TH production decreases, the thyroid gland enIarges k a compensatory
attempt to produce more hormones. The goiter that results is usually a simplei in
toxic form. People living in certain areas of the world where the soil is deficient
in iodine, the substance necessary for TH synthesis and secretion, are more prone
to become hypothyroid and develop simple goiter.
TSH stimulates the thyroid to secrete more T, (triiodothyronine) when blood T,
levels are low. Enlargement of gland will also occur in response to increased
pituitary secretion of TSH. Eventually, the gland become so large that it
compresses structures in the neck and chest, causing respiratory manifestations and
dysphagia. Reduced levels of TH are affecting to the lipid metabolism.
With reduction in TH, there is a resultant increase in serum cholesterol and
triglyceride levels and an increase in arteriosclerosis and coronary heart disease in
clients suffering from hypothyroidism.
The TIIs also play a role in the production of RBCs, so person with
hypothyroidism also show manifestations of anaemia, with possible Vit. B1, and
folate deficiency.
Decreased level of TH leads to overall slowing of the basal metabolic rate.
Clinical Manifetations
Defecthe physical development and mental retardation. Excessive sleeping,
thickened skin, and lips, squinting. Abdominal distension with vomiting, Hoarse
cry, dull facial expression. Feeding and respiratory difficulty, penpheral cyanosis,
Supraclavicular and periorbital edema, Umbil~ic91hernia and hypothermia, Large
Nursing Management in
Endocrine Disorders
k;ndocrinological. Inir~~unoirtgical
and ?Irn~~rna
Is characteri~edby an insidious and ?]on-specific slowing of body processes,
personality changes, fatigue and lethargy. Mental changes- impaired memory,
slowed speech. decreased init~ativzand somnolence, coid intolerance, hairloss, dry
dud coar3e skin, b ~ ~ t t nail\,
hoarseness. m u s c i ~kbeakness and swelling, overall
weaknesk. constipat~on,vve~ghtgain. and ~ t ~ e n o i r h a g ~ a
Semiti\ ity Ln cold, lethargy, dry skinlhair, fcjrgetfillness, depression. some wt. Gain
~vithoutincreased in food intake, inability to s\\:eat, constipation and fecal
impactic~n;increased susceptibility to infect~on.heart rate is normal/slow, B.Y.-----may be normal to subnoimal. Dysphagia and respiratory distress, Lack cf normal
physical activity. respiratory distress.
May develop in clients with undiagnosed or under treated hypothyroidism who
experience stress. Stressors include infection, drugs (barbiturates, narcotics,
anesthetics), respiratory failure. Ileart railure, cerebral vascular accident, trauma,
prolonged exposure to cold, metabolic disturbances. surgery. ant! seizures.
Myxrderila is characterized by a dry, waxy type of s\vclling ot' ski11 and other
tissues. '['he edema is of the non- pitting type and is common 'ill the pretii~ialand
facial areas. Myxedenia is most comrnonly diagnosed in hypotliyroid women in
t h e ~ r60s. Untreated n~yxeden~n
has been associated with se\.ere atherosclerosis
and has been attributed to the increase in serum choiesterch! concentration,
improves these cl~anges.
particularly low-density lipo-proteins. TI1 replac.cn~e~it
The major complication of hypothyroidisn~is niyxedema comai an extremely rare
condition with a mortality rate approaching 100%. Myxeden~acorna is
chn-acterized by a drastic decrease in metabolic rate. hypo;.-entiatio leading to
respiratory acidosis, hypotliermia and hjpotension. Complicating conditions
adrenal insufficiency,
include hyponatremia, h y p o ~ a l ~ e m i asecondary
hypoglycemia, and water intoxication. iMyxederna coma may be brought on by
stress-as ?kom surgery/ infection-or by non-compliance with tiiyroid treatment.
It includes carciiomyopathy, pericardial effilsion. and coror?ary atherosclerosis.
Rratlycardia and wealcened cardiac contractiiity icad to decreased cardiac output.
Pericardial eff~ision.however; seldom resuits in lie~nodyn>~~:iic
Incrc-ased serum cholesterol and triglyceride levels and the accanaulalioa of
rnui:opolysaccllarides in the intima of small blood vessels can resl;!t in coronary
atherosclerosis. This accumulation is seldom s\;r~!~ji:maticii.e. cl~ar:icierized hy
angina) because s f tlic decreased myocarii~i~i
C!. i<!i:sil:i;i.:,.i~:ii:r\t +:I;.
observed in hypothyroitiism.
Other feah~resinclude tlecreased (;I motilit); and ackilorliydria: < ,,n::t-:pa!r\!nl
intestina! obstructo~l.Anemiri, oti-;er 1iern~topoie:ic prc;bletns likc \ ~ i i . i;;., ~r-t);; ilnd
relate c!eficiencies, and a predisposition to bruising. T l ~ ebrain may he :~~:i.i"\.<i
diminished ct:ibral biood flow, mt.111.ii ~lugg!c;!?iics~.
inattentiveness. ~~iciirc::.~
lethargy. and changes in affcci.
Di;iilrlnstic E\/alria~irxiin~olve.; i!isiory taking-clinical complaints-like easy
increzsed nzc:! for ..rei:p.
~ n u s c ;i:eaknrs,
r11:i:;cie pai:~, hypersensitivity to aolti, i!:abilitv In trrlilcentrate, ;dc. I)i~ringthe
ij!pi.rvi~:\i.-.patients v!:icc ~hotlli! ~\.3iii:ii,:<l i\:xi. ! h i c h c s s
xp!sc'n r::?d v c ~ ~ . - a l
tone. 'The patient should tit. asked if' any changes i n \oict. qu:tlit.y have been
noticed. Menstr~la]hldories should be taken, and the patient asked ribout any
changes ir; appetite or bowel habits, Intellechial iiinctioi~in~
sholdd be c~bservcd
throcghout the interview and the parient shinrld be questioned regardiny memory
difficulties, attention span, lethargy, etc. P!lysicai exainination for coidt dry. rough,
and sc.a!y skin with brittle nails anci hair, changes In fluid and electrolyte balance
causes swelling in eyelids, hands and feet .Fdt:rna niay also be assessed by
v~eighingthe .patient and compai-ing the resuits with the previous weight recnrd.
The thyroid gland itself should be paipatzd tor enlargement. It may initially
proljferate to cornpensste for thc !u\i.er levels of thyroid hormones. The decreased
metabolic rate call be partially asseased through taking the patient's temperature
\vhich may be lower than the nonnal. The reduced body temperature causes the
skin vasculature to perform its nlajor function i.e. heat conservation. Slowness in
skin healing cj~nbe noted through observation of any cuts and scratches while
ascertaining from the patient and the time of their occurrence. The abdominal
examination may reveal gaseous distension and diminished bowel sounds as a
result of the decreased peristaltic activity. Breath sounds may be essentially
normal, although the rate and depth may be diminished. Dyspnea may be
observed in soiile patients as a result of CXF due to some other cause such as
pleural ef'fusion, anacnlia, obesity, or pulmonary, disease. Mucosa of the eye is
pale in hypothyroidism.
Perception and coordination should be assessed through muscle strength and reflex
testing. Reflex contraction and relaxation times are usually noted to be prolonged
because of the slow rate of muscle contraction and relaxation. The strength and
tone of the muscles may be normal. or they may be weak and flabby. The patient
should also be questioned regarding any weakness and poor coordination. Constant
involuntary movements of the eye(nystagmus) and intense tremors may be
observed. Thepatient shouid be questioned for sensory changes such as numbness
and tingling in the extremities.
Diagnostic tcsts thyroid f~nctiontests, basal metabolic rate, Serum T, level test,
protein-binding iodide(PBI1, butanoi-extractable iodine (BEI), T, resin uptake test.
Scniln TSFT le\rcl tcsr. Radioactive Iodide Uptake Test: (RAlU test), Scannicg
procedures 10 evalua~trcthe anatomical features of the thyroid, to recognize areas of
increased or deci.ea.scd hormone synthesis, and to identify any tissue outside the
thy~oidwhish is active in accumuiating iodide may be done. Relaxation TioleThis is especially true o f the Acllilles tendon reflex time. Its prolonged in
hypotlryroidism :~rtd shortened in hyperthyroidism. Thyroid auto-antibodies test.
