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1. Recall the DISORDERS OF ENDOCRINE SYSTEM Lecture, Listen, LCD, OHP, Can.you
anatomy ANATOMY OF ENDOCRINE SYSTEM:- discussi answe explain the
and Endocrine glands are groups of secretory on , ring. anatomy
physiolo-gy cells surrounded by an extensive network of explanat and
of capillaries that facilitates diffusion of hormones ion& phisiolog-y
Endocrine from the secretory cells into the bloodstream. question of endocrine
gland They are commonly referred as ductless glands, ing gland.
because hormones diffuse directly into the
bloodstream. Hormones are then carried in the
bloodstream to target tissues and organs that may
be quite distant, where they influence cellular
growth and metabolism.

ENDOCRINE GLANDS ARE:-

 1 Pituitary gland.
 1 Thyroid gland.
 4 Parathyroid gland.
 1 Thymus gland.
 1 pineal gland
 2 Adrenal gland.
 The Pancreatic islets.
 2 Ovaries in female.
 2 Testes in male.

1
PITUITARY GLAND:-The pituitary gland lies
in the hypophyseal fossa of the sphenoid bone
below the hypothalamus, to which it is attached
by a stalk. it is the size of a pea, weighs about 500
mg and consists of three distinct parts that
originate from different types of cells. the anterior
pituitary is an upgrowth glandular epithelium
from the pharynx and the posterior pituitary is a
downgrowth of nervous tissue from the brain.
There is a nerve fibres between the hypothalamus
and the posterior
pituitary.

2
Fig:- position of endocrine gland.

Hormones secretes from anterior pituitary:-

 Growth hormone:-
 Thyroid stimulating hormone.
 Adrenocarticotropic hormone.
 Prolactin.
 Gonadotrophins hormone.

3
 Fig:-pituitary gland and hypothalamus

Hormones secretes from posterior pituitary:-

 Oxytocin
 Antidiuretic hormone.

Pituitary and hypothalamus

the pituitary gland and the hypothalamus act as a

unit, regulating the activity of most of the other
endocrine glands. The pituitary gland lies in the
hypophyseal fossa of the sphenoid bone below the
hypothalamus, to which it is attached by a stalk.
The influence of the hypothalamus on the
pituitary gland:-

4
The influence of the hypothalamus on the release
of hormones in the anterior and posterior lob of
the pituitary gland.

The anterior pituitary:-

The hypothalamus and anterior glands are
connected by hypothalamic- hypophyseal portal
blood supply. Blood entering the anterior pituitary
gland has first passed through the hypothalamus.
The hypothalamus regulates anterior pituitary
functions by the synthesis of releasing or
inhibiting hormones and secretion into the
hypothalamic – hypophyseal portal blood supply.
These hormones are released in the anterior
pituitary gland and stimulate or inhibit release of
appropriate hormones

THE POSTERIOR PITUITARY

The hypothalamus is connected to the posterior

gland by nerve tracts that originate in the
paraventricular and supraoptical nuclei of the
hypothalamus. Posterior pituitary hormones are
actually synthesized in hypothalamus and
transported along nerve axon to the posterior
pituitary gland, where they are stored .

5
HORMONES SECRETED BY PITUITARY
GLAND AND THEIR FUNCTIONS

HORMONE FUNCTION
GH Regulates metabolism,
promotes tissue growth
especially of bone s and
muscles.
TSH Stimulates growth and activity
of thyroid gland and secretion
of T3 and T4.
ACTH Stimulates the adrenal cortex
to secrete glucocorticoids.
Prolactin Stimulates milk production in
the breasts.
FSH Stimulates production of sperm
in the testes, stimulates
secretion of oesteogen by the
ovaries, maturation of ovarian
follicles, ovulation.
LH Stimulates secretion of
testosterone by the testes,
stimulates secretion of
progesterone by the corpus
luteum
Oxytocin Stimulates uterine smooth
muscle and the muscle cells of

6
 the lactating breast after child
birth.
ADH main effect is to reduce urine
output and smooth muscle
contraction.

THYROID GLAND:-Thyroid gland is situated

in the neck in front of the larynx an trachea at the
level of the5th, 6th, and 7th cervical and 1st thoracic
vertebrae. It is highly vascular gland that weighs
is about 25g.

Hormones secretes from thyroid gland:-

 Thyroxine (T4).
 Triiodothyronine(T3 ).
 Calcitonin.

HORMONES SECRETED BY THE

THYROID GLAND AND THEIR
FUNCTIONS

HORMONES FUNCTIONS
T4 , T3 Increasing the basal metabolic
rate and heat production.
Regulating metabolism of
carbohydrates, protein s and

7
 fats.
Calcitenin it reduces the reabsorption of
calcium from bones and kidney.
PARATHYROID GLAND:-there are four small
parathyroid glands, two embedded in the posterior
surface of each lobe of the thyroid gland.

Hormones secretes from parathyroid gland:-

 Parathyroid hormone:-The main function of PTH
is to increase the blood calcium level when it is
low.

ADRENAL GLAND:-
there are two adrenal glands, one situated on the
upper pole of each kidney enclosed within the
renal fascia. They are about 4cm long and 3cm
thick.

8
 Fig:-kidney and adrenal gland.

Hormones secretes from adrenal cortex:-

 Glucocorticoid .
 Mineralocorticoid.
 Sex hormones

Hormones secretes from adrenal medulla:-

 Adrenaline.
 Nonadrenaline

Hormones Functions
Glucocoroticoid Gluconeogenesis,
lipolysis, energy
production.

9
 Promoting absorption
of sodium and water
from renal tubules.
Minerlocorticoids Maintenance of water
and electrolyte
balance in the body
Sex Contributing for onset
hormones(androgens) of puberty.
Adrenalin Adrenalin has agreater
effect on the heart and
metabolic processes.
Noradrenaline It Influence on blood
vessels.

10
Fig:-position of adrenal gland.

PANCREATIC ISLETS:-
The Pancreas is both an endocrine and
exocrine gland. The function of exocrine
pancreas is to produce pancreatic juice containing
enzymes that digest carbohydrates, proteins and
fats, proteins and fats.
Distributed through but the gland are
groups of specialized cells called the pancreatic
islets (of langerhans). The islets have no ducts, so
the hormones diffuse directly into the blood.
There are three main types of cells in the
pancreatic islets :-

11
(1) ∝ cell - That secrete Glucogon.
(2) β Cells - that secrete insulin.
(3) δ Cells - that secrete insulin.
Main Function of Glucogoni –
 Conversion of glycogen to glucose in the
liver and skeletal muscles (glycogenolysis)
 Gluconeogensis (Formation of new sugar
from – protein, fat etc.)
Main function of insulin :-
 Conversion of glucose to glycogen
 Acceleration uptake of amino acids by cells
and the synthesis of protein.
 Promoting lipogenesis.
 Decreasing glycogenolysis.
 Preventing gluconeogenesis.
 Storage of glucose in liver fat tissue and
skeletal muscles.

PINEAL GLAND OR BODY:-the pineal gland

is a small body attached to the roof of the third
ventricle. The pineal gland is about 10mm long,
is reddish brown in color.
Hormones secretes from pineal gland:-
Melatonin:- inhibition of growth and development
of the sex organs before puberty.
The gland tends trophy after puberty.

12
 THYMUS GLAND:-the thymus gland lies in the
upper part of the mediastinum and extends
upwards into the roof of the neck.

Hormones secretes from thymus gland:-

 Thymosin:-it required for the development of T-
lymphocytes.

OVARY- The two ovaries are female gonads, or

glands, and they lie in a shallow fossa on lateral
walls of the pelvis.
Hormones secretes from ovarian gland:-
 Follicle stimulating hormone.
 Luteinising hormone.

TESTES:- The Testes are suspended in the

scrotum by the spermatic cords .
Hormones secretes from testes:-
 Testosterone.

PHYSIOLOGY:- the level of hormones in the

blood is varies and self- regulating within its
normal range. A hormone is released in the
responds to a specific stimulus and usually its
action reverses or negates the stimulus through a
negative feedback mechanism .this may be
controlled either indirectly through the release of

13
hormones by the hypothalamus and the Anterior
Pituitary gland.
The effects of a positive feedback
mechanism are amplification of the stimulus and
increasing release of the hormone until a
particular process is complete and the stimulus
ceases.

Fig:-negative feedback mechanism.

14
2. Discribe DISORDERS OF ENDOCRINE GLAND Lecture, Listen, OHP, LCD Can.you
about discussi answe explain
acromegaly DISORDERS OF PITUITARY GLAND:- on , ring about
its etiology, explanat acromegaly.
clinical Disorder of anterior pituitary gland is:- ion&
manifestatio 1. Acromegaly question
n, 2. Hypopituitarism ing
pathophysio 3. Pituitary tumors
logy, 4. SIADH
diagnostic Disorder of posterior pituitary gland:-
evaluation, 1. DI
treatment,
nursing
management ACROMEGALY
.
Introduction:-

Anterior pituitary gland produces Growth

Hormone which stimulate the growth of bodily
tissues. Hyperpituitarism, also called acromegaly
and gigantism. It results in longitudinal growth of
long bones. These children may grow as tall as 8
feet. In adults excessive Growth Hormone cause
acromegaly. Because this develops after
epiphyseal closure in adults, the bones are unable
to grow longer. Instead, the bones increase in size
and width.

15
Definition
Acromegaly is the overgrowth of the bones and
soft tissues due to excessive secretion of the
growth hormone.

Etiology:-
It is caused by prolonged, excessive secretion of
growth hormone (GH). The most common cause
of acromegaly is a benign tumour (adenoma) of
the somatotroph cells, which produce growth
hormone. These cells are within the anterior
pituitary gland, located in the middle of the head
just below the brain.

Pathophysiology:-

In adults excessive Growth Hormone cause

overgrowth of bones and tissues. Because this
develops after epiphyseal closure in adults, the
bones are unable to grow longer. Instead, the
bones increase in size and width. It results in
structural changes of the skeletal system. It
develops gradually, usually during the third and
fourth decades of the life. Individuals experience
enlargement of hands and feet. The fingertips
develop a tufted or clubbed like appearance. The
enlargement of bones and cartilage may cause

16
mild joint pain to deforming, clipping arthritis.
Changes in physical appearance occur with
thickening and enlargement of bony and soft
tissue on the face and head. Enlargement of
mandible causes jaw to jut forward. The paranasal
and frontal sinuses enlarges. Enlargement of soft
tissue around eyes, nose and mouth results in
hoarsening of facial structures. Enlargement of
tongue results in speech difficulties, and the voice
deepens as a result of the hypertrophy of the vocal
cords.

Overproduction of growth hormone

-- Enlargement of viscera without increase in
height -- fingertips develop a tufted or clubbed
like appearance -- mild joint pain to
deforming, clipping arthritis -- Enlargement of
mandible -- The paranasal and frontal sinuses
enlarges --- Enlargement of soft tissue around
eyes, nose and mouth -- Change in facial
structures

17
Clinical Manifestations
 Excessive growth of soft tissue, cartilage,
and bone in the face, hands and feet.
Face and head — Facial features (nose,
lips, ears, and forehead) become broader
and larger the tongue enlarges, the space
between the teeth increases, and the lower
jaw grows, resulting in an under bite and
extended lower jaw.
 headache may be present.
 Facial hair growth increases, which may
be especially bothersome to women.

18
 Throat — Excessive soft tissue growth of
the throat and voice box can lead to a
hoarse voice or sleep apnoea (a condition in
which a person stops breathing temporarily
during sleep, causing lowered levels of
oxygen and disrupted sleep).
 Hands and feet — The hands and feet
enlarge, often requiring patients to wear
larger sized rings, gloves, and shoes.
Overgrowth of tissues in the wrist can
compress nerves to the hands, leading to
tingling or pain in the fingers (called carpal
tunnel syndro me).
 Skin — The skin may thicken, and skin
tags may appear. Excessive sweating, even
while resting, is common.
Bones — Overgrowth of the ends of bones
can damage neighbouring cartilage and lead
to arthritis.
 Tumors — Patients with acromegaly have
an increased risk of noncancerous (benign)
tumors, especially if growth hormone levels
are not controlled. Benign tumors of the
uterus (fibroids) are more common in
acromegaly. Polyps of the colon are more
common, and can become cancerous if not
surgically removed.

19
  Heart — The incidence of heart disease is
increased, likely due to enlargement of the
heart muscle, which impairs functioning of
the muscle (called cardiomyopathy). High
blood pressure is more common in
acromegaly. Some people have problems
with their heart valves. Heart failure may
occur if acromegaly is uncontrolled.
 Diabetes — Higher blood glucose levels
may be a direct result of excessive growth
hormone production, which causes insulin
resistance. Diabetes is more common in
people with acromegaly, and people with
previously diagnosed diabetes may require
higher doses of medication.
 Life expectancy may be reduced by
approximately 10 years, especially when
growth hormone levels are uncontrolled
and diabetes and heart disease are present.
Patients with controlled hormone levels
generally have a normal life expectancy.

Complication:-
 Delayed puberty

 Difficulty functioning in everyday life due

to large size and unusual features
20
  Diminished vision or total vision loss
 Embarrassment, isolation, difficulties with
relationships, and other social problems
 Hypothyroidism
 Severe chronic headaches
 Sleep apnea

Diagnostic Studies
If acromegaly is suspected based upon a person's
appearance, the diagnosis must be confirmed by
measurement of IGF-1 and growth hormone
levels. The blood level of IGF-1 can be
determined in a single blood sample drawn at any
time of day.
 Growth hormone must be measured by
taking several samples of blood, drawn
before and after drinking a glucose (sugar)
solution. In acromegaly GH concentration
do not fall.
 Plasma GH evaluation.
 MRI: Once excessive growth hormone
secretion has been confirmed, magnetic
resonance imaging (MRI) is indicated for
identification, localisation ane
determination of extension of the pituitary
tumour.
 CT scanning may also be used to locate the
tumour.
21
  A complete ophthalmologic examination,
including visual fields to assess pressure of
macroadenoma on optic nerves.
Treatment
Patients with acromegaly are treated to avoid the
risk of complications, even if there are no obvious
symptoms. The goal of therapy is to lower the
level of growth hormone and IFG-1 in the blood.
If therapy is successful, the soft tissue changes
will regress over a period of several months and
the risk of early death returns to normal.
Sometimes, initial treatment is not entirely
successful and additional treatment is needed.
There are three main forms of treatment: surgery,
medications, and radiation therapy.
Medication theray:-
There are three classes of medications used to
treat acromegaly:

 Somatostatin analogs (octreotide or

lanreotide)
 Dopamine agonists, especially cabergoline
 Growth hormone receptor antagonist
(pegvisomant)

Somatostatin analogs — Somatostatin analogs

inhibit secretion of growth hormones from the

22
growth hormone-secreting cells of the pituitary.
Ø Octreotide (Sandostatin) is made in short-acting
and long-acting forms. The short-acting form is
given three times a day by injection, and the long-
acting form is given every four weeks by
injection.
Ø Lanreotide (Somatuline) is available in a long-
acting form that is injected every four weeks.
These medications can be used as an initial
treatment, especially when an adenoma is too
large to remove completely with surgery. They
can also be used as secondary treatment for
people who have remaining adenoma tissue and
an elevated blood growth hormone concentration
after transsphenoidal surgery.
· Growth hormone receptor antagonist — Growth
hormone receptor antagonists block the effects of
growth hormone by binding to the hormone
receptor, decreasing IGF-1 production and
thereby decreasing growth effects. Pegvisomant
(Somavert®) is given daily by injection.
· Dopamine agonists — Dopamine agonists may
inhibit growth hormone secretion and therefore
decrease IGF-1 levels, although they are not
usually as effective as other classes of
medications. They can be taken orally and may be
more convenient than other forms of treatment.