Serum Cholesterol concentration, efc. May also be carried out.
Medicill .Ilinml;.rrnirnt
A$rxec/en;a (i.!ld jI-Jvrcdem:i C!.imir
Supportive measures begin in~n~cdiately
and include maintaining a patient airway,
giving O.,, and replace fluids intravenously.
The client is kept wann, and vital signs are closely monitored until the client
begins to recover.
Vasopressors are used to maintain tissue perfusion.
Levothyroxine sodium is given intravenously with glucose & corticosteroids.
When administering TN to a cljent with myxederna hear: disease. assess the client
carefully for angina. dyspnea, or orthopnea. The event that precipitated the coma
(surgery, infection, non eompliarice) must be evaluated and treated as well.
Urology. Burns, Plastics and
Reconstructive Surgery,
Entlorrinologieal, lmmu:nolcagic
and Trauma Nursing
i i)
Cor~ectThj~roidHormone Deficiency
Levothyrnxine sodium is the principal form of replacement therapy. Dosage vary
with age, the severity of the hypothyroidism, general medical condition
(particularly cardiovascular disorders), and the client's response to medical
treatment at the initiation of TH therapy. Children and other adults receive smaller
doses. Clients who respond to TH therapy receive a maintenance dose of T, daily
for life. Pharmacologic goitrogens are replaced by drugs that don't interfere with
TN function. The drug of choice for thyroid replacement ,is levothyroxine sodium,
which is converted in the body to both T, & T,. Desiccated thyroid and
liothyromine sodium (cytomel), once commonly used in replacement therapy, are
now used infrequently because of problems with fluctuating plasma levels and
side effects.
iii) Goitre Suppression
Medical management of simple goiter is focused on removing the stimulus
causing the decreased thyroid mass. Suppression of the increase in TSH is
necessary to correct the stimulus for growth of the thyroid gland. Correction also
reduces the associated increase in turnover of iodine and the increased T/ T, ratio
in thyroid secretion. With elevated TSH, the patient has remained euthyroid at the
expense of the elevated TSH and an enlarged gland. If extrinsic factors such as
goitrogenic drugs or foods are the cause, they are eliminated. Iodine deficiency,
although very rare, is ruled out and replacement is iiistituted if appropriate.
In most instances, the cause of goiter is unknown, and therapy is directed at
supplying exogenous hormone, which wiil inhibit TSH secretion. Similar therapy
is used to suppress TSH secretion in goiter associated with Hashimoto's disease.
Na L-thyroxin is usually necessary. The adequacy of the dosage in suppressing
TSH secretion is verified by an RAIU test that should have a value of less than
5%. Surgery is sometimes necessary if suppression is not accomplished with other
therapy. Surgery will result in hypothyroidism requiring life long replacement of
thyroid hormone.
Surgicul Munc~gement
Thyroidectomy may be used to treat large goiters, particularly those compressing
adjacent tissues.
Adequate nutrition (well-balanced) meals is promoted for patients with
hy-ppothyroidism. Patients are advised to follow prescribed caloric intake to achieve
goals of weigh loss if indicated. If iodine deficiency or excessive intake of
goitrogenic foods has been identified, instructions are given. In severe
hypothyroidism. apathy, ancrexia, and self care deficit may combine to limit food
intake, and attention inust be given to achieve adequate intake. Fluid restriction
and occasionally Na inodiiications are necessary in severe hyponatrernia.
Fatigue limits endurance in persons with hypothyroidism. Symptoms such as
angina and dyspnea on exertion may occur with severe fatigue. Patients should be
encouraged to increase activity gradually, building endurance and tolerance.
Appropriate referrals might include home care nursing, physical therapy, and
social services if family/ personal resources are limited.
Nursing Management in
Endwrine Disorders
Accurate assessment of patients with thyroid disease involves a history, physical
assessment and laboratory tests.
Nursing Diagnosis and Inter~,entio~l
Nursing diagnosis are determined from analysis of patient's data.
Activiky intolerance R/T poor work iapacity associated with poor curdiac
fimction, decreased breaflzi~zgrapacity and muscle stijjfness.
Promote activity to the level of patient tolerance
At first the patient will have a very limited tolerance and may only be able
to move around in the room. Activities should be increased gradually.
Monitor the cardiovascular response to new activities. If the patient
complains of chest pain or develops an unacceptable heart rate, stop the
activity and then resume at slow rate.
Body image disturbance R/T change in appearance (weight gain, hair and
skin clzanges), changes in futrctioning (decreased mental and physical
Promote positive body image.
Provide infoi-mation that helps the patient and significant others understand
the relationship of body changes to hypothyroidism.
Educate about reversible body changes.
Stress the +ve changes that have occurred.
. 3)
Constipation R;T decreased peristaltic action, decreused physical activity.
/ n l e r ~cntions
Promote nonl~albowel elimination:
Monitor bowel elimination.
iMaint~111adeqalate fluid intake
Increase bu!k in the diet.
Hypotlzermiu R/T decreased Ireat production associated with decreased
nretaboiic rate.
I n t e i ~tir1n.s
Treat hypothei~nia.
Monitor temperature every 2-4 hours
Maintain an environmental temperatt11.e i.e., co~nfortablefor the patient
Use blankets to increase body temperature if necessary
1 rolrjn>. I<.irslc. t'i.r\tic* ..M
U ~ C S J ~ % ~ I .\urLt-b>~
A n o w l ~ d ~.de$cit;
disease, rreatment, evpected outcomes, self-mortitoring,
fb&nt. LIP. W T new interventions with no previous evposure to information.
Cndrtcrino!c~girJI. Irnrnonr~i~~a~c
cnd Trauctxa \ur\ing
Teach the patient and Ilis caregivers;
Nature of the disorder, diagnostic tests, and treatment; need for life long
replacement therapy:
Medications, dosage, method of admitlistration,, and side-effects;
Self-monitorung of vital signs, weight. skin integrity and bowel function:
Methods to prevent skin breakdown and constipation;
Need for periods of rest alternating with activity;
Need for continlied follow-up care.
"41terednutrition mtwe than body requirements R/T decreased metabolic
rate. (As ulreadj~rliscussed earlier)
7) Pain
Headaclze, and joint pain associated with chronic thyroid
Promote cornfort:
Use non-medicinal comfort measures such as massage, cool or warm heat
and distraction to promote pain control.
If medications are used, monitor, the patient carefully. Patient will have lower
tolerance for sedative and depressant medications.
Se!Fcare deficit, total(varies); bathing-hygiene; dressing-grooming, feeding,
Provide for self-care needs. At first the patient may require complete care for
Ip~giene.tolleting, and dietary needs.
Se-xuol dy.~unctiunWT alt~rationsin menstruul cycle, sperm production
and libidq.
Facilitate patjent's: understanding of the relacionship between the sexual problems
and the kypiithyroiclisrn.
10) impaired skin integrity I"t/T mucinous deposits in skin, decreased
circrrlation, imtnohiIitytu
Mail~tainskin integrity:
Monitor skin condition each shift.
Institute preventive care measures such as sheep skin pads and soft sheets.
If patient is unable toldoes not turn by self, assist in turning every 2 hours.
I I ) Impaired tltought process, R R slowing of inteliecfualfunctions assoduted
with chronic deficit of thyraid hormana
Facilitate a safe cnvlronrnent and orientation and monitor neurological status evely
Reorient the patient frequently, use resources such as current events, clochs.
and newspapers.
Maintain a safe environment: remove any clutter, keep bed low; and keep
bed rails up.
Check on patient frequently, especially ar night, and use nightlights to
prevent confusion.
Inform significant others of relationship between irlental status and
Involve patient, as possible, in decisions about care.
Check Your Progress 1
Enumerate signs and symptoms of hypothyroidism in adult.
B s n i n g Management in
Endocrine Disorders
Plastics and
coma is a life threatening complication of hypothyroidism. Severe
hypothyroidism is associated with respiratory failure, usually in the presence
of myxedema coma.