23
Surgery:-
Surgery offers the chance of a cure if the
somatotroph adenoma can be completely
removed. Surgery is also the first choice of
treatment when the adenoma is very large and
impairing or threatening vision.
During surgery, a small incision is made in the
nose. The incision is extended through the
sphenoid sinus, allowing the surgeon to visualize
and remove the adenoma. An endoscope (a thin,
lighted tube with a camera) may be used to ensure
that the adenoma has been removed completely.
Alternately, the entire procedure may be
performed using the endoscope.
Surgery is usually effective in reducing growth
hormone levels, although levels do not always
return to normal. The chance that the growth
hormone levels will be normal after surgery is
directly related to the size of the adenoma before
surgery. The levels of growth hormone and IGF-1
will return to normal in about eighty percent of
people with small adenomas (less than 1 cm [0.5
inch]). On the other hand, only about 30 percent
of people who have larger adenomas that extend
beyond the pituitary will have normal hormone
levels after surgery.
If the adenoma is completely excised, the blood

24
GH level falls to normal within hours after
surgery and the blood IGF-1 level returns to
normal within weeks to months.

Radiation therapy:-Radiation therapy has been

used for many years for treatment of pituitary
adenomas, including somatotrophadenomas.
Radiation can be delivered in one of several ways:
A linear accelerator
A cobalt source (gamma radiation)
A cyclotron (proton beam)
Radiation can be given as a single large dose or in
multiple smaller doses. Whatever the source and
number of doses, the radiation is directed
stereotactically (three-dimensionally) to the
adenoma by a computerized program.
Radiation therapy is usually effective in stopping
or even reversing adenoma growth, and in
decreasing growth hormone and IGF-1
production. However, the decline in growth
hormone secretion (and clinical improvement) is
very slow. Even 10 to 15 years after radiation,
only a small percentage of patients achieve a
normal blood growth hormone level.

Nursing Assessment:-
o Assess the body changes of the patient.

25
o Assess the sensory perception status of the
patient
o Assess the fluid and electrolyte status of the
patien
o Assess the sleeping pattern of the patient.
o Assess the anxiety level of the patient.
o Assess the coping ability of the patient.
o Assess the knowledge level of the patient
regarding features and treatment of the disorder.

Nursing Diagnosis
1. Disturbed body image related to enlargement of
body parts as manifested by enlarged hands, feet
and jaw.
2. Disturbed sensory perception related to
enlarged pituitary gland as manifested by
protrusion of eye balls .
3. Fluid volume deficit related to polyuria as
manifested by excessive thirst of the patient.
4. Disturbed sleeping pattern related to soft tissue
swelling as manifested by verbalization of the
patient about insomnia.
5. Anxiety related to change in appearance and
treatment as manifested by verbalization of the
patient about body appearance.
6. Ineffective coping related to change in
appearance as manifested by verbalization of

26
negative feeling about the change in appearance.
7. Knowledge deficit regarding development of
disease and treatment as manifested by repeated
questions by the patient regarding disease and
treatment.

Nursing Interventions :-

1. Disturbed body image related to

enlargement of body parts as manifested by
enlarged hands, feet and jaw.
o Assess the body changes of the patient.
o Give psychological support.

2. Disturbed sensory perception related to

enlarged pituitary gland as manifested by
protrusion of eye balls.
o Assess the sensory perception status of the
patient
o Administer medications if ordered

3. Fluid volume deficit related to polyuria as

manifested by excessive thirst of the patient.
o Assess the fluid and electrolyte status of the
patient.
o Provide more oral fluids to the patient.
o Administer IV fluids if ordered.

27
4. Disturbed sleeping pattern related to soft
tissue swelling as manifested by verbalization
of the patient about insomnia.
o Assess the sleeping pattern of the patient.
o Provide comfortable position to the patient.
o Provide calm and quiet environment.

5. Anxiety related to change in appearance and

treatment as manifested by verbalization of the
patient about body appearance.
o Assess the anxiety level of the patient
o Explain the patient about progressive features of
the disorder
o Divert the attention of the patient by talking.

6. Ineffective coping related to change in

appearance as manifested by verbalization of
negative feeling about the change in
appearance.
o Assess the coping ability of the patient.
o Provide psychologic support to the patient.

7. Knowledge deficit regarding development of

disease and treatment as manifested by
repeated questions by the patient regarding
disease and treatment.
o Assess the knowledge level of the patient

28
 regarding features and treatment of the disorder.
o Explain the patient about progressive features of
the disorder.
o Clarify patient’s doubts and questions regarding
hyperpituitary disorder.

Prognosis:-
Prognosis is good in patients who receive prompt
treatment. Surgery is successful in up to 80% of
the patients depending on the size of the tumor
and the skill of the surgeon. Remission rates
mainly depend upon the initial size of the pituitary
adenoma, the GH level, and the skill of the
neurosurgeon. Microadenomas have 80-85%
remission rate, while macroadenomas have 50-
65% remission rates. A postoperative GH
concentration of less than 3 ng/dL was associated
with a 90% remission rate.

3. Discribe HYPOPITUITARISM:- Lecture, Listen, LCD OHP, Can.you

about discussi answe Videos. explain
hypopituitar Introduction:- Hypopituitarism is rare disorder on , ring about
ism its that involves a decrease in one or more of the explanat clinical
etiology, anterior pituitary hormones. any combination of ion& manifestatio
clinical deficit of six hormones may occur in question n of
manifestatio Hypopituitarism. ing hypopituitar
n, ism.

29
pathophysio Definition:- Hypopituitarism is that involve a
logy, decrease in one or more of the anterior pituitary
diagnostic hormones such as GH, ACTH, GTH, PRL, TSH
evaluation, Hormones.
treatment,
nursing Etiology:-
management  Tumor:-Craniopharyngioma; primary CNS
. tumors; nonsecreting pituitary tumors.
 Ischemic changes:-Sheehan’s syndrome
ischemic changes following PPH or
infection related shock.
 Developmental abnormalies.
 Infections:- viral encephalitis, bacteremia
and tuberculosis.
 Autoimmune disorders.
 Radiation:-Damage, particularly after
treatment of secreting adenomas of
pituitary gland.
 Trauma:-including surgery.

Pathophysiology

The sequential loss of anterior pituitary hormones

secondary to a mass effect occurs with the loss of
the least important hormones initially: namely,
GH and gonadotrophins (LH and FSH). This is
subsequently followed by the loss of more

30
important hormones: namely, ACTH and TSH.
The hormones least needed for survival are lost
first and the ones critical for survival are
preserved till later.

Pituitary adenomas may present with a typical

clinical syndrome, such as acromegaly, Cushing's
syndrome, prolactinoma syndrome,
thyrotrophinoma, or gonadotrophinoma
syndromes, resulting from hypersecretion of one
or more anterior pituitary hormones. Alternatively
they may present more insidiously with mass
effect or with tumour expansion leading to
compression of surrounding structures, including
normal pituitary tissue with destruction of
hormone-producing cells. Hypopituitarism
resulting from pituitary adenomas is thought to be
related to impaired blood flow to the normal
pituitary tissue, compression of normal tissue, or
interference with the delivery of hypothalamic
hormones via the hypothalamus-hypophysial
portal system.

Pituitary apoplexy presents with sudden onset of

an excruciating headache, visual disturbance, or
ophthalmoplegia due to cranial nerve palsies (III,
IV, VI). Sudden onset of ACTH deficiency and

31
subsequent cortisol deficiency is serious and can
cause life-threatening hypotension,
hyponatraemia, and hypoglycaemia.
Hypopituitarism caused by pituitary infarction
may develop immediately or after a delay of
several years, depending on the degree of tissue
destruction.

CLINICAL MANIFESTATION:-

 Presentation varies from asymptomatic to

acute pituitary failure with acute collapse
and coma, depending on the aetiology,
rapidity of onset, and predominant
hormones involved.
 Initially, a patient with any hormone
deficiency may be asymptomatic.
 May present with endocrine dysfunction:
1. Adrenocorticotrophic hormone
(ACTH) deficiency:
 Chronic: fatigue, pallor,
anorexia, weight loss
 Acute: weakness, dizziness,
nausea, vomiting, circulatory
collapse, fever, shock
 Children: delayed puberty,
failure to thrive

32
  Hypoglycaemia, hypotension,
anaemia, lymphocytosis,
eosinophilia, hyponatraemia
2. Thyroid-stimulating hormone (TSH)
deficiency:
 Tiredness, cold intolerance,
constipation, hair loss, dry
skin, hoarseness, cognitive
slowing
 Weight gain, bradycardia,
hypotension
 Children: retarded
development, growth
retardation
3. Gonadotropin deficiency:
 Women: oligomenorrhoea,
loss of libido, dyspareunia,
infertility, osteoporosis
 Men: loss of libido, impaired
sexual function, mood
impairment, loss of facial,
scrotal, and body hair;
decreased muscle mass,
osteoporosis, anaemia
 Children: delayed puberty
4. Growth hormone deficiency:
 Decreased muscle mass and

33
 strength, visceral obesity,
fatigue, decreased quality of
life, impairment of attention
and memory
 Dyslipidaemia, premature
atherosclerosis
 Children: growth retardation
5. Antidiuretic hormone deficiency:
 Polyuria, polydipsia
 Decreased urine osmolality,
hypernatraemia
6. May also present with features
attributable to the underlying cause:
 Space-occupying lesion:
headaches or visual field
deficits
 Large lesions involving the
hypothalamus: polydipsia and
inappropriate secretion of
antidiuretic hormone

Hypopituitary coma

 Usually occurs in a patient known to have

hypopituitarism and often develops
gradually but may occur suddenly due to

34
 pituitary apoplexy.
 May be triggered by infection, trauma,
surgery, hypothermia or pituitary
haemorrhage.
 Clinical features include hormone
deficiencies, meningism, visual field
defects, ophthalmoplegia, reduced
consciousness, hypotension, hypothermia
and hypoglycaemia.
 Treatment is required urgently in the form
of intravenous hydrocortisone. Thyroid
replacement (T3) should only be started
once hydrocortisone therapy has been
given. Pituitary apoplexy requires urgent
surgery.

Complications

 Morbidity is variable depending on the

degree of hormone deficiency and the
underlying cause.
 Susceptibility to infection is increased.

DIAGNOSTIC EVALUATION:-

 Blood glucose, renal function and

electrolytes (disturbances of renal function,

35
 glucose and electrolytes are common).
 Hormonal assays:
o Thyroid function tests, prolactin,
gonadotrophins, testosterone,
cortisol.
o Measurement of gonadotrophins,
TSH, growth hormone, glucose and
cortisol following triple stimulation
with gonadotrophin-releasing
hormone, TRH (thyrotropin-
releasing hormone) and insulin-
induced hypoglycaemia.
 Cranial MRI scan should be performed to
exclude tumours and other lesions of the
sellar and parasellar region after
hypopituitarism has been confirmed.[1]

Management

 Acute resuscitation, including intravenous

saline boluses,[7] may be required.
 If hypopituitarism has been caused by a
tumour, pituitary function may be restored
after successful surgical or medical removal
of the lesion.
 Medical care consists of hormone
replacement as appropriate and treatment of

36
 the underlying cause.
 Glucocorticoids are required if the ACTH-
adrenal axis is impaired, especially in acute
presentations. Increased doses of
glucocorticoids are required following any
form of emotional or physical stress (eg
during an infection) to prevent acute
decompensation.[7]
 Secondary hypothyroidism: thyroid
hormone replacement.
 Gonadotropin deficiency: testosterone
replacement for men and oestrogens, with
or without progesterone, for women
(combined oral contraceptive pill for
premenopausal women).
 Growth hormone replacement for children.
 Surgical
o In pituitary apoplexy, prompt
surgical decompression may be life-
saving.
o Extirpate macroadenomas that do not
respond to medical therapy.

Nursing management:-

Assessment:-

 Assess the severity of the condition and

37
 support system.
 Assess the vitals like temperature, pulse,
BP etc.
 Take the patient history about illness, their
habit, their life pattern etc.
 Assess the patient understanding of
management plan, coping with the
diagnosis and support from other.
 Assess for changes in energy level or
decrease in mobility.
 Assess for knowledge level related to
disorder, treatment, and potential outcome
of treatment.

Nursing diagnosis:-

1. Hypotension related to disease condition as

manifested by BP is 100/60 mm of hg.
2. Dehydration related to inadequate renal
function secondary to inadequate adrenal
function as manifested by polyuria and
polydepsia.
3. Imbalanced nutrition; less than body
requirement related to decreased metabolic
rate as manifested by anorexia.
4. Generalized weakness related to
progressive disease condition as manifested

38
 by fatigue.
5. Anxiety related to the presence condition as
manifested by verbalization.

Nursing intervention:-

Maintaining Adequate Fluid Volume

 Measure fluid intake and output
accurately.
 Obtain daily weights and central venous
pressure, and other measurements.
 Provide patient with ample water to drink
and administer I.V. fluids as indicated.
 Monitor results of serum and urine
osmolality and serum sodium tests.
 Administer or teach self administer of
medication as prescribed and document
patient response.
maintain cardiac output
 monitor hemodynamic status like vital
sign , hemodynamic parameter CVP,
PCWP, AND CO.
 .Implement fluid replacement regimens
 Monitor hydration status .
Balance blood electrolyte level
 Implement fluid replacement regimen.
 Administer hypotonic fluids initially.
 Monitor all vital parameters during fluid
39
 replacement therapy.
 Encourage for oral intake of fluid.
 Monitor cardiac status- overhydration.
dehydration.
 Administer ADH replacement therapy as
prescribed.
Improve the nutritional status of the patient
 Assess the nutritional status of the patient.
 Plan for provide balance diet.
 Encourage patient to take more water and
full diet.
 Take history about patient’s like and
dislike.
Reducing anxiety:-
 Provide emotional support through the
diagnostic process and answer questions about
treatment options
 Prepare patient for surgery or other treatment
by describing nursing care thoroughly.
 Stress likelihood of positive outcome with
ablation therapy.