F ~ ~ ~ ~ c r l nlmmunolo%ical
~ % ' ~ ~ ~ i ~ ~ ~ . Myxedema
~ 1 . 0 : ';rb#..
Cardiovascular disease in chronic hypothyroidism.
Primaw prevention: Its concerned with the prevention of Iodine deficiency
and its consequences. Iodine is necessary for proper growth and development
of the brain of the fetus, infant and child.
Soconduly prevention: Target population for 2" prevention of hypothyroidism
dre newborn infants and persons older than age 60, especially women, and
these persons with risk factors. Prompt treatment of newborns with congenital
deficiencies of thyroid hormone is necessary to prevent irreversible brain
damage and dwarfism (cretinism).
Tertiary prevention: It includes iodine replacement in patients with iodine
deficient states and the administration of thyroid hormone to those with
thyroid hormone deficiency. . .
Efforts to increase compliance with thyroid hormone replacement drugs are
important measures to prevent complications.
Evaluation outcomes are that the successful client shows no evidence of heart
failure, edema, or skin impairment, temperature and urine output are normal for
the client. and the client shows no further evidence of myxedema.
Hyperthyroidism forms a well defined disease entity. commonly identified as
Grave's disease or exophthalmic goiter. The cause of this condition is believed to
be the excessive secretion of thyroid hormones due to abnormal stimulation of
thyrold gland by the circulating immuno globulins, though the actual cause is
unknown. This mainly affects women than men i.e; in the ratlo 5:1, which denotes
that, women are 5 times more prone to hyperthyroidism than men. This is said to
appear after an emotional shock, stress, or an infection, still the exact relations are
not clear. It mainly affects the women members in between 20 years and 40 years
of age. Myperthyrctidism is a highly preventable disorder.
Hyperthyroidism may be due to the over fbnctioning of the entire gland or may
be single or multiple functioning adenoma of thyroid cancer. It can use be caused
due to the over treatment of Myxedema with thyroid hormone.
The most common form of hyper thyroidism is Grave's disease caused by hyper
thyroidism, enlargement of thyroid gland and exophthalmos i.e; abnormal
protrusion of eyes. Grave's disease is said to be an auto immune disorder
mediated by IgG, that binds with thyroid stimulating hormone and activates it.
Other causes that precipitate hyperthyroidism are: Nodular goiter, toxic adenoma,
thyroid carcinoma, sub-acute and chronic thyroiditis, ingestion of thyroid hormone,
and ingestion of Amiodarone hydrochloride.
Grave's disease may be due to excessive stimulation of adrenergic nervous system
or excessive levels of circulatiilg TII. Hyperthyroidism is characterized by loss of
the normal regulatory coiltrols of TH secretion. The action of thvroid hormone
stimulates and causes hypermetabolism with increased sympathetic neiTrous system
In hyperthyroidism, the cardiac system is stimulated which increases Beta
adrenergic receptor. This increases the pulse rate and cardiac output, stroke
volume, responsiveness and peripheral blood flow. Increase in metabolism, leads
to negative nitrogen balance. lipid depletion and ultimately leading to nutritional
Hyper thyroidism also results in the alteration bf secretion and metabolism of
hypothalamics, pituitary and gonadal hormones. If hyperthyroidism occurs before
puberty, sexual development is delayed in both sexes and if after puberty, it
results in decreased libido and will also cause menstrual irregularity and decreased
fertility in women.
Clinical Manifestations
Patient's with well-developed hyperthyroidism exhibits a characteristic group of
symptoms and signs, sometimes called as Thyrotoxicosis. Hyperthyroidism is
manifested by nervousness. emotionally hyper excitable, irritable, apprehensive,
Restless, suffer from palpitation's, tachycardia, heat intolerance, profuse
diaphoresis, incoordination, skin-warm, smooth and moist, increased appetite and
food intake, progressive weight loss, abnormal muscular fatigability, weakness, a
menorrhea, changes in bowel function, increased B.P. and cardiac decompensation.
Goiter is said to be the 2nd major manifestation of hyperthyroidism. In this, the
gland is enlarged and excessive TH is released into blood.
Exophthalmos is the 3rd major manifestation of hyperthyroidism. This causes
protruding of eyes with a fixed stare, anxiety.
Diagnostic Assessment
Diagnostic assessment of hyperthyroidism is based on:
Physical appearance: enlarged neck, protruding eyes, agitated expression.
Presence of symptoms like agitation, restlessness, weight loss etc.
Laboratory findings include:
TSH -decreased
Serum T4 -increased
Serum T3 -increased
Free T4 -increased
Free T3 -inc~-eased
(Hers TWI-thyroid releasing hormone; TSH-thyrt2id stiinulari~lgi~!~rruoiie.T4thyroid; T3-triiodothyroxine.]
Nursing Management in
Endocrine Uisordesi
r.bgy. Burns. Vlaciiic* and
I:cconcitrul'liri htargcr).
Fndocrlnulogicv\ ~wmunelogical
and Tra~t:.-dF - & ~ v ~ ~ E
The major complications of hyperthyroidism are:
It develops as a result of proptosis lid reaction, muscle swelling and tissue edema
from a prolonged hyper thyroid condition. Manifestations may include a gritty
sensation in the eye, photophobia, lacrimation, inflammatory changes and dyslexia.
These cannot be easily corrected with therapy. Diuretics may elevate some
periorbital edema. When glucocorticoides are administered, as their side effect,
they can cause acute psychoses. Radiation therapy may also be given. Other than
this a se\leral nursing measures help the patient to recover. They include providing
sleeping mask, reduce discomfort and reduce eye ulceration and infection;
elevation of the head end and avoid salt intake and providing eye care if
Heart disease has a serious threat. Tachycardia accompanies thyrotoxicosis and
arterial fibrillation. This is most common among the old age patients with
longstanding thyrotoxicosis. Propranol is the drug used but this is contra indicated
if the patient has heart failure or asthma pre-existingly.
iii) Thyroid Storm
Thyroid storm is a potentially fatal, acute episode of increased thyroid activity
characterized by high fever; severe tachy cardia, delirium, dehydration, and
extreme irritability. Factors that cause thyroid storm include untreated
hypei~hyroidism.infection, thyroid ablation, metabolic catastrophy, surgery, trauma,
labor and delivery, myocardial infarction, pulmonary embolus, medication
overdose, ctc. Thyroid storm is a clinical diagnosis, no laboratory test differentiate
hyper thyroidism from this in general. It is called as Thyrotoxicosis and thyroid
Medical Managenzeitt
Treatment for hyperthyroidism has not been discerned yet which combats its basic
cause. Howeker, reduction of thyroid hyperactivity provides effective for
sym2torn':tlc relief and removes the principal source of its important
ca!c;;iicatisns. The medical management aims at:
Curtail excessive secretion of thyroid hormone.
Prej~cntand treat con~plications.
Tandgement aspect is discussed in detail In subsequent section on Nurses'
.ole in pi~innaco!ogical management of endocrine disorders.
Check Your Progress 2
bi~circlerhe correct ansaer (TrueFalse):
Myxedelna ccms is characterized by a drastic decrease in the
metabolic rate.
Decreased lipid levels may lead to deuelopment of cardiac problems
Graves disease is an autoimmune disorder mediated by IgG.
Diuretics may decrease periorbitai edena
Hyperthyroidism leads to increased fertility in women.
4.3.3 Adrenal Disorders
Cushing's Syndrome
Cushing's syndrome was first described by Harvey cushing in 1932. It results
from overactivity of the adrenal gland, with consequent hypersecretion of
glucocorticoids. It may result from excessive administration of' cortisone or ACTH
or from hyperplasia of the adrenal cortex. It can also cause turnor of adrenal
gland that secrete cortisol. This condition 1s characterized by breakdown of muscle
protein and redistribution of body fat. It causes various changes as facial skin
flushed, abdomen stretch marks, wound healing is poor, susceptible to infectio~.
Cushing syndrome is a relatively rare condition. It occurs mainly in chilcken and
women, the average age of onset in women is 20 to 40 years of age. It can,
however be seen up to age 60 years.
The Anterior pituitary gland secretes honnones that regulate a wide range of
bodily activities. Release of anterior pituitary .gland hormones is stimulated by
releasing hormones and suppressed by inhibiting hormones from the
hypothalamus. (ACTH) or adrenocortico tropic hormone or corticotrophin, which
stimulates the adrenal cortex to secrete glucocorticoids, is synthesized by
corticotrophs. Secretioil of ACTH occur by a negative feedback in the form of
hormones released by target glands adjust secretion of anterior pituitary gland
cells. In this (ACTH) stimulate the adrenal cortex of the adrenal gland to secrete
glucocorticoids mainly cortisol.
The hypersecretion of cortisol can be caused by the following factorsA cortisol-secreting adrenal tumors are responsible for approximately 30% of
cases of cushing's syndrome. Most (85%) are benign, but 15 percent are
Adrenal hyperplasia is caused by overproduction of ACTI1. The two sources
of excessive ACTH secretion arepituitary hypersecretion and pituitary tumors causes approximately 70 percent
cases of cushing's syndrome.
ectopic secretion of ACTH. ACTH - secreting tumors located outside the
pituitary gland constitute a rare cause of cushing's syndrome.
iatrogenic cushing's syndrome, another form of.the disorder, results from
exogenous administration of synthetic glucocorticoids in supraphysiologic
Risk Factors
One of the major risk factors for increased level of cortisol is the administration
of exogenous steroids. Whenever steroids are administered: a degree of excess is
present. Placing the client on the lowest amount of steroids possible can help to
control this problem. Other risk factors are related to hyperplasia of the adrenal
gland either as priinaiy disorder or secondary to excessive amount of ACTH.
When cushing's syndrome develops the normal f~nctionof the glucocorticoids
becomes exaggerated and the classic picture of the syndrome emerges. This
exaggerated phyqiologic action of glucocortico~dsappear aq:
Persistent hyperglycemia
Wursine %\.lanagernenti n
Enducrine Disorders
Urology, Burns,
Plastics alnd
Reconstructive Surgery,
Endo'rrinologlral, Immuno~ogical
and 'Rnuma Nursing
Protein tissue wasting, which results in weakness due to musde wasting;
capillary fragility, resulting in ecchymosis;
osteoporosis due to bone matrix wasting
Potassium depletion, leading to hypokalemia, arrythmias, muscle weakness
and renal disorder.
Sodium and water retention, which causes edema and hypertension.
The normal feed back mechanism that control the function of adrenal cortex
become ineffective and the usual diurnal pattern of cortisol is lost. The signs and
symptoms of cushing syndrome are primarily a result of unregulated secretion of
glucocortiroids and androgens or sex hormones, although there may also be
altered mineralo-corticoid secretion.
Clinical ~Mcrnifestations
When overproduction of the adrenal cortical hormone occurs, growth arrest,
obesity and musculoskeletal changes occur.
Cushing syndrome patient has obesity with a fatty 'buffallo hump' in the
neck and supraclavicular areas, a heavy trunk and relatively thin extremities
The skin is thinned, fragile and easily traumatized; ecchymoses and straie
The patient complains of weakness and lassitude. S!tc;p is disturbed because
of altered diurnal secretion of cortisol.
Kypblosis, backache and compression fiactures of the vertebrae may result.
The patient takes on a 'moon-faced' appearance and may experience
increased oiliness of the skin and acne. There is increased susceptibility to
In female of all ages, virilization may occur as a result of excess androgens.
Virilization is characterized by the appearance of masculine traits and the
recession of feminine traits. There is an excessive growth of hair on the face.
The breasts atrophy, menses cease, the clitoris enlarges, and the patient voice
deepens. Libido lost in males and females.
Changes occur in mood and mental activity. A psychosis may develop on
The patient reports of weight changes an& slow healing of minor cuts and
Diagnostic Evaluutisn
Hyperglycemia, fluid and eleclroly-te disturbance and immunosuppressive responses
that characterize excessive gliucocorticoid secretion.
Count of WBC increases lQ,000/m1n3but count of eosinophil below 50 cells/
Clients with cushing syndrome have elevated plasma cortisol levels
throughout the day and can demonstrate a loss of diurnal variation.
Urinary frce cortisol measurement is used as a screening test to [email protected]
elevdcd uri~laryexcretion of free cortisol.
De\arncthasone ssppression test is done in which a low dose and a potent
syntlrctic glucocorticoids are administered and plasma cortisol and urine 17(11
L ~.ctrticosteroidlevels are obtained.
> \
CT scan can be done to localize adrenal tissue and detect tumors of adrenal
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The inferior petrosal sinus sampling test (IPSS) is a radiologic test used to
isolate the source of ACTH secretion. The left and right petrosal sinuses
carry blood from the pituitary glands to the jugular veins. By sampling
ACTH levels drawn from the right and left petrosal sinuses, the side of the
pituitary gland producing ACTH can be identified.
Medical Management
Radiation therapy can be used to treat primary pituitary tumors and other ACTH
secreting adenomas. Radiation can be either ~nternally'or externally applied to
pituitary gland for tumors. Internally the radiation is applied through a
transphenoidal implant. Radiations must be used with care because of the
proximity of the optic nerve. Medications that interfere with ACT13 production or
adrenal hormone synthesis are avai_lable. Mitotane is a cytotoxic antihormonal
agent that inhibit corticosteroid synthesis without destroying cortical cells.
Aminogluthamide and tritostane are other cytotoxic agent that block the synthesis
of glucocorticoids and adrenal steroids. Cyproheptadine is used commonly to treat
hypersecretion due to pituitary abnormalities resulting in increased ACTH levels
This agent appears to interfere with the ACTH production thereby decreasing the
effect on the adrenals.
Surgical Management
The resection of most pituitary tumors causing cushing's syndrome is performed
via transsphenoidal hypophysectomy; large or anatomically complex tumors are
excised. For cushing syndrome due to adrenal tumor, an adrenalectomy can be
performed to remove the gland containing the tumor. In case of ectopic ACTHsecreting tumors, the tumors can be difficult to localize. If no source is found, a
bilateral adrenalectomy can be performed to intempt the production of cortisol in
response to ACTH produced by the tumor, or the client can be treated with
antiglucocorticoids while continuing to search the tumor.
Nursing Management
Assessment: The history includes information about the patient level of activity
and ability to cany out routine and self-care activities. The patient skin is
observed and assessed for trauma, infection, breakdown, brushing and edema.
Changes in physical appearance are noted, and the patient's responses to these
changes are elicited.
Nursing Diagnosis
Impaired ability to carry out self-care activities r;t weakness, fatigue. muscle
wasting and altered sleep patterns.
Impaired skin integrity rit edema, impaired healing and thin, fragile skin.
Increased susceptibility to injury and infection rit altered protein metabolism
and inflammatory response.
Altzred body irnage r/t altered physical appearance, impaired sexual
functioning and decrease in activity level.
Altered mental fullction r/t mood swiligs irritability and depression.
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Patient should be encouraged for moderate work to avoid complication of
immobility and promote self care and increased self esteem.
Rest periods should be planned and spaced throughout the day. Efforts are
made to promote a relaxing, quiet environment for rest and sleep.
Meticulous skin care is necessary to avoid trauniatizing the patient's f::.,ile
skin. The skin and bony-prominences are assessed frequently and the patient
is encouraged to change position frequently to prevent skill breakdown.
A protective environment rnust be established to prevent falls, fractures, and
other injuries to bones and soft &sues.
If removal of the cause of cushing's syndrome is possible and is carried out,
the major changes will disappear in time.
Explanation to the patient and family member about the cause of emotional
instability are important in helping them cope with the mood swings,
irritability and depression that may occur.
Addison's Disease
Glandular hypo function and hyper function characterize the major disorders of
the adrenal cortex. Understanding of the adrenal cortex results in a deficiency of
glucocorticoids, Mineralocorticoids and adrenal ac5rogens. Over activity results in
excessive production of glucocorticoids, mineralocorticoids. and androgens or
Chronic primary adrenal insufficiency or Addisons's disease is a condition that
occurs as a result of hypofunction of the adrenal cortex that can originate from a
disorder with the adrenal gland itself, or it may be due to hypofunction of the
pituitary-hypothalamic unit. Adrenocortical insufficiency can be either chronic or
acute. Addison's disease strikes only 4 of 100,000 persons & affects all age
groups and both sexes.