Prognosis:-

Mortality is increased by a factor between 1.3 and

2.2 when compared with age-sex controls

If adequately replaced, prognosis in

40
 hypopituitarism is good. Prognosis is therefore
usually dependent on the underlying cause
4. Discribe PITUITARY TUMORS:- Lecture, Listen, Tell me
about discussi answe about types
pituitary INTRODUCTION:- on , ring of pituitary
tumors its Pituitary tumors represent various cell types. explanat tumors.
etiology, Symptoms reflect tumor effects on target tissues ion&
clinical or on local structure surrounding the pituitary question
manifestatio gland. ing
n,
pathophysio DEFINITION:-
logy, A spontaneous growth or enlargement in pituitary
diagnostic gland known as pituitary tumors.
evaluation, Pituitary tumors are usually benign, although their
treatment, location and effects on hormone production by
nursing target organs can cause life threatening effects.
management
. Pituitary tumors are divided into three groups:

1. Benign pituitary adenomas: Tumors that are

not cancer. These tumors grow very slowly
and do not spread from the pituitary gland
to other parts of the body.
2. Invasive pituitary adenomas: Benign
tumors that may spread to bones of the
skull or the sinus cavity below the pituitary
gland.

41
Pituitary carcinomas: Tumors that are malignant
(cancer). These pituitary tumors spread into other
areas of the central nervous system (brain and
spinal cord) or outside of the central nervous
system. Very few pituitary tumors are malignant.

Pituitary tumors may be either non-functioning or

functioning.

 Non-functioning pituitary tumors do not

make hormones.
 Functioning pituitary tumors make more
than the normal amount of one or more
hormones. Most pituitary tumors are
functioning tumors. The extra hormones
made by pituitary tumors may cause certain
signs or symptoms of disease.

ETIOLOGY:

1. Unknown cause.
2. Some time hereditary is occurs.
3. Hypersecreation.

PATHOPHYOLOGY:-

42
 Humoral factors are affects normal pituitary
gland.
 Hyperplasia occurs in takeplace and that
lead to microadenoma.
 Addition mutation in occurs and then
microadenoma convert into macroadenoma
than after gland become malignant.
CLINICAL MANIFESTATION:-

Symptoms can be caused by the growth of the

tumor and/or by hormones the tumor makes.
Some tumors may not cause symptoms.

43
Conditions other than pituitary tumors can cause
the symptoms listed below. A doctor should be
consulted if any of these problems occur.

Signs and symptoms of a non-functioning

pituitary tumor

Sometimes, a pituitary tumor may press on or

damage parts of the pituitary gland, causing it to
stop making one or more hormones. Too little of a
certain hormone will affect the work of the gland
or organ that the hormone controls. The following
symptoms may occur:

 Headache.
 Some loss of vision.
 Loss of body hair.
 In women, less frequent or no menstrual
periods or no milk from the breasts.
 In men, loss of facial hair, growth of breast
tissue, and impotence.
 In women and men, lower sex drive.
 In children, slowed growth and sexual
development.

Most of the tumors that make LH and FSH do not

make enough extra hormone to cause symptoms.

44
These tumors are considered to be non-
functioning tumors.

Signs and symptoms of a functioning pituitary

tumor

When a functioning pituitary tumor makes extra

hormones, the symptoms will depend on the type
of hormone being made.

Too much prolactin may cause:

 Headache.
 Some loss of vision.
 Less frequent or no menstrual periods or
menstrual periods with a very light flow.
 Trouble becoming pregnant or an inability
to become pregnant.
 Impotence in men.
 Lower sex drive.
 Flow of breast milk in a woman who is not
pregnant or breast-feeding.


Too much ACTH may cause:

 Headache.

45
  Some loss of vision.
 Weight gain in the face, neck, and trunk of
the body, and thin arms and legs.
 A lump of fat on the back of the neck.
 Thin skin that may have purple or pink
stretch marks on the chest or abdomen.
 Easy bruising.
 Growth of fine hair on the face, upper back,
or arms.
 Bones that break easily.
 Anxiety, irritability, and depression.

Too much growth hormone may cause:

 Headache.
 Some loss of vision.
 In adults, acromegaly (growth of the bones
in the face, hands, and feet). In children, the
whole body may grow much taller and
larger than normal.
 Tingling or numbness in the hands and
fingers.
 Snoring or pauses in breathing during sleep.
 Joint pain.
 Sweating more than usual.
 Dysmorphophobia (extreme dislike of or
concern about one or more parts of the

46
 body).

Too much thyroid-stimulating hormone may

cause:

 Irregular heartbeat.
 Shakiness.
 Weight loss.
 Trouble sleeping.
 Frequent bowel movements.
 Sweating.

Other general signs and symptoms of pituitary

tumors:

 Nausea and vomiting.

 Confusion.
 Dizziness.
 Seizures.
 Runny or "drippy" nose (cerebrospinal fluid
that surrounds the brain and spinal cord
leaks into the nose).

COMPLICATION:-

47
diabetes insipidus:

Diabetes insipidus happens when pituitary

gland and the gland found just above it, the
hypothalamus, don't produce enough
vasopressin, a hormone that's in charge of
maintaining the body's water balance. The
most common symptom is constant thirst,
which ca lead to frequent bathroom stops
from drinking so many fluids. This is
because without vasopressin, the kidneys
aren't able to hold onto water as they should
and you get dehydrated, triggering you to
be thirsty. This condition can also be a
complication of some pituitary tumor
treatments.

 permanent hormone deficiency: It's

possible for a pituitary tumor to cause a
permanent hormone imbalance. If this
happens, may need to take medication to
replace the depleted hormone. For example,
if patient’s pituitary tumor causes a thyroid-
stimulating hormone (TSH) deficiency, he
may need to take thyroid hormone
replacement to get your thyroid levels back
to normal.

48
  Pituitary apoplexy: This is a rare but
serious complication that causes sudden
bleeding into the pituitary tumor. Pituitary
apoplexy typically needs immediate
treatment—usually corticosteroids or
surgery. Symptoms include a severe
headache and vision problems, such as
double vision or vision loss and also have
symptoms of hypopituitarism (when
pituitary gland releases low amounts of
certain hormones). Symptoms of
hypopituitarism can include excessive thirst
(from diabetes insipidus), lightheadedness
(from adrenal insufficiency), and cold
intolerance (from hypothyroidism).

.DIAGNOSTIC EVALUATION:-

Imaging studies and tests that examine the blood

and urine are used to detect (find) and diagnose a
pituitary tumor.

The following tests and procedures may be used:

 Physical exam and history: An exam of the

body to check general signs of health,
including checking for signs of disease,
such as lumps or anything else that seems

49
 unusual. A history of the patient’s health
habits and past illnesses and treatments will
also be taken.
 Eye exam: An exam to check vision and the
general health of the eyes.
 Visual field exam: An exam to check a
person’s field of vision (the total area in
which objects can be seen). This test
measures both central vision (how much a
person can see when looking straight
ahead) and peripheral vision (how much a
person can see in all other directions while
staring straight ahead). The eyes are tested
one at a time. The eye not being tested is
covered.
 Neurological exam: A series of questions
and tests to check the brain, spinal cord,
and nerve function. The exam checks a
person’s mental status, coordination, and
ability to walk normally, and how well the
muscles, senses, and reflexes work. This
may also be called a neuro exam or a
neurologic exam.
 MRI (magnetic resonance imaging) with
gadolinium: A procedure that uses a
magnet, radio waves, and a computer to
make a series of detailed pictures of areas
50
 inside the brain and spinal cord. A
substance called gadolinium is injected into
a vein. The gadolinium collects around the
cancer cells so they show up brighter in the
picture. This procedure is also called
nuclear magnetic resonance imaging
(NMRI).
 CT scan (CAT scan): A procedure that
makes a series of detailed pictures of areas
inside the brain, taken from different
angles. The pictures are made by a
computer linked to an x-ray machine. A
dye may be injected into a vein or
swallowed to help the organs or tissues
show up more clearly. This procedure is
also called computed tomography,
computerized tomography, or computerized
axial tomography.
 Blood chemistry study: A procedure in
which a blood sample is checked to
measure the amounts of certain substances,
such as glucose (sugar), released into the
blood by organs and tissues in the body. An
unusual (higher or lower than normal)
amount of a substance can be a sign of
disease in the organ or tissue that makes it.
 Blood tests: Tests to measure the levels of

51
 testosterone or estrogen in the blood. A
higher or lower than normal amount of
these hormones may be a sign of pituitary
tumor.
 Twenty-four-hour urine test: A test in
which urine is collected for 24 hours to
measure the amounts of certain substances.
An unusual (higher or lower than normal)
amount of a substance can be a sign of
disease in the organ or tissue that makes it.
A higher than normal amount of the
hormone cortisol may be a sign of a
pituitary tumor.
 High-dose dexamethasone suppression test:
A test in which one or more high doses of
dexamethasone are given. The level of
cortisol is checked from a sample of blood
or from urine that is collected for three
days.
 Low-dose dexamethasone suppression test:
A test in which one or more small doses of
dexamethasone are given. The level of
cortisol is checked from a sample of blood
or from urine that is collected for three
days.
 Venous sampling for pituitary tumors: A
procedure in which a sample of blood is

52
 taken from veins coming from the pituitary
gland. The sample is checked to measure
the amount of ACTH released into the
blood by the gland. Venous sampling may
be done if blood tests show there is a tumor
making ACTH, but the pituitary gland
looks normal in the imaging tests.
 Biopsy: The removal of cells or tissues so
they can be viewed under a microscope by
a pathologist to check for signs of cancer.
 Immunohistochemistry study: A laboratory
test in which a substance such as an
antibody, dye, or radioisotope is added to a
sample of cancer tissue to test for certain
antigens. This type of study is used to tell
the difference between different types of
cancer.
 Immunocytochemistry study: A laboratory
test in which a substance such as an
antibody, dye, or radioisotope is added to a
sample of cancer cells to test for certain
antigens. This type of study is used to tell
the difference between different types of
cancer.
 Light and electron microscopy: A
laboratory test in which cells in a sample of
tissue are viewed under regular and high-

53
 powered microscopes to look for certain
changes in the cells.

TREATMENT:

Pituitary tumors are usually not cancerous and

therefore won't spread to other areas of the body.
However, as they grow, they may place pressure
on important nerves and blood vessels.

Surgery to remove the tumor is often necessary,

especially if the tumor is pressing on the optic
nerves, which could cause blindness.

Most of the time, pituitary tumors can be removed

through the nose and sinuses. However, some
tumors cannot be removed this way and will need
to be removed through the skull (transcranial).

Radiation therapy may be used to shrink the

tumor, either in combination with surgery or for
people who cannot have surgery.

The following medications may shrink certain

types of tumors:

 Bromocriptine or cabergoline are the first-

line therapy for tumors that release

54
 prolactin. These drugs decrease prolactin
levels and shrink the tumor.
 Octreotide or pegvisomant is sometimes
used for tumors that release growth
hormone, especially when surgery is
unlikely to result in a cure.

Nursing assessment:-
 Obtain sign and symptoms.
 Perform thorough neurological examination
and general physical examination to
identify signs of hormone deficiency or
excess.
 Assess patient’s understanding of the
management plan, coping with the
diagnosis, and support from others.
 Assess for temporal headache of moderate
intensity, arthralgias, backache.
 Assess for changes in energy level or
decrease in mobility.
 Assess for knowledge level related to
disorder, treatment, and potential outcome
of treatment.
Nursing diagnosis:-
 Fluid volume deficit related to poor
perfusion.
 Imbalance nutrition; less than body
55
 requirement related to anorexia .
 Anxiety related to ablation treatment.
 Readiness for Enhanced Management of
Therapeutic regimen.

Nursing interventions:-
Maintain adequate fluid volume
 Measure fluid intake and output
accurately.
 Obtain daily weights and central venous
pressure, and other measurements.
 Provide patient with ample water to drink
and administer I.V. fluids as indicated.
 Monitor results of serum and urine
osmolality and serum sodium tests.
 Administer or teach self administer of
medication as prescribed and document
patient response.
Improve the nutritional status of the patient
 Assess the nutritional status of the patient.
 Plan for provide balance diet.
 Encourage patient to take more water and
full diet.
 Take history about patient’s like and
dislike.
Reducing anxiety:-
 Provide emotional support through the

56
 diagnostic process and answer questions about
treatment options
 Prepare patient for surgery or other treatment
by describing nursing care thoroughly.
 Stress likelihood of positive outcome with
ablation therapy.

Promoting management of the therapeutic

regimen:-
 -Teach patient the nature of hormonal
deficiencies after treatment and the purpose
of replacement therapy.
 -Instruct patient about the early signs and
symptoms of cortisol of thyroid hormone
deficiency or excess and the need to report
them.
 -Describe and demonstrate the correct
method of administering prescribed
medications.
 -Encourage patient in assuming active role
in self- care through information – seeking
and problem solving.

Patient Education and Health Maintenance:-

 Advise patient on temporary limitations
in activities.
 Teach patient the need for frequent

57
 initial follow up visits and lifelong
medical management when on hormonal
therapy.
 If applicable, advise patient on the need
for postsurgery radiation therapy and
periodic follow-up MRI and visual field
testing.
 Teach patient to notify health care
provider if signs of thyroid or cottisol
imbalance become evident.
 Advise patient to wear Medical Alert
bracelet.
 Help patient identify sources of
information and support available in the
community.

PROGNOSIS:-

The prognosis (chance of recovery) depends on

the type of tumor and whether the tumor has
spread into other areas of the central nervous
system (brain and spinal cord) or outside of the
central nervous system to other parts of the body

5. Discribe SIADH Lecture, Listen, LCD, OHP, Explain the

about Introduction:- discussi answe pathophysio
SIADH its The syndrome of inappropriate antidiuretic on , ring logy
etiology, hormone secretion or SIADH (other names: explanat ofSIADH.
58
clinical Schwartz-Bartter syndrome, SIAD—syndrome of ion&
manifestatio immoderate antidiuresis) is characterized by question
n, excessive release of antidiuretic hormone from the ing.
pathophysio posterior pituitary gland or another source. The
logy, result is hyponatremia and sometimes fluid
diagnostic overload. It is usually found in patients diagnosed
evaluation, with pneumonia, brain tumors, head trauma,
treatment, strokes, meningitis, encephalitis, or small-cell
nursing carcinoma of the lung.
management Definition
. Syndrome of inappropriate antidiuretic hormone
secretion (SIADH) is caused by excessive or
inappropriate secretion or action of antidiuretic
hormone (ADH), resulting in:

 Dilutional hyponatremia without clinically

apparent hypervolemia (also known as
euvolemic)
 Reduced plasma osmolality
 Impaired water excretion with decreased
volumes of urine that is inappropriately
concentrated for the prevailing plasma
osmolality and volume status.