At one time, most cases of Addison's disease were complication of tuberculosis.
Today 70% are considered idiopathic in origin. Since one half of two thirds of
clients with idiopathic Addison's disease have circulating auto antibodies and so
may havc an autoimmune basis. In addition, a kw cases of Addison's disease are
caused by Neoplasm, Amyloidosis, Systemic Fungal Infections,
The risk factors for primary adrenal insufficiency include:
It is commonly seen in people with AIDS.
Tuberculosis is the cause in about 20% of cases of Addison's disease.
A history of other endocrine insufficiency include this disorder.
Taking glucocorticoids for more than 3-weeks with sudden cessation.
Taking glacocorticoids more than once every other day.
IZfSecls qf ,4tIdi.~on
S Disease
Aliicaterone deticier~cycauses numerous fluid and electrolyte imbalance.
Aldostcrone normally promotes consenration of sodium (Na') and consequently
water and excretion of potassium (Kt).
A deficiency of aldosterone causes
increased sodium excretion, which results in the following chain of events.
Water excretion increases
Extra cellular volume becomes depleted
hypotension develops
Cardiac output decreases
The heart becomes smaller as a result of its diminished workload.
Eventually, hypotension becomes severe and cardiovascular activity weakens,
leading to circulatory collapse, shock and death. Although the body excretes
excess sodium, it retains excess potassium.
Glucocorticoid deficiency causes widespread metabolic disturbances. When
glucocorticoids become deficient, gluconeogenesis decreases with resultant /
hypoglycemia and liver glycogen deficiency. The client grows weak, exhausted
and suffers from anorexia, weight loss, nausea and vomiting. Finally cortisol
deficiency results in a failure to inhibit .anterior pituitary secretion of
adrenocorticotrapic hormone (ACTH).
Melanocyte stimulating hormone (MSH) stimulates the epidennal melanocytes,
which manufacture melanine. Increased ACTH secretion leads to increased
pigmentation of the skin and mucous membranes.
Androgen deficiency fails to produce symptoms in men with Addison's disease
because the testes supply adequate amounts of sex hormones. However, women
depend on the adrenal cortex for an adequate secretion of androgens. The
hormones secretion by the adrenal cortex are essential to life. IJntreated Addison's
disease is ultimately fatal.
Clinical Manifestations
The onset of Addison's disease is usually insidious. The client experiences-mild
fatigue. Imtability, Weight loss, Nausea, Vomiting, Postural hypotension. These
symptoms can be seen for weeks or months before diagnosis of the disease: It can
become an acute emergency sch adrenats crisis.
As the disorder progresses; symptoms intensify. In most of the cases, it causes
gradual fall of general health. Person becomes weak, indisposed to either bodily
or mental exertion. Appetite is impaired or entirely lost. pulse small and feeble,
slight pain or uneasiness is from time to time referred to the region of the
stomach. There is occasionally vomiting , discoloration of skin.
Diagnostic Assessment
Diagnosis of Addison's disease depends primarily on blood and urine hormonal
assays. Diagnostic tests of adrenocortical function include.
ACTH stimulation test: This is the most reliable screening test for Addisonas
disease. In the AC'TH stimulation test, synthetic corticotropin is administered
parenterally. Normally, plasma cortisol levels rise markedly after
administration. However, in a client with Addison's disease, the plasma
cortisol response is low or absent.
Plasma ACTH: Failing the screening test plasma ACTH determination will
accurately categorize clients with primary and secondary high for primary
and normal or low for adrenal insufficiency.
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Serurn electrolytes: Serum sodium level is usually decreased, whereas
potassiunl and calcium levels are usually increased.
Other diagnostic tests may be ordered to evaluate the effects of hypofunction
of the adrenals on the body viz. Blood glucose. X-ray studies; computed
tomography. Magnetic resonance imaging of the adrenals.
Medical Management
Addison's disease was once fatal within months. Today with the manufacture of
synthetic corticosteroids, clients with Addison's disease can live normal, active
lives provided they receive adequate glucocorticoid replacement. Clients shoi~ldbe
carefully assessed for signs of hypercortisolism that can result from excessive
long-term cortisol therapy. Fludrocortisone acetate also should be taken daily
1 OOug by mouth, as miaeralocorticoid replacement therapy.
Assessment: The client's vital signs should be monitored closely while the disease
being diagnosed. Check the pulse carefully, at least every 4 hours. Report drops
in blood pressure below the baseline. Assess for signs and symptoms of increased
physical vitality and emotional well-being.
.\ssess bony prominences to avoid pressure sores in immobilized clients with
therapy: listlessness and exhaustion should gradually lessen and diszppear.
Carefully assess for signs of sodium and potassium imbalance. If steroid
replacement therapy is inadequate, sodium loss and potassium retention continue
uncorrected. If steroid dosage is too high, excessive amounts of sodium and water
are retained and potassium excretion is high.
Nursing Diagnosis and Interventions
", Knowledge deficit R/T self-administeration of steroid medications.
'(ursing Intervention
Provide the client and significant others with written instructions for self~dministrationof steroids. This information should include the:
Importance of taking the medications daily, without fail; exactly as
Principles of self-administration of oral medications
Signs of over and under dosage
Need for an intramuscular self-injection kit to be available at all times.
Actions of prescribed hormones.
~ e e for
d a medic alert bracelet worn to indicate the diagnosis or need
for cortisol replacement.
Znjrtry, High Risk for W T acute adrenal insufficiency seconday to
addison 's crisis.
The nurse should closely monitor for signs and sympton~sof addisonian crisis;
including: Sudden prof~undweakness. Severe abdominal, back and leg pain, hyper
pyrexia follo\;ved by hypothermia, peripheral vascular collapse, coma, Renal
shutdown and death.
The development of an adrenal crisis constitutes a medical emergency that must
be treated rapidly and vigorously. The three major goals of interventions are to:
Reverse shock.
Restore blood circulation: The client usually suffers from a deficit of at least
20% of ECF volume.
Replenish the body with essential steroids.
Immediately on admission, a rapid inksion of 1000 ml of normal saline is
administered with water-soluble glucocorticoid added. The dosage of the
prescribed glucocorticoid is gradually reduced. With rapid, efficient intervention,
addisonian crisis usually passes by 12-hours. The client's condition stabilizes and
the convalescent period begins. When the client is able to tolerate food and fluids
by mouth, steroid replacement can be administered orally.
Activity intolerance R/Tdecreased cortisol production and fitigue.
Nursing Interventions
Assist the patient with activities of daily livi~~g.
Provide for periods of rest and activity to avoid over exertion.
c) ,Provide for high-calorie, high-protein diet.
Instruct the patient about manifestations of excessive use of medications and
reportable symptoms.
Self-steem disturbance'R/T change in functional ability, change in body
Nursing Interventions
Help patient and significant others understand relationship between changes
in self and the disease process; explain that physical changes are reversible.
Help patient set short-term realistic goals.
Compliment patient on accomplishments
Involve patient in decision making, even if patient is unable to perform
physical activities.
Fluid volume deficit R/T sodium and water loss associated with deficiency
of adrenal cortex hormones.
Nursing Interventions
To promote fluid balance, monitor for fluid deficit.
weight every day
intake and output every 1 to 8 hours.
laboratory values for signs of hemoconcentration every day.
skin turgor every 4-hour.
vital signs eveiy 1 to 4 hour.
Report signs of increasing fluid deficit immediately.
Maintain fluid intake at several liters a day
Provide diet with a normal sodium level.
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Altered Nutrition less than body reyuirements R/T Decreased intake
associated with anorexia, nausea, vomiting.
firsing Interventions
Promoting g o d nutrition:
after patient's condition is stable, provide a high-calorie diet idcorporating
food from all food groups.
Provide good oral hygiene before meals.
Provide an environment conducive to eating.
Pain R/T abdominal discomfort.
Nursing Itzterventions
Promoting comfort
Give back rubs
Relaxation techniques
Stress reduction
PatiendFamily Education
The initial teaching during the acute phase relates to proposed diagnostic tests and
immediate interventions. After the patient's condition is stable. information is
given about the disease and long-term needs viz.