Etiology

SIADH is actually caused due to increased levels

of the ADH hormone. ADH or Antidiuretic

59
hormone is released by the pituitary gland and
helps the kidney to function properly. It helps
maintain the balance of water and minerals like
sodium and potassium in the urine and the
bloodstream. An excess of this hormone leads to
the expulsion of large amounts of sodium through
urine while the water level remains almost
unchanged. A healthy amount of sodium is vital
for proper functioning of the body. Naturally, low
sodium level can be very harmful for the body.

SIADH arises when the sodium level drops due to

some reason. Some of the most common causes
for a reduction in sodium level are:

Tumors

Cancerous tumors, particularly small cell lung

tumors, can give rise to SIADH. This happens
because tumors may begin creating their own
ADH (Antidiuretic Hormone) or impact the
pituitary gland to boost ADH production.

Medicines

Some anti-epileptic drugs, anti-depressants and

certain drugs that are used to treat diabetes,

60
dkepression and blood pressure may also activate
ADH secretion. General anesthesia may be
another ADH enhancer. Some of these medicines
affect liquid output from kidneys thereby bringing
on this syndrome.

Lung Disease

Lung disorders such as lung cancer and lung

abscess may also give rise to increased ADH
production in some cases.

Infections

Certain infections of the CNS (Central Nervous

System) such as Guillain-Barre Syndrome result
in swelling of the nerves and trigger a release of
the ADH hormone.

Malignancy

Malignant conditions like Prostate cancer,

Pancreatic cancer, Leukemia and Lymphoma can
also lead to this condition.

Chest Disorders

In some cases, chest diseases like tuberculosis and

61
Pneumonia can be causes of SIADH.

Brain Diseases

Brain disorders like Meningitis are another reason

behind the appearance of SIADH syndrome in
many patients. Head injuries and brain tumors are
other possible causes.

Mental Disorders

Major mental diseases like Psychosis are often

held responsible for the showing up of this
disease.

Encephalitis

This condition is characterized by an

inflammation of the brain. It is caused by lead
poisoning or the bite of an infected mosquito.

Pathphysiology

Certain disease states can upset the delicate

balance of water and salt in the body. If there is
too much ADH in the body, or if the kidneys
overreact to the ADH they receive, the body
retains excess water and the serum sodium
62
concentration becomes diluted and falls to
abnormal levels. The patient with SIADH
develops symptoms based on the degree of
abnormality in the serum sodium concentration
and the speed with which this concentration falls.

clinical manifestation:-

People suffering from SIADH experience a

number of symptoms. Some of the most
commonly observed SIADH signs and symptoms
are:

Headache

The low sodium levels may give rise to headaches

in affected people.

Fatigue

Most SIADH sufferers experience a tiredness or

lethargic feeling which impairs their daily
activities.

Restlessness

63
Reduced sodium level may cause the suffering
perso7n fidget and have an uncomfortable feeling.

Nausea

People having SIADH may also feel nauseous.

Many sufferers feel like vomiting while they are
having an abnormally reduced sodium level.

Confusion

The physical discomfort can also lead to mental

confusion in some patients.

Hallucinations

Physical symptoms and mental confusion also

make some affected people suffer from mild
hallucinations.

Seizures and Fainting

If the condition is not timely treated, the affected

people may suffer from loss of consciousness and
seizures.

Spasms

64
A person may also experience muscular cramps or
spasms due to low sodium levels in the body.

Complications

 Complications of hyponatremia
o Depend on the rapidity of onset and
absolute decrease in serum sodium
concentrations
 Obtundation or coma
 Seizures
 Death
 Complications of treatment
o Central pontine myelinolysis
 Acute, potentially fatal
neurologic syndrome
characterized by:
 Quadriparesis
 Ataxia
 Abnormal extraocular
movements
 Characteristic findings
on MRI
o May occur with rapid correction of
hyponatremia if it has been present
for > 24–48 hours
o Thought to be a result of rapid
osmotic fluid shifts
65
Diagnosis

Laboratory findings in diagnosis of SIADH

include:

 Euvolemic hyponatremia <134 mEq/L, and

POsm <275 mOsm/kg OR ( POsm - Serum
[Urea]mmol/l < 280 mOsm/kg )
 Urine osmolality >100mOsm/kg of water
during hypotonicity
 Urine sodium concentration >40 mEq/L
with normal dietary salt intake

Other findings:

 Clinical euvolemia without edema or

ascites

 Low blood urea nitrogen (BUN)

 Normal serum creatinine
 Low uric acid
 Normal Acid-Base, K+ balance
 Normal Adrenal, Thyroid function

Management

Management of SIADH includes:

66
 Treating underlying causes when possible.
 Long-term fluid restriction of 1,200–1,800
mL/day will increase serum sodium
through decreasing total body water.
 For very symptomatic patients (severe
confusion, convulsions, or coma)
hypertonic saline (3%) 1-2 ml/kg IV in 3-4
h should be given.
 Drugs
o Demeclocycline can be used in
chronic situations when fluid
restrictions are difficult to maintain;
demeclocycline is the most potent
inhibitor of Vasopressin (ADH/AVP)
action. However, demeclocycline has
a 2-3 delay in onset with extensive
side effect profile, including but not
limited to new onset Nephrogenic
Diabetes Insipidus (70%), skin
photosensitivity, and nephrotoxicity.
o Urea: oral daily ingestion has shown
favorable long-term results with
protective effects in myelinosis and
brain damage. Limitations noted to
be undesirable taste and is
contraindicated in patients with
cirrhosis to avoid initiation or
67
 potentiation of hepatic
encephalopathy.
o Conivaptan - an antagonist of both
V1A and V2 vasopressin receptors. Its
indications are "treatment of
euvolemic hyponatremia (e.g. the
syndrome of inappropriate secretion
of antidiuretic hormone, or in the
setting of hypothyroidism, adrenal
insufficiency, pulmonary disorders,
etc.) in hospitalized patients.".
Conivaptan, however, is only
available as a parenteral preparation.
o Tolvaptan - an antagonist of the V2
vasopressin receptor. A randomized
controlled trial showed tolvaptan is
able to raise serum sodium in
patients with euvolemic or
hypervolemic hyponatremia in 2
different tests. Combined analysis of
the 2 trials showed an improvement
in hyponatremia in both the short
term (primary sodium change in
average AUC: 3.62+/- 2.68 and 4.35
+/-2.87) and long term with long
term maintenance (primary sodium
change in average AUC: 6.22 +/-

68
 4.22 and 6.20 +/- 4.92), at 4 days and
30 days, respectively. Tolvaptan’s
side effect profile is minimal.
Discontinuation of the Tolvaptan
showed return of hyponatremia to
control values at their respective time
frames.

No head to head study is currently available to

quantify and compare the relative efficacies of V2
vasopressin receptor antagonists with
demeclocycline or other treatment options.

Care must be taken when correcting

hyponatremia. A rapid rise in the sodium level
may cause central pontine myelinolysis. Avoid
correction by more than 12 mEq/L/day. Initial
treatment with hypertonic saline may abruptly
lead to a rapid dilute diuresis and fall in ADH.
Rapid diuresis may lead to over-rapid rise in
serum sodium, and should be managed with
extreme care.

Nursing management:-

Assessment:-

 Assess the severity of the condition and

69
 support system.
 Assess the vitals like temperature, pulse,
BP etc.
 Take the patient history about illness, their
habit, their life pattern etc.
 Assess the patient understanding of
management plan, coping with the
diagnosis and support from other.
 Assess for changes in energy level or
decrease in mobility.
 Assess for knowledge level related to
disorder, treatment, and potential outcome
of treatment.

Diagnosis:-
 Fluid volume deficit related to poor
perfusion.
 Imbalance nutrition; less than body
requirement related to anorexia.
 Anxiety related to ablation treatment.
 Constipation related to decreased bowel
motility caused by IADH.
Intervention:-
Maintaining Adequate Fluid Volume

70
  Measure fluid intake and output accurately.
 Obtain daily weights and central venous
pressure, and other measurements.
 Provide patient with ample water to drink
and administer I.V. fluids as indicated.
 Monitor results of serum and urine
osmolality and serum sodium tests.
 Administer or teach self administer of
medication as prescribed and document
patient response.

Improve the nutritional status of the patient

 Assess the nutritional status of the patient.
 Plan for provide balance diet.
 Encourage patient to take more water and
full diet.
 Take history about patient’s like and
dislike.Reducing anxiety:-
 Provide emotional support through the
diagnostic process and answer questions about
treatment options
 Prepare patient for surgery or other treatment
by describing nursing care thoroughly.
 Stress likelihood of positive outcome with

71
ablation therapy.
Prognosis:-Underlying associated disorder
o Severity of hyponatremia
 Mortality rate
 Serum sodium
concentration < 120
mmol/L: 25%
 Serum sodium
concentration > 120
mmol/L: 12.5%
o Rate of development of
hyponatremia
 Mortality rate of acute
hyponatremia: 5–50%

72
6. Discribe DIABETES INSIPIDUS:- Lecture, Listen, OHP,LCD, Enlist the
about DI its discussi answe VIDEOS symptoms
etiology, INTRODUCTION:-Pituitary diabetes incipidus on , ring of DI.
clinical results from lack of sufficient ADH either from explanat
manifestatio inadequate levels of circulating ADH, insufficient ion&
n, pituitary release of ADH or accelerated question
pathophysio degradation of circulating ADH. ing
logy,
diagnostic DEFINITION:- DI is a disorder of the posterior
evaluation, lobe of the pituitary gland characterized by a
treatment, deficiency of ADH, also called vasopressin.
nursing
management CLASSIFICATION
.
The several forms of DI are:

Neurogenic

Neurogenic diabetes insipidus, more commonly

known as central diabetes insipidus, is due to a
lack of vasopressin production in the brain.

Nephrogenic

Nephrogenic diabetes insipidus is due to the

inability of the kidney to respond normally to
vasopressin.

73
Dipsogenic

Dipsogenic DI is due to a defect or damage to the

thirst mechanism, which is located in the
hypothalamus. This defect results in an abnormal
increase in thirst and fluid intake that suppresses
vasopressin secretion and increases urine output.
Desmopressin is ineffective, and can lead to fluid
overload as the thirst remains.

Gestational

Gestational DI only occurs during pregnancy.

During pregnancy, all women produce
vasopressinase in the placenta, which breaks
down ADH. Gestational DI is thought to occur
with excessive vasopressinase production.

ETIOLOGY:-

1. Causes of central diabetes insipidus

Central diabetes insipidus is the most common

type of diabetes insipidus. It occurs because of
damage to the pituitary gland and poor regulation
of vasopressin. Damage to the pituitary can result
from:

74
  Brain surgery
 Genetics
 Head injury
 Infection
 Tumor

2. Causes of nephrogenic diabetes insipidus

In nephrogenic diabetes insipidus, the kidneys

cannot properly process vasopressin. Damage to
the kidney’s vasopressin response mechanism can
result from:

 Genetics
 Hypercalcemia (too much calcium in the
blood)
 Kidney failure or certain kidney diseases
 Medication side effects, such as side effects
from lithium
 Other causes not currently known

3. Causes of dipsogenic diabetes insipidus

Dipsogenic diabetes insipidus happens when there

is damage to the body’s sense of thirst. The sense
of thirst is located in a part of the brain called the
hypothalamus. Damage to the hypothalamus can

75
occur due to:

 Brain surgery
 Genetics
 Head injury
 Infection
 Tumor

4. Causes of gestational diabetes insipidus

Gestational diabetes insipidus arises in pregnant

women when the placenta manufactures an
enzyme that attacks the mother’s vasopressin,
leading to poor fluid regulation

The risk factors for diabetes insipidus

A number of factors increase the risk of

developing diabetes insipidus. Not all people with
risk factors will get diabetes insipidus. Risk
factors for diabetes insipidus include:

 Brain surgery
 Family history of diabetes insipidus
 Head injury
 Infection of the brain
 Kidney disease (includes any type of

76
 kidney problem, such as kidney stones,
kidney failure, and kidney anomalies)
 Pregnancy (gestational diabetes insipidus)

PATHOPHYSIOLOGY

1. Vasopressin (Anti-Diuretic Hormone) is

produced by the hypothalamus in response to
increased serum osmolality

2. Vasopressin is then transported to the

posterior pituitary gland

3. It is then released into the circulatory system

via the posterior pituitary gland

4. It then travels to the kidneys where it binds

to vasopressin receptors on the distal
convoluted tubules

5. This causes Aquaporin-2 channels to move

from the cytoplasm into the apical membrane
ofthe tubules.

 These aquaporin-2 channels allow water to

be reabsorbed out of the collecting ducts &
back into the blood stream.
 This results in both a decrease in volume &

77
 an increase in osmolality (concentration) of
the urine been excreted

6. The extra water that has been reabsorbed

re-enters the circulatory system, reducing the
serum osmolality

7. This reduction in serum osmolality is

detected by the hypothalamus & results in
decreased production of vasopressin.

78
 CLINICAL MANIFESTATION :-

The two main symptoms of diabetes insipidus

are:

 needing to pass large amounts of urine

often

79
  feeling thirsty all the time

These and other symptoms patient may

experience if he/she have diabetes insipidus are
outlined below.

Passing excess urine

Patient may pass pale, watery urine as often as

every 15-20 minutes. The amount of urine passed
can range from 3 litres (5.2 pints) in mild cases to
up to 20 litres (35 pints) in severe cases.

Constant thirst

Patient may be constantly thirsty and have a 'dry'

feeling that is always present, no matter how
much water he drink.

Trouble sleeping and carrying out daily activities

If patient need to pass urine often and always feel

thirsty, patient’s sleeping patterns and daily
activities may be disrupted as a result. This can
cause tiredness, irritability and difficulty
concentrating, which can affect his daily life
further.

80
Generally feeling unwell

If patient have diabetes insipidus, he may feel

generally unwell and 'run down' much of the time
for no apparent reason.

COMPLICATION

Dehydration
Except for dipsogenic DI, which causes to retain
too much water, diabetes insipidus can cause
body to retain too little water to function properly,
and can become dehydrated. Dehydration can
cause:

 Dry mouth
 Muscle weakness
 Low blood pressure (hypotension)
 Elevated blood sodium (hypernatremia)
 Sunken appearance to your eyes
 Fever
 Headache
 Rapid heart rate
 Weight loss

Electrolyte imbalance
Diabetes insipidus can also cause an electrolyte

81
imbalance. Electrolytes are minerals in blood —
such as sodium, potassium and calcium — that
maintain the balance of fluids in your body.
Electrolyte imbalance can cause symptoms, such
as:

 Headache
 Fatigue
 Irritability
 Muscle pains

Water intoxication
Excessive fluid intake in dipsogenic diabetes
insipidus can lead to water intoxication, a
condition that lowers sodium concentration in
blood, which can damage brain.

DIAGNOSTIC EVALUATION:-

Water deprivation test

A water deprivation test involves not drinking any

liquid for several hours to see how your body
responds. If you have diabetes insipidus, you will
continue to pass large amounts of dilute urine,
when normally you would only pass a small

82
amount of concentrated urine.

During the test, the amount of urine

you are producing is measured. You may also
need a blood test to assess the levels of
antidiuretic hormone (ADH) in your blood.

Your blood and urine may also be tested for

substances such as blood sugar (glucose), calcium
and potassium. If you have diabetes insipidus,
your urine will be very diluted, with low levels of
other substances. However, a high amount of
sugar in your urine may be a sign of type 1 or type
2 diabetes, not diabetes insipidus.

Antidiuretic hormone (ADH) test

After the water deprivation test, you may be

given a small dose of ADH, usually as an
injection. This shows how your body reacts to the
hormone which helps identify the type of
diabetes insipidus you have.

If the dose of ADH stops you producing urine, it

is likely your condition is due to a shortage of
ADH. If this is the case, you may be diagnosed

83
with cranial diabetes insipidus.

However, if you continue to produce urine,

despite the dose of ADH, it suggests there is
already enough ADH in your body, but your
kidneys are not responding to it. In this case, you
may be diagnosed with nephrogenic diabetes
insipidus.

MRI scan

Magnetic resonance imaging (MRI) is a scan that

uses a strong magnetic field and radio waves to
produce images of the inside of your body,
including your brain.

You may need an MRI scan if your GP or

endocrinologist thinks you have cranial diabetes
insipidus as a result of damage to your
hypothalamus or pituitary gland.

If your condition is due to an abnormality in your

hypothalamus or pituitary gland, such as a
tumour, it may need to be treated before you can
receive treatment for diabetes insipid

TREATMENT:-

84
Mild cases of diabetes insipidus may not require
medical treatment, or they may require that you
drink extra water during the day. In more serious
cases of diabetes insipidus, the treatment depends
on the type of diabetes insipidus.

Treatment of central and gestational diabetes

insipidus

Gestational diabetes insipidus only occurs during

pregnancy and will resolve after birth. During
pregnancy, artificial vasopressin can be taken.
Central diabetes insipidus is also generally treated
with medications designed to mimic vasopressin,
such as:

 Desmopressin injection (DDAVP)

 Desmopressin nasal spray (Stimate,
Minirin)
 Desmopressin pill (DDAVP)

Treatment of nephrogenic diabetes insipidus

Nephrogenic diabetes insipidus cannot be treated

with artificial vasopressin. Instead, treatments for
nephrogenic diabetes insipidus include:

85
  Anti-inflammatory drugs, such as
indomethacin (Indocid, Indocin)
 Diuretics, such as hydrochlorothiazide
mixed with amiloride (Moduretic)
 Increasing fluid intake

Treatment of dipsogenic diabetes insipidus

Effective treatments for dipsogenic diabetes

insipidus are not known. However, careful fluid
regulation is important to prevent dehydration.

What you can do to improve your diabetes

insipidus

Diabetes insipidus prevents your body’s fluid

regulation mechanisms from working properly. If
you have diabetes insipidus, regulating or
increasing your fluid intake may help with
symptoms. Fluid intake should only be modified
on the advice of a health care professional, as
some medications may interfere with fluid
regulation.

Nursing Assessment

86
 1. Obtain complete health to determine
possible cause of DI.
2. Assess hydration status.
3. Assess the vital signs
4. Assess nutritional status of the patient .
Nursing Diagnosis
1. Risk for deficient fluid volume related to
disease process.
2. Decreased cardiac output related to
severely intravascular volume.
3. Electrolyte imbalance related to excessive
water loss.
4. Skin integrity related to diarrhea.
5. Imbalanced nutrition; less than body
requirement related to anorexia, nausea
associated with hypernatremic state.

Nursing Interventions
Maintaining Adequate Fluid Volume
 Measure fluid intake and output
accurately.
 Obtain daily weights and central venous
pressure, and other measurements.
 Provide patient with ample water to drink
and administer I.V. fluids as indicated.
 Monitor results of serum and urine
osmolality and serum sodium tests.

87
  Administer or teach self administer of
medication as prescribed and document
patient response.
maintain cardiac output
 monitor hemodynamic status like vital
sign , hemodynamic parameter CVP,
PCWP, AND CO.
 .Implement fluid replacement regimens
 Monitor hydration status .
Balance blood electrolyte level
 Implement fluid replacement regimen.
 Administer hypotonic fluids initially.
 Monitor all vital parameters during fluid
replacement therapy.
 Encourage for oral intake of fluid.
 Monitor cardiac status- overhydration.
dehydration.
 Administer ADH replacement therapy as
prescribed.
Maintain the skin intergrity
1. Initiate skin care regimen:-
-frequent turning and positioning.
-active / passive ROM exercises.
-initiate pressure relief device.
2. monitor nutritional intake.
Patient education and health maintenances:-
1. Inform patient to that metabolic status must

88
 be monitored on long term basis because
the severity of DI changes from time to
time.
2. Advise patient to avoid limiting fluids to
decrease urine output; thirst is a protective
function.
3. Advise patient to wear a Medic Alert
bracelet stating that the wearer has DI.
4. Teach patient to be alert for the sign of
dehydration decreased weight decreased
urine output, increased thirst, dry skin and
mucous membrane; and overhydration
increased weight, increased edema and
report these to health care provider.
5. Tell the patient to consider eliminating
coffee and tea from diet –may have an
exaggerated diuretic effects.
6. Give written instruction on Vassopressin
administration. Have the patient
demonstrate intranasal and injection
technique.
Diabetes Insipidus Prognosis

Diabetes insipidus may be latent, especially if

there is associated lack of anterior pituitary
function; and may be transient, eg, following head
trauma. The ultimate prognosis is essentially that
89
of the underlying disorder. Since many cases are
associated with organic brain disease, the
prognosis is often poor. Surgical correction of the
primary brain lesion rarely alters the diabetes
insipidus.

90
7. Discribe DISORDERS OF THYROID GLAND:- Lecture, Listen, OHP, LCD, What are the
about  Hypothyroidism. discussi answe VEDIOS. etiological
hypothyroid Hyperthyroidism. on , ring. factor of
ism its Hashimoto's Thyroiditis. explanat hypothyroid
etiology,  Cancer of the thyroid. ion& ism.
clinical  Thyroid tumors. question
manifestatio Goiter ing
n, HYPOTHYROIDISM:-
pathophysio
logy, INTRODUCTION:-This is a condition that
diagnostic arises from inadequate amounts of thyroid
evaluation, hormone in the bloodstream. Hypothyroidism
treatment, results from suboptimal levels of thyroid
nursing hormone. Thyroid deficiency can affect all body
management functions and can range from mild, subclinical
. forms to myxedema.

DEFINITION:-hypothyroidism is a condition
characterized by abnormally low thyroid hormone
production. Thyroid hormone levels decrease
metabolic and increase the risk of other health
issues such as heart disease and problem in
pregnancy.

ETIOLOGY :-
1. Primary hypothyroidism is the most common
form of this condition and is generally caused by:-
a. -Autoimmune disease (Hashimoto’s thyroiditis).
91
8. Discribe HYPERTHYROIDISM:-
about Lecture, Listen, OHP, LCD, Explain the
hyperthyro INTRODUCTION hyperthyroidism literally discussi answe VEDIOS. pathophysio
its etiology, means “too much thyroid hormones. Under the on , ring. logy of
clinical normal condition thyroid gland produce normal or explanat hyperthyroi
manifestatio exact amout of thyroid hormone, but in case of ion& dism.
n, hyperthyroidism, the gland produces excessive question
pathophysio amount of one or both hormone. ing
logy,
diagnostic DEFINATION
evaluation, This hyper metabolic condition is characterized
treatment, by excessive amount of thyroid hormones in
nursing bloodstream.
management
.
ETIOLOGY :-

The major causes in humans are:

 Graves' disease. An autoimmune disease.

 Toxic thyroid adenoma
 Toxic multinodular goitre

High blood levels of thyroid hormones (most

accurately termed hyperthyroxinemia) can occur
for a number of other reasons:

92
  Inflammation of the thyroid is called
thyroiditis.
 Oral consumption of excess thyroid
hormone tablets is possible (surreptitious
use of thyroid hormone), as is the rare event
of consumption of ground beef
contaminated with thyroid tissue, and thus
thyroid hormone (termed "hamburger
hyperthyroidism").
 Amiodarone, an anti-arrhythmic drug, is
structurally similar to thyroxine and may
cause either under- or overactivity of the
thyroid.
 Postpartum thyroiditis (PPT) occurs in
about 7% of women during the year after
they give birth. PPT typically has several
phases, the first of which is
hyperthyroidism. This form of
hyperthyroidism usually corrects itself
within weeks or months without the need
for treatment.
 A struma ovarii is a rare form of
monodermal teratoma that contains mostly
thyroid tissue, which leads to
hyperthyroidism.

Hypersecretion of thyroid stimulating hormone

93
(TSH), which in turn is almost always caused by a
pituitary adenoma, accounts for much less than 1
percent of hyperthyroidism cases.

PATHOPHYSIOLOGY:-
The typothalmus releases a hormone called
thyrotropic releasing hormone. In turn,TSH sends
a signal to the pituitary to release thyroid
stimulating hormone. In turn, TSH sends a signal
to the thyroid to release thyroid hormones. If
overactivity of any these three gland occurs, an
excessive amount of thyroid hormones can be
produced, thereby resulting in hyperthyroidism.

94
95
CLINICAL MANIFESTATIONS:-

Nervousness, emotional liability,

apprehension.
Difficulty in setting quietly.
Rapid pulse at rest and on exertion;
palpitations.
Heat intolerance; profuse perspiration;
flushed skin.
Fine tremors in hand; changes in bowl
habits-constipation or diarrhea.
Increased appetite and progressive weight
loss; frequent stool.
Muscles fatigability and weakness;
amenorrhea.
Atrial fibrillation possible (cardiac
decompression is common in older
patients).
Bulging eyes (exopathalmos) –seen only
in Graves disease.
Thyroid gland may be palpable and bruit
may be auscultated over the gland.
Course may be mild, characterized by
remissions and exacerbations.
It may progress to emaciation, extreme
form of hyperthyroidism, is
characterized by hyperpyrexia, diarrhea,

96
 dehydration, tachycardia, arrhythmia,
extreme irritation, delirium coma, shock,
and death, if not adequately treated.
Thyroid storm may be precipitated by
stress or inadequate preparation for
surgery in a patient with known
hyperthyroidism.
Complications

Thyroid crisis (storm), also called thyrotoxicosis,

is a sudden worsening of hyperthyroidism
symptoms that may occur with infection or stress.
Fever, decreased mental alertness, and abdominal
pain may occur. Immediate hospitalization is
needed.

Other complications of hyperthyroidism include:

 Heart-related complications including:

o Rapid heart rate
o Congestive heart failure
o Atrial fibrillation
 Increased risk for osteoporosis, if
hyperthyroidism is present for a long time
 Surgery-related complications, including:
o Scarring of the neck
o Hoarseness due to nerve damage to

97
 the voice box
o Low calcium level due to damage to
the parathyroid glands (located near
the thyroid gland)
 Treatments for hypothyroidism, such as
radioactive iodine, surgery, and
medications to replace thyroid hormones
can have side effects.

DIAGNOSTIC EVALUATION:-

Physical examination may reveal:

 High systolic blood pressure (the first

number in a blood pressure reading)
 Hyperactive reflexes
 Increased heart rate
 Thyroid enlargement
 Tremor

Blood tests are also done to measure levels of

thyroid hormones.

 TSH (thyroid stimulating hormone) level is

usually low
 T3 and free T4 levels are usually high

This disease may also affect the results of the

98
following tests:

 Cholesterol test
 Glucose test
 Radioactive iodine uptake

TREATMENT:-
OBJECTIVE OF TREATMENT:-
 Goal of therapy is to bring normal
metabolic rate to normal as soon as possible
and to maintain it at this level.
 Treatment depends on causes, age of
patient, severity of the diseases, and
complications.
 Remission of hyperthyroidism occurs
spontaneously within one to two years;
however, relapse can be expected in half of
the patients. Antithyroid drugs, radiation, or
surgery may be use for treatment.
 Nodular toxic goiter- surgery or use of
radioiodine is preferred.
 Thyroid carcinoma –surgery or radiation is
used.

Pharmacotherapy:-
 Drugs that inhibit hormones formation.
 Thioamides – propylthiouracil (PTU),

99
 Methimazole.
 Act by depressing the synthesis of thyroid
hormone by inhibiting peroxidase.
 May be given in divided daily dose or in a
single daily dose.
 Duration of treatment is determined by
clinical criteria.
 Thyroid gland becomes smaller.
 Uptakes of T4 and T3 are measured to
determine the adequacy of dose.
 Treatment continues until patient becomes
clinically euthyroid; this varies from 3
months to 2 years; if euthyroidism can not
be maintained without treatment, then
radiation or surgery is recommended.
 Therapy is withdrawn gradually to prevent
exacerbation.
 Drugs to control peripheral manifestation of
hyperthyroidism:-
o Propranolal-
 Acts as a beta-adrenergic blocking agent.
 Inhibits peripheral conversion of T4 to T3.
 Abolishes tachycardia, tremor, excess
sweating, nervousness.
 Controls hyperthyroid symptoms until
antithyroid drugs or radioiodine can take
effect.

100
  Glucocorticoids:-decrease the peripheral
conversion of T4 to T3, a more potent
thyroid hormone.
Radioactive iodine:-
 Action – limits secretion of thyroid
hormone by destroying thyroid tissue.
 Dosage is controlled so that
hypothyroidism does not occur.
 Chief advantage over thioamides is that
lasting remission can be achieved.
 Chief disadvantage is that permanent
hypothyroidism can be produced.