Follow medication regimen:
Take drugs with meals or snacks
Glucocorticoids take 213 of dose at approximately 8 AM and 113 of dose
at approximately 4 PM
Mineralocorticoids: take medication in the morning.
Do not omit a drug dose.
Keep sufficient medication on hand
If unable to retain oral form of drug, take parenteral fonn as instructed.
Carry drugs on person or in carry on luggage when traveling; do tiot
ship drugs with luggage; make sure traveling companion knows how to
give the injectable form of glucocorticoid.
Carry extra doses in case of delays or illness.
Wear a medic alert bracelet or necklace that lists condition, drugs and
dosage, and name and phone number of physician.
Monitor self for presence of increased stressors (fever. infections, dental
work, accidents, or family or persunai c:-lszs). And :Elrrecise dose of
elucocorticoid as instructed or consult phycician.
Monitor self daily for signs and symptoms of insufficient dnig therapy
(anorexia, nausea, vomiting, weakness, depression, dizzit~ess.yr.fyuria. and
weight loss) and report immediately.
Monitor self daily for slgns and s v q t o r n s of insufficien! drug therap1
. !anorexia. nausea, vomiting. weakness, depression, dizziness, polqwria, ,!?d
weight loss) and report immediately.
Monitor self daily for signs and sylnptonls of excessive drug therapy (rapid
~veightgain, round face, edcma or hypertension) arid report immediately.
Eat a well-balanced diet. choosing foods from all food groups
Maintain a regular schedule with adequate sleep, regular meals and irregular
Eliminate as many work and home confrontations as possible to decrease
stress response that increase glucocorticoid needs.
See physician as instructed; consult as ncccssp-y if questions arise concerning
Surgery rcsults in complete remission of syrnptoms in most patients; therefore
discharge teaching for most patients is focused on helping the patient plan for
patient resumption of normal activities, maintenance of an adequate diet, and
follow up care.
Additional teaching should include the effect of stressors on the disease and
inetl~odsto reduce or eliminate stress. The patient and significant others should be
able to describeHome medication program, the need for continued treatment if replacement is
necessary, and situatioils that require and increase ii: medication dosage.
Medications follow up plan.
Symptoms indicating adrenal crisis and the need for medical attention.
Need for continual n1edica.l follow up
Need to carry identification card with infornlation concerning physician and
current medication.
Some physicians have the patient to keep a parented form of cortisol at home
and instruct significant others in its administration for emergency purpose. Patients
may also carry a vial of hydrocortisone with a syringe for use when away from
4.3.4 Pituitary Disorders
The hypothalamus and pituitary gland f o m ~a unit that control the function of
several endocrine glands thyroid, adrenals and gonads-as well as a wide range of
physiological activities. This section describes the brain endocrlne interactions or
Types of Pituitary 1)isc~rders
Different types of pituitary disorders depend on the secretion of hormone. If
the hormone is secreted. above the norma4 level it is called Hypersecretion. If
the llormone is secreted, below the normal level it is called Hjposecretion.
Pituitary dwxders are also class~fied on the basis of lobes viz. Anterior
pituitary lobe disordcr that includzs IIypersecretion and Ilyposecretion
disorder.. Posterior pitultar? lobe d~sorderswhich includes Hypersecretion and
Hyyorecretion drsorders Eg kiypcrfimct~onof the pituitary gland (Anterior
lobe), Prolacim I-Iyperse~retion(ilnti'r~orlobe). Growth hornlone Hypersecretion
(Anterior lobe), syndrome of Inappropriate antidiuretic lio.mone secret~on
lobe). Hyposecret~ondisorders inwlws Anterior lobe disorder.
Diabetes lnsipidus (Postenor lobe). Hyperfunction of the Pituitary Gland.
Hypopituitarism is a deficiency of one or more of' the hormones produced by
the anterior lobe of the p~tuitary.
prolactin and growth hormones are the hormones most commonly overproduced
by adenomas. They lead to hyper prolactinemia and acron~egaly.Increased
amounts of growth hormone lcad to rapid growth of all body tissues. This
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increased growth leads to gigantism, if it occurs before closure of the epiphysis
and acromegaly, if it occurs after epiphyseal closure. Pituitary adenomas are intracellular adenomas less than 1 cm in diameter that present with manifestations of
hormonal excess without enlargement or external extension. Pituitary
macroadenomas are tumors larger than 1 cm in diameter and cause generalized
enlargement. Alterations in physiological functioning that occur with pituitary
tumors result from the presence of a space occupying mass in the cranium and
from the effects of the excessive secretion of hormones by functional neoplasm.
Hypopituitarism may result due to Invasion. Infarction. Infiltration, sarcoidosis.
Injury, Iatrogenic, Infections, Idiopathic-familial, Isolated-deficiency of hormones.
In hypopituitarism, the endocrine dysfunction may be the result of hypothalamic
damage or primary pituitary diseases.
Clinical Mangestations
Pituitary tumors produce both systemic and local effects. Systemic Effects lncludeexcessive or abnormal growth patterns related to overproduction of growth
hormone, abnormal milk secretion, over stimulation of one or more of the target
gland. Local Effects includes Pituitary tumors produce manifestations because the
bony cranium that houses the tumor cannot expand to accommodate a growing
mass. Visual field abnormalities resulting from pressure on the optic chiasm.
Headache and somnolence. Neurological manifestations include visual defects with
progression to hemianopia or scotomas finally to total blindness, Headache,
Somnolence, rarely signs of increased intra sranial pressure. With very large
tumors, disturbance in appetite, sleep, temperature regulation and emotional
balance because of hypothalamic involvement may occur. Behavioural changes and
seizures with expansion causing compression of the temporal or frontal lobe may
also occur.
The pituitary gland has enormous functional resume; therefore manifestations of
hypopituitarism usually do not appear until 75% of the pituitary has been
obliterated by tumor or thrombosis. The various manifestations of hypopituitarism
may include short stature - severely stunted growth resulting from either
congenital lack of growth hormone or the development of a space-occupying intracranial tumor; Sexual and reproductive disorder - deficiencies of the gonadotropins
can produce sterility, diminished sex drive and decreased secondary sex
characteristics; Hypothyroidism; Secondary adreno-corticai insufficiency; Prolactin
Diagnostic Evaluation involves History Taking. Physical Examination. Pituitary
Function Testing, Skull Xrays, Computerised Tomography and MRl, Laboratory
tests eg. ACTH Levels can be measured to diagnose secondary adrenal
insufficiency; Cortisol levels are low in both primary and secondary
hypothyroidism, etc.
Pituitary adenomas are treated with surgery, radiation, or drugs to suppress
hypersecretion by the adenoma. Goals of therapy are to correct hypersecretion of
other anterior pituitary hormone and to remove or suppress the adenoma. Medical
Management of pituitary adenomas became feasible with the availability of
bremocriptine, a dopamine agonist. This drug is most successful in the treatment
of hyperprolactinemia and is also useful in selected patients with acromegaly or
cushing's disease. Surgical Management involves tumor resection. A variety of
approaches can be used to remoLe a pituitary tumor. Usually a transphenoidal
hypo-physectomy is performed in which the surgeon approaches the pituitary porn
dnd the nasal cavity through the sphenoid-sinus, removes the anterior inferior
sellar floor and incises the dura to remove the adenoma. Pituitary radiation is
usually reserved for patients with larger tumors, who have had an incomplete
resection of large pituitary adenolnas. Heavy particle irradiation with alpha
particles or protons is used. An advantage of this technique is the ability to focus
the radiation beam precisely, limiting the radiation exposure of surrounding
structures. Disadvantages are the limited availability and the smaller radiation
field; which precludes use of this technique in patients with tumors larger than 1.5
cm in diameter and in those with extrasellar extension.
Management of hypopituitarism involves medical treatment which include
injectioi~sof human growth honnone to treat growth hormone deficiency.
Medications are prescribed to replace hormone include Corticdsteroids to correct
secondary adrenocortical insufficiency, thyroid hormone to treat myxedema and
sex hormones to correct hypogonadism. Surgical management includes surgical
resection of the tumor. Pituitary radiations are also done.