Surgery:-
 Used for those have large goiters,or for
those for whom the use of radioiodine or
thioamide is contraindicated.
 Subtotal thyroidectomy involves of
removal of most of thyroid gland.
 Emergency management of thyroid storm:-
 Inhibition of new hormone synthesis with
thioamides [PTU].
 Inhibition of thyroid hormone release using
iodine[Lugol’s solution.
 Inhibition of peripheral effect of thyroid
hormones with propranolol, corticosteroids,
and thioamides[PTU].
 Treatment aimed at systemic effect of
101
 thyroid hormonesand prevent of
decompensation.
 .Hyperthermia- cooling blanket,
acetaminophen.
 .Dehydration- administration of I. V. fluids
and electrolytes.
 Treatment of precipitating events.
NURSING MANAGEMENT
Nursing assessment
 Obtain history of symptoms, family history
of thyroid disease, medication, any recent
physical stress, particularly infection.
 Perform multisystem assessment that
includes cardiac, respiratory, GI and
neurological systems.
 Closely monitor the patient’s temperature
for thyroid strom .
 Assess the vital sign.
 Assess the symptom of the patient.
 Assess the level of understanding of their
disease.
 Assess all function of the body.
Nursing diagnosis
 Imbalanced nutrition : less than body
requirements related to hypermetabolic
state and fluid loss through diaphoresis.
 Risk for impaired skin integrity related to

102
 diaphoresis, hyperpyrexia, restlessness and
rapid weight loss.
 Disturbed through processes related to
insomnia, decreased attention span, and
irritability.
 Anxienty related to condition and concern
about upcoming surgery/ radioiodine
treatment.
Nursing intervention
Providing adequate nutrition
 Determine the patient’s food and fluids
preferences.consistent with the patient’s
requirements.
 Provide high- calorie foods and fluids
consistent with the patient’s requirements.
 Provide a quiet, calm environment at meals.
 Restrict stimulants(tea, coffee,
alcohol) ;explain rationale of requirements
and restrictions to patient.
 Encourage and pe to detrmit the patient to
eat alone if embarrassed or if otherwise
disturbed by voracious appetite.
 Monitor I.V. infusion when prescribed to
maintain fluid and electrolyte balance.
 Monitor fluid and nutritional status by
weighing the patient daily and by keeping
accurate intake and output record.

103
  Monitor vital signs to detect change in fluid
volume status.
 Assess skin turgor, mucous membranes,
and neck veins for signs of increased or
decreased fluid volume.
Maintain skin integrity
 Assess skin frequently to detect
diaphoresis.
 Bathe frequently with cool water; change
linen when damp.
 Avoid soap to prevent drying and use
lubricant skin lotion to pressure points.
 Protect and relieve pressure from bony
prominences when immobilized or while
hypothermia blanket is used.
Promoting normal thought processes
 Explain procedure to patient in an
unhurried, calm manner.
 Limit visitors; avoid stimulating
conversations or television programs.
 Reduce stressors in the environment;
reduce noise and light.
 Promote sleep and relaxation through use
of prescribed medication, massage, and
relaxation exercises.
 Minimize disruption of the patient’s sleep
or rest by clustering nursing activity.

104
  Use safety measures to reduce risk of
trauma or falls.
Relieving anxiety
 Encourage patient to verbalize concerns
and fears about illness and treatment.
 Support the patient who is undergoing
various diagnostic tests.
 Explain the purpose and requirements of
each prescribed test.
 Explain the result of tests if unclear to the
patient or if questions arise.
 Clear up misconceptions about treatment
options.
Patient education and health maintenance
 Instruct patient as follows:
 When to take medications.
 Signs and symptoms of insufficient and
excessive medications.
 Necessity of having blood evtaluations
periodically to determine thyroid levels.
 Signs of agranulocytosis (fever, sore throat,
upper respiratory infection ) or rash, fever,
urticaria, or enlarged salivary glands caused by
thioamide toxicity.
 Signs and symptoms of thyroid strom (i.e.
tachycardia, hyperpyrexia, extreme irritation)
and predisposing factors to thyroid storm (i.e.

105
 infection, surgery, stress, abrupt withdrawal of
antithyroid medication and adrenergic
blockers.
 Reinforce teaching by providing written
instructions as well.
 Assist patient in identifying source of
information and support available in the
community.

Prognosis
Hyperthyroidism is generally treatable and only
rarely is life threatening. Some of its causes may
go away without treatment.

Hyperthyroidism caused by Graves disease

usually gets worse over time. It has many
complications, some of which are severe and
affect quality of life.

9. Discribe HASHIMOTO’S THYROIDITIS:- Lecture, Listen, OHP, LCD, Explain

about Hashimoto’s thyroiditis is a chronic discussi answe VEDIOS. clinical
hashimoto’s progressive disease of the thyroid gland caused by on , ring. manifestatio
thyroiditis infiltration of lymphocytes; it results in explanat n of
its etiology, progressive destruction of the parenchyma and ion& hashimoto’s
clinical hypothyroidism if untreated. question .thyroiditis
manifestatio ing
n, DEFINITION:-
106
pathophysio Hashimoto's thyroiditis is the most common cause
logy, of hypothyroidism in the United States. It is
diagnostic named after the first doctor who described this
evaluation, condition, Dr. Hakaru Hashimoto, in 1912.
treatment,
nursing ETIOLOGY:-
management
 Chronic thyroiditis or Hashimoto's disease
.
is a common thyroid gland disorder. It can
occur at any age, but is most often seen in
middle-aged women. It is caused by a
reaction of the immune system against the
thyroid gland.
 The disease begins slowly. It may take
months or even years for the condition to
be detected. Chronic thyroiditis is most
common in women and in people with a
family history of thyroid disease. It affects
between 0.1% and 5% of all adults in
Western countries.
 Hashimoto's disease may, in rare cases, be
related to other endocrine (hormonal)
disorders caused by the immune system.
Hashimoto's disease can occur with adrenal
insufficiency and type 1 diabetes. In these
cases, the condition is called type 2
polyglandular autoimmune syndrome (PGA
II).

107
  Less commonly, Hashimoto's disease
occurs as part of a condition called type 1
polyglandular autoimmune syndrome (PGA
I), along with:

 Adrenal insufficiency (poor function of the

adrenal glands)
 Fungal infections of the mouth and nails
 Hypoparathyroidism (underactive
parathyroid gland)

Marked by a slowly developing, firm

enlargement of the thyroid gland.Usually
no gross nodules. Basal metabolic rate is
usually low.Period of hyperthyroidism
caused by large amount of T3 and T4 being
released into bloodstream.

PATHOPHYSIOLOGY:-
 Genetic predisposition and environment
factor breakdown the immune tolerance.
 And by this breakdown of immune
tolerance is happened.
 Large number of autoreactive T-helper
cells, cytotoxic T-lymphocytes and
autoantibody producing B-cells.
 Accumulation of immune cells in the
thyroid gland.

108
  Prevalence of Thi medicated autoimmune
response and cytotoxic effects of Tc cells in
the thyroid.
 Apoptosis of thyrocytes that lead to
hashimoto’s thyroidis.

109
110
The symptoms of Hashimoto's thyroiditis?

Patients with mild hypothyroidism may have no

signs or symptoms. The symptoms generally
become more obvious as the condition worsens
and the majority of these complaints are related to
a metabolic slowing of the body. Common
symptoms are listed below:

 Fatigue
 Depression
 Modest weight gain
 Cold intolerance
 Excessive sleepiness
 Dry, coarse hair
 Constipation
 Dry skin
 Muscle cramps
 Increased cholesterol levels
 Decreased concentration
 Vague aches and pains
 Swelling of the legs

Complications
 This condition can occur with other
autoimmune disorders. In rare cases,
thyroid cancer may develop. Progressive

111
 hypothyroidism.
 Without treattment, hashimoto’s thyroiditis
may progress from goiter and
hypothyroidism to myxedema.

DIAGNOSTIC EVALUATION

Laboratory tests to determine thyroid function

include:

 Free T4 test
 Serum TSH
 T3
 Thyroid autoantibodies:
o Antithyroid peroxidase antibody
o Antithyroglobulin antibody

Imaging studies are generally not needed to

diagnose Hashimoto's thyroiditis.

This disease may also change the results of the

following tests:

 Complete blood count

 Serum prolactin
 Serum sodium
 Total cholesterol

112
TREATMENT:-
 Thyroid hormone replacement agents such
as levothyroxine or desiccated thyroid
extract. A tablet taken once a day generally
keeps the thyroid hormone levels normal.
In most cases, the treatment needs to be
taken for the rest of the patient's life.
 A gluten-free diet may reduce the
autoimmune response responsible for
thyroid degeneration.
 Thyroid medications to maintain a normal
level of circulating thyroid hormones; this
is done to suppress production of TSH, to
prevent enlargement of thyroid and
maintain a euthyroid state.
 Surgical resection of goiter if tracheal
compression, cough or hoarseness occurs.
 Careful follow- up to detect and treat
hypothyroidism.

NURSING MANAGAMENT:-
NURSING ASSESSMENT-
 Assess for signs and symptoms of
hyperthyroidism and hypothyroidism.
 Assess size of thyroid gland and symptoms of
compression – neck tightness, cough, and

113
 jewelry or scarves around neck, and avoiding
excessive neck flexion or hyperextension,
which may aggravate feeling of compression
 Assess the vitai sign for any sign of infection.
 Assess the pain level acute, continue.
 Assess the severity of the condition.
 Assess the level of understanding of the
patient.
Nursing diagnosis:-
1. Hyperthermia related to disease
condition as manifestation by
axillaries temperature is 103 degree
salacious.
2. Fluid volume deficit related to
inflammatory process as evidence by
increased thirst.
3. Pain related to progressive disease
condition as manifested by pain
scale-3.
4. Risk of infection related to
inflammatory condition.
5. Anxiety related to outcome of
disease as evidence by continues ask
related question.

Nursing intervention:-

114
Maintain normal body temperature:-
 Assess the temperature by different sides.
 Encourage patient to drink more water.
 Give antipyretic medication along with
antibiotics.

Restore fluid volume:-

 Encourage to intake more water.
 Maintain electrolyte level by taking ORS or
I.V.administation.
 Monitor body weight daily.
 Monitor vital signs.
Relieve for pain:-
 Assess the level of pain.
 Assess the tolerance of pain.
 Take history of alcoholism, any side effect
of any drugs.
 Administer analgesia.
Providing adequate nutrition
 Determine the patient’s food and fluids
preferences.consistent with the patient’s
requirements.
 Provide high- calorie foods and fluids
consistent with the patient’s requirements.
 Provide a quiet, calm environment at meals.
 Restrict stimulants(tea, coffee,

115
 alcohol) ;explain rationale of requirements
and restrictions to patient.
 Encourage and pe to detrmit the patient to
eat alone if embarrassed or if otherwise
disturbed by voracious appetite.
 Monitor I.V. infusion when prescribed to
maintain fluid and electrolyte balance.
 Monitor fluid and nutritional status by
weighing the patient daily and by keeping
accurate intake and output record.
 Monitor vital signs to detect change in fluid
volume status.
 Assess skin turgor, mucous membranes,
and neck veins for signs of increased or
decreased fluid volume.

Relieving anxiety
 Encourage patient to verbalize concerns
and fears about illness and treatment.
 Support the patient who is undergoing
various diagnostic tests.
 Explain the purpose and requirements of
each prescribed test.
 Explain the result of tests if unclear to the

116
 patient or if questions arise.
 Clear up misconceptions about treatment
options.

Patient education and health maintenance:en-

 Teach signs of tracheal compression that
should be reported to health care
 Explain outcome of hypothyroidism and
necessity of taking thyroid hormones every
day for life.
 Explain the need of regular medical follow- up
visit to monitor thyroid hormones and TSH
levels.
 Assist patient in identifying sources of
information and support available in the
community.
PROGNOSIS:-

The outlook for those with Hashimoto's disease is

good. While long-term thyroid hormone
replacement therapy will likely be needed, with
regular blood tests and monitoring of symptoms,
side effects are minimal and the long-term
prognosis is good.

10. Discribe THYROID TUMORS Lecture, Listen, OHP, LCD, Enlist the
about discussi answe VEDIOS complicatio
117
thyroid on , ring. n of thyroid
tumors its Introduction:-Most thyroid tumors are benign, explanat tumors.
etiology, but 5% are malignant and it is important to ion&
clinical distinguish this sinister minority. question
manifestatio Definition:-A thyroid tumor is a growth (lump) in ing
n, the thyroid gland. The thyroid gland is located at
pathophysio the base of the neck.
logy,
diagnostic Pathophysilogy:-
evaluation,
treatment,  Most thyroid nodules are adenomatous.
nursing Most are multiple and that is usually shown
management on ultrasound, scintigraphy and at surgery.
. The nodules are usually non-functioning
(cold at scintigraphy), although a few may
be hyper-functioning toxic adenomas (hot
on scintigrams). They may also be a hyper-
functioning adenoma in a multinodular
goitre.
 When solid, the nodules are poorly
encapsulated and not well-defined, and
themerge into the surrounding tissue.
Cystic adenomatous nodules are
haemorrhagic, with irregular internal walls
and particulate fluid content. Intratumoral
calcification is occasionally seen.
 Follicular adenomas are the most common

118
 and arise from follicular epithelium. They
are usually single, well-encapsulated
lesions. On ultrasound, adenomas may be
hyperechoic or hypoechoic solid nodules
with a regular hypoechoic area surrounding
ring called the halo sign. Rarely, a
parathyroid adenoma has an ectopic
intrathyroid location.
 Whether solitary adenomas transform into
follicular carcinoma is uncertain. In
particular, whether aneuploid cells, which
are present in approximately 25% of
follicular adenomas, represent carcinoma in
situ is unclear.
 Follicular adenomas are further classified
according to their cellular architecture and
relative amounts of cellularity and colloid
into fetal (microfollicular), colloid
(macrofollicular), embryonal (atypical), and
Hürthle (oxyphil) cell types.

Clinical manifestation:-

 Most patients with thyroid nodules are

asymptomatic, and most nodules are found
on clinical examination or self-palpation.
 A single dominant or solitary nodule is
more likely to represent carcinoma
119
 (malignancy incidence 2.7-30%), than a
single nodule within a multinodular gland
(malignancy incidence 1.4 to 10%).[2]
 Thyroid lumps are often asymptomatic and
are noticed by family members or seen in
the mirror.
 They may sometimes cause pain and rarely
present with features of compression of the
trachea.
 Ask about previous radiation.
 Ask the patient to drink some water and
note the thyroid move as they swallow.
 Note enlargement or asymmetry.
 Stand behind a seated patient and use the
2nd and 3rd fingers of both hands to
examine the gland as they swallow again.