Nursing management focuses on assisting the patient to effectively cope with
changes in body image and teaching about treatment protocols. Patient educaliU,,
, is another focus of care. The patient must be prepared for various diagnostic tests.
Patient/ Family Education of the patient with a pituitary adenoma includes
teaching and support to deal with a variety of issues including body image
changes, anxiety, sexual functioning, activity intolerance and home going
medications. The individual patient and type of tumor and treatment used will
determine which issues are of priority. The family should be involved with
teaching so they will be better equipped to assist the patient at home. If the
patient has been treated surgically with transphenoidal resection, activities causing
increased intracranial pleasure must be avoided. Bending over at the waist.
blowing the nose forcefully, coughing and straining with defecation can increase
intracranial pressure. Teaching should include strategies to prevent constipation
and avoidance of such activities. Assistance may be needed with activities of daily
living because of generalized weakness or neurological deficits. The patient will
generally need regular follow up care to monitor progress and hormone level. The
patient need to be taught about prescribed medications.
Check Your Progress 3
Fill in the blanks with appropriate words:
................. of
Aldosterone promotes
Increased ACTH secreatins ................. pigmentation of skin and mucous
membranes. (increased/decreased)
................. and ................. hormones are the hormones overproduced by
admomas. (Growth, Prolactin, TSH, ACTH)
Hypopituitarisrn is deficiency of hormones of .................lobe of
pituitary. (anterior, posteror)
potassium. (increase/excretion)
intracranial pressure. (increases, decreases).
List down kommon sign and symptoms of endocrine disorders.
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5.Iedical Managemelit of thyroid or other endocrinal disorders aims at:
curtailing excessive secretion of thyroid hormone.
preventing and treating complications.
curtailing Excessive Secretion of 'Thyroid Hormone
The three major forms of therapy used are Antithyroid medications, Radioiodine
therapy and surgery.
hnti-thyroid drugs are often used to control hyperthyroidism during an anticipated
remission and before a thyroidectomy. Since these drugs do not interfere with the
reiease or activity of the previously released thyroid hormones, the relief and
withdrawal of symptoms takes place very slowly and gradually. The therapy is
bnsed or the clinical criteria like changes in pulse rate, pulse pressure, body
weight, function. Toxic effects of the anti-thyroid drugs are very less but the
periodical examination is necessary because, drug sensitization is followed by
fever, rash, urticaria, thrombocytopenia, etc.
Patient's on antithyroid drugs are instructed not to use decongestants for nasal
stiffness because they are poorly tolerated. Antf-thyroid drugs are contra-indicated
in pregnancy because they may produce goiter and cretinism in fetus.
'I'llyroid hormoile may occasionally be given with antithyroid drugs to put the
thyroid gland at. rest. In this approach, hyperthyroidism from excess antithyroid
diug is avoided, as is stimulation of thyroid gland by TSH.
R'ursing Implications
Assess: Pulse, B.P. and temperature, 110, Blood counts, response of the
Wit11 any drug that causes agranulocytosis.
with meals to decrease GI upset.
at some time to maintain drug level.
fluids 3-4 I/day
lowkst dose that relieves symptoms.
medication storcd in light-tight container.
medication must not be given in the last trimester of pregnancy or
during lactation.
report if any symptom of infection.
monitored continually for improvement.
Evaluate: Therapeutic responses like weight gain, decreased pulse, decreased
T3 and T4 level.
Teach patient / family:
to abstain from breast feeding ,after delivery.
to take pulse quarter hourly.
- to-report if any redness, swelling, sore throat, mouth lesions, etc.
to avoid substance with iodine
not to discontinue medication abruptly
that the relief and curing will take time.
to use medic alert ID.
medicine is contraindicated in pregnancy and lactation
- all other medications are stopped before 1 week or 5-7 days.
Thyroid functioning is determined empty stomach.
Institute radiation precaution in the body secretion for 3 days after
Limited contact with the patient i.e 1/2 hr/day.
Adequate rest after treatment.
- Fluid intake 3-4 I/day for 48hrs. to remove agent from body.
to avoid close and prolonged contact with children for a week.
To report in case of redness, swelling, rashes, fever, etc.
Preventing and Treating Complications
Adrenergic Blocking Agents
Adrenergic blocking agents are given to control the activity of the sympathetic
nervous system. They also help to cure 'hyperthyroid heart', because of it's
increased sensitivity to catecholamines and increased no. of B-adrenergic receptor
site. These agents help lessen distressing manifestations like tachycardia and
palpitations. Tretnor and nervousness can also be cured with these agents. The
medication included are Propranolol and Reserpine.
Dietary Therapy
The patient with hyperthyroidism is given high calorie and high protein diet. This
prevents the nitrogen balance and weight loss. Sea foods and other food items
with iodine must be restricted.
Treating Thyroid Stor-m
Heroic intervention is needed for treating thyroid storm since it is an emergency.
High fever and diarrhea and treated with hypothermia blanket and with
intravenous fluid respectively. Managing thyroid storm means suppression of
hormone release, inhibiting hormone synthesis, blocking conversion of T4 $3 'T3.
Inhibiting the effect of TH on body, treating precipitating cause. etc.
Blocking of TH secretion is done using iodine. Sodium iodide is given
intravenously and glucocorticoids, Dexamethasone, propylthiolrracil are
administered orally.
Surgica! management involves surgery for hyperthyroidism bas been performed
from a long perid. The person selected for operation must be young, and free
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from any condition it may cause postoperative risks. A thyroidectomy may be
total or partial. Total thyroidectomy is done to remove cancer. Clients who have
undergone this surgery must take thyroid drugs permanently. Subtotal
thyroidectomy is done to correct hyperthyroidism and extreme cases of simple
goiter. About 5/6 th of the whole gland is removed but since there is a little bit
remaining, hormonal replacement is not necessary.
Preoperative prepar:<tion of thyroidectomy is very important. The patient must get
euthyroid before the operation. If not done, the chances of occurring of thyroid
storm post-operatively are high. The client must be provided with adequate rest
and optimal weight and in good and sound health before operation. Surgical
management is effective in the case of most of the patient. A negligible no of
patients remain with hyperthyroidism and some other develops hypothyroidism.
Very rarely only paralysis of vocal cord or hypoparathyroidism is reported.
Nursing management includes nursing assessment, nursing diagnosis, planning,
implementation and evaluation.
Assessment is done by obtaining a complete client history, which includes
questioning about weight, appetite, activity heat tolerance and bowel activity.
Nurse also observes the patient for the signs and symptoms of hyper thyroidism.
Watch or observe the patient for the clinical manifestations of Grave's disease. He
should also be questioned regarding visual difficulties, fatigue, weakness, tremors
or insomnia. 'The fanlily members of the patient must be asked about any mood
alteration, irritability decreased attention in the patient.
:V~frsingDicg~tosisand lnten~entions
.Iltered r~utrition:less than body requirement R/T accelerated metabolic
provide high calorie and balanced diet.
Six lull meals a day is needed.
Provicle foods that arc nutritious with ample amount of protein,
cnrbc&drates, fats and minerals to maintain nitrogen balance.
Discourage eating of those foods that increase peristalsis.
he weight of the patient must be checked regularly.
If weight is reduced, vitamin B complex must be administered.
intolerance WT exhaustion 2' to accelerated metabolic rate.
provide the client with restful environment.
Help the patient to relax physically and mentally.
Allow them to do their favourite things.
Assign them a quite rootn away from others.
Provide the things, which they need.
High risk for injury: corneal ulceration, infection and possible blindness R/
T inability to close the eyelids secondary to exophthalmos.
The treatment must be started as soon as possible.
The patient must use artificial tears and eye patches to prevent irritation.
The patient must use sleeping masks to induce sleep and also for
Plastic covers can also be used.
Hyperthermia R/T accelerated metabolic rate.
Provide the patient with a cool environment.
Use a light-weight top sheet
Light and loose clothings must be given to the patient.
If the patient is diaphoretic, change the bed linen regularly.
Increase the ventilation of the room by opening the windows, curtains,
. Social
interaction, impaired R/T extreme agitation, hyperactivity and mood
maintain a quite and caring environment while doing the procedures.
Help the family members to cope up with this situation.
Accept their irritation and emotional disturbance as normal expression.
Include occupational therapy in the procedures.
Encourage the patient to ask more questions.
Provide simple activities for the patient to do.
Encourage the patient to interact with his family members.
High risk for injury R/T preoperative preparation, euthyroid state and
surgical procedure.
The client is treated with antithyroid drugs, iodine therapy.
The patient is given adequate bed rest, nutritious diet with vitamins, etc.
The patient with good health has no risk of developing complications.
The postoperative care includes
maintain airway patency.
decrease the strain in the suture line.
relieve discomfort from sore throat and tracheal irritation.
prevent accumulation of respiratory secretions.
prevent complications of thyroidectomy.
Nursing hlanagement id
Endocrine rJisorders
a7aelokv,Burns, Piastics and
e t Surgerj,
PI& T e e TT Yersing
Knowledge deficit R/Tmedications, eye care, possible medication.
Teach the patient to balance the weight of the head and neck when
sitting up
Show them how to flex the neck by the placing the hands at the back of
Instruct the client in range in motion.
Prevent contractures.
Teach the client to move the head forward and laterally.
Ask the patient to do this regularly and every day.
Give instructions of thyroid drugs.
Health Education
Health Education is given to the patient when is about to take care of himself It
lZsli the patient not to have food with iodine.
Ask hiin to avoid sea foods.
Ask hini to stop cigarette smoking.
'k11 him to do the small exercises regularly.
'Ieil hi111 lo avoid over execution.
Teach him the sign and symptoms.
Teach him how to do self-medication
Tell him to visit the doctor regularly.
'reach and tell him about the risk factors also.
Rr1trse.5 RO?P it1 Corticosfrroid Therapy
r-iicrapy may be adn~inisteredorally, Parenterally, Sublmgually,
iCzc~.ally?'by inhalation and by direct application to skin or mucous membrane.
i3pctbre adrnt:listi.r~ngany of the adrenal agents, the nurse should perform a
: i ~ ~ r o u gph\sici~I
a~stssmentto determine the patient's baseline weight, intake
a i d otitpr~t,rta~us,vital s i g ~ ~(especially
B.P.), hydration status, skin condition, and
immune status Important baseline laboratory values include the serum Na, K,
RUN. and tlb levels and lict. All this is crucial for ensuring the safe and most
effective use \>f these adrenal agents and for identifying any specific cautions or
i.ot~trdinJictir:niis111 advance of treatment, as well as ibr monitoring the patient's
rcspcjn3e to the t~-cd~~nt'nt.
Any edema or electrolyte imbalances need to be
docilmented and brought to the attention of the physician. Because glucocorticoids
~ 3 ! iclevatc a patient's blood glucose level, a baseline level must be determined.
The nurse should find out whether the patient has a history of ulcer disease,
gastritis or heartburn.
7 here are many drugs that interact with corticosteroids, so the nurse should
always find out \\]hat prescription and over the counter medications the patient is
currently taking to prevent their interactions from occurring.
Xursing Management
Nursing Diagnosk and Intervetrtions
Risk fir infection related to side efl'ects qf gliicocorricnid tlrerapy.
Encourage the patient to avoid crowd and the possibility of exposure to
Encourage exercise to prevent venous stasis.
Be aware that signs of infection1 inflammation may be masked by fever.
redness and swelling.
Excess fluid volume related to increased cardiac oittprtt .from increased
volume or fluid retention associated with mine~alocorticoid.
Restrict Na intake and increase K intake by
Avoiding saline as diluent in preparing injectable medications
Give lemon juice, which is high in K and low in Na.
Check blood pressure ftequently and weigh the patient daily.
Observe for edema.
hqaintain I/O chart.
Impaired skin integrity relafed to side eficts of glucocorticoids.
Monitor the client's skin meticulously for breakdown
Avoid using tape or other irritants that may tear or excoriate the skin.
Sterile technique should be used while applying topical agents if skin is
not intact.
Altered thought processes {memory loss, cognitive impairmerzt. mood
swings, depression) related to increased level of glucocorticoids and ACTH
resulting in an inability to make decisions and remember.
Recognize and report any brood that deviates from the usual behaviour
Report unusual behaviour, dreams withdrawal or suicidal tendencies.
Advise the patient to avoid extremes of temperature and upsetting
Reassure the patient and give psychological support.
Activity intolerance related to fafigue and muscle weakttess .from profri~r
upasting, persistent hyperglycemia and K depletir,~resulting it# arr irrubilig
fu maintain a normal astir*@level.
Drornotc inental and pl~ysicalrcst by giving colnfc~r',:ll~:\~using recreational therapy.
Endocrine Disordl.7
Urologv, Burns, Plastics and
Reconstructive Surgery,
Endocrinological, Immunological
and Trauma Nursing
Minimize stress and confusion so that client can achieve maximal
periods of rest.
Recommend a program of activities of daily living and weight bearing;
norrnal range of motion and safe repositioning for the bed ridden.
Patient Teaching Tips
Because of their suppressed immune system, patients taking
corticosteroid should avoid people with infections and report any fever,
increased weakness and lethargy or sore throat.
Encourage patients to tell about unpleasant side effects and changes in
Encourage patients to get adequate rest, exercise and nutrition.
They should understand the importance of their nutritional status,
weight, fluid volume, electrolyte balance, and skin turgor and glucose
1et.t.l~during therapy.
Encourage patients to keep a daily log of their general feelings of wellbeing and any questions for the physician.
Patients should take all adrenal medications exactly as prescribed and at
the same time every day. Oral agents are to be taken with meals / foods.
Patients should wear medical alert tags at all times.
Check Your Progress 4
List down general nursing implications involved in pharmacologicat management
o f endocrine cdiscders.
You have read in their put unit on various common endocrinal disorders and
almost in each of them, various changes when take place in the physical and
mental characteristics of the individual that poses a great conccrn not only for the
individual but also the health team including nurses. It poses a challenge for the
health team to deal with such chronic changes as these affect other body functions
also. Skilled and imaginative nursing care and close supervision hastens early
recovery and prevents various complications. Nurse plays an important role as a
liaison between the client and other health team members in the management of
such disorders.
Congenital condition due to lack of thyroid
secretion, characterized by arrested physical and
mental development.
Profuse seveating
An imprecise term concerning a condition in which
an individual with normal vision is unable to
interpret written language.
Normal functioning of thyroid gland
Elargement of thyroid gland
Rolling of the 'eye ball
An involuntary movement of a part of parts of the
body resulting from alternate contractions of
opposing muscles.
Check Your Progress 1
Personality changes
Mental changes-impaired
and sonnolence,
memory, slowed speech, decreased initiative
Others-hairloss, dry and coarse skin, brittle nails, hoarseness, cold
intolerance, muscle weakness B: swelling, constipation, weight gain,
Activity intolerance
Body image disturbance
Knowledge deficit
Altered Nutrition
Urology, Burns. Plastics and
Reconstructive Surgery,
Endacrinologicai, Immunological
and lkauma Nursing
Self care deficit
Sexual dyshction
Impaired skin integrity
Impaired thought process
Check Your Progress 2
Check Your Progress 3
Prolactin, Growth
Mental status changes--extreme alterations in consciousness e.g. coma,
lability of mood, mental confusion, depression
Changes in vital signs-increased body temperature, fatigue, tremoss,
palpitation, tachycardia, deeprapid breathing
iii) Weight ciiznges-gaidloss
of weight
iv) Polydipsil, polyuria, changes in bowel status
v) Menstrual irtegularities, loss of libido, impotence and infertility
vi) Hyperpigmentation, edema, hirsutism
vii) Exophalmos, bone pain, cyst, tiac'ture
viii) Renal colic and stones
ix) Tetany, parsthesia, muscle cramps
Check Your Progress 4
General nursing implications involved in farmacological management of patient
with endocrille disorders:
Assess vital signs
Administer with meals to decrease GI upset
Increase fluids 3-4 litresiday
Check for weight changes
Avoid giving in 1st and last trimester of pregnancy
Ensure adherance to diug regimen
Watch for complications or side-effects
Give high calorie high protein diet
Ensure regular follow up.
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