 Note lumps, asymmetry, size and

tenderness.
 Check for regional lymphadenopathy.

Examination findings that increase the concern for

malignancy include:

 Nodules larger than 4 cm in size.

 Firmness to palpation.
 Fixation of the nodule to adjacent tissues.
 Cervical lymphadenopathy.

120
  Vocal fold immobility.

Investigations

 TFTs will show most patients to be

euthyroid - refer those which are abnormal
for endocrine opinion.[3]
 Ultrasound is useful to detect and
characterise most thyroid nodules.[2] It can
show cystic lesions 2 mm wide and solid
lesions 3 mm wide. Ultrasound
examination is far more sensitive than
clinical examination and only 4-7% of
nodules detected by ultrasound are
clinically palpable.
 Fine-needle aspiration (FNA) gives tissue
for cytology. It is performed under
ultrasound guidance (for maximum
accuracy).[4] It is safe, inexpensive and
provides direct information. The false-
negative rate varies with the experience of
the person performing the procedure.
However, the false-negative rate for cancer
can vary from 1% to 6% (owing to wrong
diagnosis or sampling errors) even when
the operator is experienced and the sample
is sufficient for diagnosis. These errors
occur more commonly in nodules smaller
121
 than 1 cm or larger than 4 cm.
 Radionuclide isotope scanning looks at
iodine uptake by the thyroid and has a
limited role in the diagnosis of thyroid
cancer. The British Thyroid Association
(BTA) does not support its routine use - it
is "usually non-diagnostic of cancer".[3] The
American Thyroid Association
recommends its use only in specific
situations.[5]
 CT scans and MRI scans are valuable to
detect local and mediastinal spread and
regional lymph nodes.

Management

General measures

 The BTA recommends that patients with

non-palpable nodules smaller than 1 cm
that are discovered incidentally on imaging
of the neck and with no worrying features,
can be managed in primary care.[3] The
American Thyroid Association's guidelines
state that usually no further investigations
are required.[5]
 New thyroid lumps that have been growing
over a period of months, or patients with a

122
 sudden onset of pain in a nodule (which is
usually due to a bleed into a cyst), should
be referred to a specialist thyroid clinic
with provisions for ultrasound and fine-
needle aspiration (FNA) assessment, where
they should be seen within four weeks of
referral.[3]
 Urgent referral to secondary care is
necessary when:
o There is a solitary nodule increasing
in size.
o There is history of neck irradiation.
o There is a thyroid nodule or goitre in
a child or teenager.
o A family history of an endocrine
tumour exists.
o Unexplained hoarseness or voice
changes are noted.
o There is cervical lymphadenopathy
(usually deep cervical or
supraclavicular).
o The patient is aged 65 years or older.
o There has been enlargement of a
painless thyroid mass over a period
of weeks (may be indicative of
thyroid cancer).

123
Pharmacological

 Biochemical abnormalities of TFTs need to

be treated in the usual way. Beta-blockers
may be needed to control symptoms in
some severely toxic patients.
 Patients with benign solitary thyroid
nodules may have suppression therapy with
thyroxine, although there is currently little
evidence to support the practice.

Surgical

Solitary thyroid nodules that are malignant,

suspicious, or indeterminate on FNA require
removal. There is controversy about which
operation, with advocates for thyroid lobectomy,
total or subtotal thyroidectomy.

Complications

Both surgery and alcohol injection can cause

recurrent laryngeal nerve palsy, which should
occur in fewer than 5% of procedures. With
alcohol injection it is usually transient with full
recovery within 1-3 months. The primary disease
can cause nerve damage in both benign and

124
malignant conditions.

Nursing management

Nursing assessment:-

 Obtain history of symptoms, family history

of thyroid disease, medication, any recent
physical stress, particularly infection.
 Perform multisystem assessment that
includes cardiac, respiratory, GI and
neurological systems.
 Closely monitor the patient’s temperature
for thyroid strom .
 Assess the vital sign.
 Assess the symptom of the patient.
 Assess the level of understanding of their
disease.
 Explore patient’s feelings and concerns
regarding the diagnosis, treatment, and
prognosis.

Nursing diagnosis:-

 Disturbed body image related to visible

swelling and actual change in structure of
neck.

125
  Anxiety related to change in health status or
progressive growth of mass.
 Imbalance nutrition; less than body
requirement related to decreased ability to
ingest and difficulty swallowing.
 Knowledge deficit related to lack of
information of disease process.

Nursing intervention:-

 explain patient to this swelling is because

of the disease condition and after taking
proper treatment it may be cure.
 Assess the patient knowledge level about
the disease condition and according to
provide health related information.
 Determine the patient’s food and fluids
preferences.consistent with the patient’s
requirements.

 Provide high- calorie foods and fluids

consistent with the patient’s requirements.
 Provide a quiet, calm environment at meals.
 Restrict stimulants(tea, coffee,
alcohol) ;explain rationale of requirements
and restrictions to patient.
 Encourage and pe to detrmit the patient to
eat alone if embarrassed or if otherwise

126
 disturbed by voracious appetite.
 Monitor I.V. infusion when prescribed to
maintain fluid and electrolyte balance.
 Monitor fluid and nutritional status by
weighing the patient daily and by keeping
accurate intake and output record.
 Monitor vital signs to detect change in fluid
volume status.
 Assess skin turgor, mucous membranes,
and neck veins for signs of increased or
decreased fluid volume.
 Explain procedure to patient in an
unhurried, calm manner.
 Limit visitors; avoid stimulating
conversations or television programs.
 Reduce stressors in the environment;
reduce noise and light.
 Promote sleep and relaxation through use
of prescribed medication, massage, and
relaxation exercises.
 Minimize disruption of the patient’s sleep
or rest by clustering nursing activity.
 Use safety measures to reduce risk of
trauma or falls.
 Encourage patient to verbalize concerns
and fears about illness and treatment.
 Support the patient who is undergoing

127
 various diagnostic tests.
 Explain the purpose and requirements of
each prescribed test.
 Explain the result of tests if unclear to the
patient or if questions arise.
 Clear up misconceptions about treatment
options.
Prognosis

After exclusion of anaplastic carcinoma,

prognosis for thyroid disease is excellent.

11. Discribe CANCER OF THE THYROID:- Lecture, Listen, OHP, LCD, Describe
about cancer discussi answe VEDIOS. types of
of the INTRODUCTION:- on , ring. thyroid
thyroid its Thyroid cancer is unique among cancers, in fact, explanat cancer.
etiology, thyroid cells are unique among all cells ion&
clinical of the human body. They are the only cells that question
manifestatio have the ability to absorb Iodine. Iodine ing
n, is required for thyroid cells to produce thyroid
pathophysio hormone, so they absorb it from the
logy, bloodstream and concentrate it inside the cell.
diagnostic Most thyroid cancer cells retain this ability
evaluation, to absorb and concentrate iodine. This provides a
treatment, perfect "chemotherapy" strategy.
nursing Radioactive Iodine is given to the patient and the

128
management remaining thyroid cells .
.
DEFINITION

Thyroid cancer is a disease in which the cells of

the thyroid gland become abnormal, grow
uncontrollably, and form a mass of cells called a
tumor.

Stages of cancer of the thyroid

Once cancer of the thyroid is found (diagnosed),

more tests will be done to find out if cancer cells
have spread to other parts of the body. This is
called staging. A doctor needs to know the stage
of the disease to plan treatment.

The following stages are used for papillary

cancers of the thyroid:

Papillary and Follicular Thyroid Cancer in

Patients Younger than 45 Years of Age:

Stage I Papillary and Follicular

In stage I papillary and follicular thyroid cancer,

the tumor is any size, may be in the thyroid, or
may have spread to nearby tissues and lymph
nodes. Cancer has not spread to other parts of the
129
body.

Stage II Papillary and Follicular

In stage II papillary and follicular thyroid cancer,

the tumor is any size and cancer has spread from
the thyroid to other parts of the body, such as the
lungs or bone, and may have spread to lymph
nodes.

Papillary and Follicular Thyroid Cancer in

Patients Older than 45 Years of Age:

Stage 1 Papillary and Follicular

In stage I papillary and follicular thyroid cancer,

cancer is found only in the thyroid and the tumor
is 2 centimeters or smaller.

Stage II Papillary and Follicular

In stage II papillary and follicular thyroid cancer,

cancer is only in the thyroid and the tumor is
larger than 2 centimeters but not larger than 4
centimeters.

Stage III Papillary and Follicular

130
In stage III papillary and follicular thyroid cancer,
either of the following is found:

 the tumor is larger than 4 centimeters and

only in the thyroid or the tumor is any size
and cancer has spread to tissues just outside
the thyroid, but not to lymph nodes; or
 he tumor is any size and cancer may have
spread to tissues just outside the thyroid
and has spread to lymph nodes near the
trachea or the larynx (voice box).

Stage IV Papillary and Follicular

Stage IV papillary and follicular thyroid cancer is

divided into stages IVA, IVB, and IVC.

 In stage IVA, either of the following is

found:
o the tumor is any size and cancer has
spread outside the thyroid to tissues
under the skin, the trachea, the
esophagus, the larynx (voice box),
and/or the recurrent laryngeal nerve
(a nerve with two branches that go to
the larynx); cancer may have spread
to nearby lymph nodes; or

131
 o the tumor is any size and cancer may
have spread to tissues just outside the
thyroid. Cancer has spread to lymph
nodes on one or both sides of the
neck or between the lungs.
 In stage IVB, cancer has spread to tissue in
front of the spinal column or has
surrounded the carotid artery or the blood
vessels in the area between the lungs;
cancer may have spread to lymph nodes.
 In stage IVC, the tumor is any size and
cancer has spread to other parts of the body,
such as the lungs and bones, and may have
spread to lymph nodes.

∫Medullary Thyroid Cancer

Stage 0 medullary

Stage 0 medullary thyroid cancer is found only

with a special screening test. No tumor can be
found in the thyroid.

Stage I medullary

Stage I medullary thyroid cancer is found only in

the thyroid and is 2 centimeters or smaller.

132
Stage II medullary

In stage II medullary thyroid cancer, either of the

following is found:

 the tumor is larger than 2 centimeters and

only in the thyroid; or
 the tumor is any size and has spread to
tissues just outside the thyroid, but not to
lymph nodes.

Stage III medullary

In stage III medullary thyroid cancer, the tumor is

any size, has spread to lymph nodes near the
trachea and the larynx (voice box), and may have
spread to tissues just outside the thyroid.

Stage IV medullary

Stage IV medullary thyroid cancer is divided into

stages IVA, IVB, and IVC.

 In stage IVA, either of the following is

found:
o the tumor is any size and cancer has
spread outside the thyroid to tissues
under the skin, the trachea, the
133
 esophagus, the larynx (voice box),
and/or the recurrent laryngeal nerve
(a nerve with 2 branches that go to
the larynx); cancer may have spread
to lymph nodes near the trachea or
the larynx; or
o the tumor is any size and cancer may
have spread to tissues just outside the
thyroid. Cancer has spread to lymph
nodes on one or both sides of the
neck or between the lungs.
 In stage IVB, cancer has spread to tissue in
front of the spinal column or has
surrounded the carotid artery or the blood
vessels in the area between the lungs.
Cancer may have spread to lymph nodes.
 In stage IVC, the tumor is any size and
cancer has spread to other parts of the body,
such as the lungs and bones, and may have
spread to lymph nodes.

Anaplastic

Anaplastic thyroid cancer grows quickly and has

usually spread within the neck when it is found.
Stage IV anaplastic thyroid cancer is divided into
stages IVA, IVB, and IVC.

134
  In stage IVA, cancer is found in the thyroid
and may have spread to lymph nodes.
 In stage IVB, cancer has spread to tissue
just outside the thyroid and may have
spread to lymph nodes.
 In stage IVC, cancer has spread to other
parts of the body, such as the lungs and
bones, and may have spread to lymph
nodes.

Etiology

Thyroid cancer can occur in all age groups.

Radiation increases the risk of developing thyroid

cancer. Exposure may occur from:

 Radiation therapy to the neck (especially in

childhood)
 Radiation exposure from nuclear plant
disasters

 Growth is slow, and spread is confined to

lymph nodes that surround thyroid area.
 Cure rate is excellent after removal of involved
areas.
 Occurs predominantly in middle-aged and

135
 older persons.
 Brief encouraging response may occur with
irradiation.
 Progression of disease is rapid; high mortality.
 Parafollicular-medullary thyroid carcinoma.
 Rare, inheritable type of thyroid malignancy,
which can be detected early by a
radioimmunoassay for calcitonin.
 Undifferentiated a anaplastic carcinoma.
 The most aggressive and lethal solid tumor
found in humans.
 Least common of all thyroid cancers.
 Usually fatal within months of diagnosis.
Clinical Manifestations
 On palpation of the thyroid, there may be a
firm, irregular, fixed painless mass or
nodule.
 The occurrence of signs and symptoms of
hyperthyroidism is rare.

Complications:-

 Injury to the voice box and hoarseness after

thyroid surgery
 Low calcium levels from accidental
removal of the parathyroid glands during
surgery
 Spread of the cancer to the lungs, bones, or
136
 other parts of the body

DIAGNOSTIC EVALUATION

CLINICAL EVALUATION

A critical part of detecting and diagnosing thyroid

disease is the clinical evaluation conducted by a
trained practitioner. As part of a thorough clinical
evaluation, practitioner typically should do the
following:

 Feel (also known as “palpating”) neck.

 Listen to thyroid using a stethoscope.
 Test your reflexes.
 Check heart rate, rhythm and blood
pressure.
 Measure weight.
 Measure body temperature.
 Examine face.
 Examine eyes.
 Observe the general quantity and quality of
hair.
 Examine skin.
 Examine nails and hands.
 Review other clinical signs

Find out more about the specifics of the clinical

137
evaluation for thyroid disease in this article.

THYROID BLOOD TESTS

The blood tests that may be done as part of a

thyroid diagnosis include the following:

 Thyroid Stimulating Hormone (TSH) Test

 Total T4/ Total Thyroxine
 Free T4 / Free Thyroxine
 Total T3 / Total Triiodothyronine
 Free T3 / Free Triiodothyronine
 Thyroglobulin/Thyroid Binding
Globulin/TBG
 T3 Resin Uptake (T3RU)
 Reverse T3
 Thyroid Peroxidase Antibodies (TPOAb) /
Antithyroid Peroxidase Antibodies
 Antithyroid Microsomal Antibodies /
Antimicrosomal Antibodies
 Thyroglobulin Antibodies /
Antithyroglobulin Antibodies
 Thyroid Receptor Antibodies (TRAb)
 Thyroid-Stimulating Immunoglobulins
(TSI)

THYROID IMAGING TESTS

138
A number of imaging tests are performed for
diagnosis of various thyroid conditions. These
tests include:

 Nuclear Scan / Radioactive Iodine Uptake

(RAI-U) – which can tell whether a person
has Graves' disease, toxic multinodular
goiter, or thyroiditis.
 CT Scan – to help detect and diagnose a
goiter, or larger thyroid nodules.
 MRI / Magnetic Resonance Imaging – to
evaluate the size and shape of the thyroid
 Thyroid Ultrasound – to evaluate nodules,
lumps and enlargement of your gland.
Ultrasound can tell whether a nodule is a
fluid-filled cyst, or a mass of solid tissue.

Find out more about these imaging tests for

thyroid disease in this article.

THYROID BIOPSY/ASPIRATION

A needle biopsy, also known as fine needle

aspiration (FNA) is used to help evaluate lumps or
cold nodules. In a needle biopsy, a thin needle is
inserted directly into the lump, some cells are
withdrawn and they are evaluated for cancer.
(Some practitioners use ultrasound while

139
conducting a biopsy in order to ensure that the
needle goes into the right position.) Cancer can be
definitively diagnosed about 75 percent of the
time from FNA. Evaluation of biopsy results can
also show cells indicative of Hashimoto’s
thyroiditis.

Find out more about fine needle aspiration (FNA)

biopsy of the thyroid in this Q&A article.

OTHER DIAGNOSTIC TESTS AND

PROCEDURES

Practitioners sometimes use other diagnostic tests

and procedures to identify thyroid dysfunction.
The use of these tests is considered controversial
to mainstream practitioners, but many of these
tests are well-accepted and in use among
alternative, integrative and holistic physicians.
These tests include:

 Iodine Patch Tests

 Saliva Testing
 Urinary Testing
 Basal Body Temperature Testing

THYROID SELF-TESTS/ORDERING YOUR

140
OWN TESTS

Some patients need to be highly involved in their

thyroid diagnosis and care, which is where self-
tests and the ability to order your own tests can be
a critical tool for an empowered patient. Among
the options for patients include:

 The Thyroid Neck Check – A check you

can perform yourself.
 MyMedLab.com Blood Tests, including
Anti-Thyroid Antibodies (Thyroglobulin
Antibodies and Thyroid Peroxidase
Antibodies), Free T4, Free T3, Reverse T3,
and more
 ZRT Laboratory’s Saliva and Bloodspot
Testing, including TSH, Free T4, Free T3,
and Thyroid Peroxidase (TPO) Antibody.
 Diagnostechs Saliva Testing, including
TSH, Free T4, Free T3, and antimicrosomal
antibodies.

Treatment

There are treatments for all patients with cancer of

the thyroid. Four types of treatment are used:

141
  surgery (taking out the cancer)
 radiation therapy (using high-dose x-rays or
other high-energy rays to kill cancer cells)
 hormone therapy (using hormones to stop
cancer cells from growing)
 chemotherapy (using drugs to kill cancer
cells)

Surgery is the most common treatment of cancer

of the thyroid. A doctor may remove the cancer
using one of the following operations:

 Lobectomy removes only the side of the

thyroid where the cancer is found. Lymph
nodes in the area may be taken out
(biopsied) to see if they contain cancer.
 Near-total thyroidectomy removes all of the
thyroid except for a small part.
 Total thyroidectomy removes the entire
thyroid.
 Lymph node dissection removes lymph
nodes in the neck that contain cancer.

Radiation therapy uses high-energy x-rays to kill

cancer cells and shrink tumors. Radiation for
cancer of the thyroid may come from a machine
outside the body (external radiation therapy) or

142
from drinking a liquid that contains radioactive
iodine. Because the thyroid takes up iodine, the
radioactive iodine collects in any thyroid tissue
remaining in the body and kills the cancer cells.

Hormone therapy uses hormones to stop cancer

cells from growing. In treating cancer of the
thyroid, hormones can be used to stop the body
from making other hormones that might make
cancer cells grow. Hormones are usually given as
pills.

Chemotherapy uses drugs to kill cancer cells.

Chemotherapy may be taken by pill, or it may be
put into the body by a needle in the vein or
muscle. Chemotherapy is called a systemic
treatment because the drug enters the
bloodstream, travels through the body, and can
kill cancer cells outside the thyroid.

Treatment by stage

Treatment of cancer of the thyroid depends on the

type and stage of the disease, and the patient's age
and overall health.

Standard treatment may be considered because of

143
its effectiveness in patients in past studies, or
participation in a clinical trial may be considered.
Not all patients are cured with standard therapy
and some standard treatments may have more side
effects than are desired. For these reasons, clinical
trials are designed to find better ways to treat
cancer patients and are based on the most up-to-
date information. Clinical trials are ongoing in
many parts of the country for some patients with
cancer of the thyroid. To learn more about clinical
trials, call the Cancer Information Service at 1-
800-4-CANCER (1-800-422-6237); TTY at 1-
800-332-8615.

STAGE I PAPILLARY THYROID CANCER

Treatment may be one of the following:

1. Surgery to remove one lobe of the

thyroid (lobectomy), followed by hormone
therapy. Radioactive iodine also may be
given following surgery.
2. Surgery to remove the thyroid (total
thyroidectomy).

144
STAGE I FOLLICULAR THYROID
CANCER

Treatment may be one of the following:

1. Surgery to remove the thyroid (total

thyroidectomy).
2. Surgery to remove one lobe of the
thyroid (lobectomy), followed by hormone
therapy. Radioactive iodine also may be
given following surgery.

STAGE II PAPILLARY THYROID CANCER

Treatment may be one of the following:

1. Surgery to remove one lobe of the

thyroid (lobectomy) and lymph nodes that
contain cancer, followed by hormone
therapy. Radioactive iodine also may be
given following surgery.
2. Surgery to remove the thyroid (total
thyroidectomy).

145
STAGE II FOLLICULAR THYROID
CANCER

Treatment may be one of the following:

1. Surgery to remove the thyroid (total

thyroidectomy).
2. Surgery to remove one lobe of the
thyroid (lobectomy) and lymph nodes that
contain cancer, followed by hormone
therapy. Radioactive iodine also may be
given following surgery.

STAGE III PAPILLARY THYROID

CANCER

Treatment may be one of the following:

1. Surgery to remove the entire thyroid

(total thyroidectomy) and lymph nodes
where cancer has spread.
2. Total thyroidectomy followed by
radiation therapy with radioactive iodine or
external beam radiation therapy.

146
STAGE III FOLLICULAR THYROID
CANCER

Treatment may be one of the following:

1. Surgery to remove the entire thyroid

(total thyroidectomy) and lymph nodes or
other tissues around the thyroid where the
cancer has spread.
2. Total thyroidectomy followed by
radioactive iodine or external beam
radiation therapy.

STAGE IV PAPILLARY THYROID

CANCER

Treatment may be one of the following:

1. Radioactive iodine.
2. External beam radiation therapy.
3. Hormone therapy.
4. A clinical trial of chemotherapy.

STAGE IV FOLLICULAR THYROID

147
CANCER

Treatment may be one of the following:

1. Radioactive iodine.
2. External beam radiation therapy.
3. Hormone therapy.
4. A clinical trial of chemotherapy.

MEDULLARY THYROID CANCER

Treatment will probably be surgery to remove the

entire thyroid (total thyroidectomy) unless the
cancer has spread to other parts of the body. If
lymph nodes in the neck contain cancer, the
lymph nodes in the neck will be removed (lymph
node dissection). If the cancer has spread to other
parts of the body, chemotherapy may be given.

ANAPLASTIC THYROID CANCER

Treatment may be one of the following:

1. Surgery to remove the thyroid and the

148
 tissues around it. Because this cancer often
spreads very quickly to other tissues, a
doctor may have to take out part of the tube
through which a person breathes. The
doctor will then make an airway in the
throat so the patient can breathe. This is
called a tracheostomy.
2. Total thyroidectomy to reduce symptoms
if the disease remains in the area of the
thyroid.
3. External beam radiation therapy.
4. Chemotherapy.
5. Clinical trials studying new methods of
treatment of thyroid cancer.

RECURRENT THYROID CANCER

The choice of treatment depends on the type of

thyroid cancer the patient has, the kind of
treatment the patient had before, and where the
cancer comes back. Treatment may be one of the
following:

1. Surgery with or without radioactive

iodine.

149
 2. External beam radiation therapy to
relieve symptoms caused by the cancer.
3. Chemotherapy.
4. Radioactive iodine.
5. Radiation therapy given during surgery.
6. Clinical trials.

NURSING MANAGEMENT

Nursing Assessment

 Obtain history of symptoms, family history

of thyroid disease, medication, any recent
physical stress, particularly infection.
 Perform multisystem assessment that
includes cardiac, respiratory, GI and
neurological systems.
 Closely monitor the patient’s temperature
for thyroid strom .
 Assess the vital sign.
 Assess the symptom of the patient.
 Assess the level of understanding of their
disease.
 Explore patient’s feelings and concerns
regarding the diagnosis, treatment, and
150
 prognosis.

Nursing Diagnosis
 Imbalanced nutrition : less than body
requirements related to hypermetabolic
state and fluid loss through diaphoresis.
 Risk for impaired skin integrity related to
diaphoresis, hyperpyrexia, restlessness and
rapid weight loss.
 Disturbed through processes related to
insomnia, decreased attention span, and
irritability.
 Anxiety related to concern about cancer,
upcoming surgery.

Nursing Interventions
Providing adequate nutrition
 Determine the patient’s food and fluids
preferences.consistent with the patient’s
requirements.
 Provide high- calorie foods and fluids
consistent with the patient’s requirements.
 Provide a quiet, calm environment at meals.
 Restrict stimulants(tea, coffee,
alcohol) ;explain rationale of requirements

151
 and restrictions to patient.
 Encourage and pe to detrmit the patient to
eat alone if embarrassed or if otherwise
disturbed by voracious appetite.
 Monitor I.V. infusion when prescribed to
maintain fluid and electrolyte balance.
 Monitor fluid and nutritional status by
weighing the patient daily and by keeping
accurate intake and output record.
 Monitor vital signs to detect change in fluid
volume status.
 Assess skin turgor, mucous membranes,
and neck veins for signs of increased or
decreased fluid volume.

Maintain skin integrity

 Assess skin frequently to detect
diaphoresis.
 Bathe frequently with cool water; change
linen when damp.
 Avoid soap to prevent drying and use
lubricant skin lotion to pressure points.
 Protect and relieve pressure from bony
prominences when immobilized or while

152
 hypothermia blanket is used.

Promoting normal thought processes

 Explain procedure to patient in an
unhurried, calm manner.
 Limit visitors; avoid stimulating
conversations or television programs.
 Reduce stressors in the environment;
reduce noise and light.
 Promote sleep and relaxation through use
of prescribed medication, massage, and
relaxation exercises.
 Minimize disruption of the patient’s sleep
or rest by clustering nursing activity.
 Use safety measures to reduce risk of
trauma or falls.

Relieving anxiety
 Encourage patient to verbalize concerns
and fears about illness and treatment.
 Support the patient who is undergoing
various diagnostic tests.
 Explain the purpose and requirements of
each prescribed test.
 Explain the result of tests if unclear to the

153
 patient or if questions arise.
 Clear up misconceptions about treatment
options.
 Provide all explanations in a simple,
concise manner and repeat important
information as necessary because anxiety
may interfere with patient’s processing of
information.
 Stress the positive aspects of treatment,
high cure rate as outlined by health care
provider.
 Encourage support by significant other,
clergy, social worker, nursing staff, as
available.
Patient Education and Health
Maintenance
 Instruct the patient on thyroid hormone
replacement and follow-up blood tests.
 Stress the need for periodic evaluation for
recurrence of malignancy.
 Supply additional information or suggest
community resources dealing with cancer
prevention and treatment.
 Assist patient in identifying sources of
information and support available in the
community.

154
Prognosis

Most thyroid cancers are very curable. In fact, the

most common types of thyroid cancer (papillary
and follicular thyroid cancer) are the most
curable. In younger patients, both papillary and
follicular cancers have a more than 97% cure rate
if treated appropriately. Both papillary and
follicular thyroid cancers are typically treated
with complete removal of the lobe of the thyroid
that harbors the cancer, in addition to the removal
of most or all of the other side.

The bottom line is that most thyroid cancers are

papillary thyroid cancer, and this is one of the
most curable cancers of all cancers. Treated
correctly, the cure rate is extremely high.

Medullary thyroid cancer is significantly less

common but has a worse prognosis. Medullary
cancers tend to spread to large numbers of lymph
nodes very early on, and therefore require a much
more aggressive operation than the more localized
thyroid cancers, such as papillary and follicular
thyroid cancer.

This cancer requires complete thyroid removal

plus a dissection to remove the lymph nodes of

155
 the front and sides of the neck.

The least common type of thyroid cancer is

anaplastic thyroid cancer, which has a very poor
prognosis. Anaplastic thyroid cancer tends to be
found after it has spread, and it is incurable in
most cases.
It is very uncommon to survive anaplastic thyroid
cancer, as often the operation cannot remove all
of the tumor. These patients often require a
tracheostomy during the treatment, and treatment
is much more aggressive than for other types of
thyroid cancer

12. Discribe GOITER Lecture, Listen, OHP, LCD, Explain the

about goiter INTRODUCTION:- discussi answe VEDIOS. diagnostic
its etiology, on , ring. evaluation
clinical A goitre or goiter , is a swelling of the thyroid explanat of goiter.
manifestatio gland, which can lead to a swelling of the neck or ion&
n, larynx (voice box). Goitre is a term that refers to question
pathophysio an enlargement of the thyroid (thyromegaly) and ing
logy, can be associated with a thyroid gland that is .
diagnostic functioning properly or not.
evaluation,
treatment, DEFINITION:-

156
nursing A goiter is an abnormal enlargement of the
management thyroid gland and can occur for a number of
. different reasons.

Diffuse hyperplasia of the thyroid

TYPES OF GOITER:-

Regarding morphology, goitres may be classified

either as the growth pattern or as the size of the
157
growth:

Growth pattern

 Uninodular (struma uninodosa): can be

either inactive or a toxic nodule.
 Multinodular (struma nodosa): can likewise
be inactive or toxic, the latter called toxic
multinodular goitre.
 Diffuse (struma diffuse): the whole thyroid
appearing to be enlarged.

Size

 Class I (palpation struma): in normal

posture of the head, it cannot be seen; it is
only found by palpation.
 Class II: the struma is palpative and can be
easily seen.
 Class III: the struma is very large and is
retrosternal; pressure results in compression
marks.

158
 Struma nodosa (Class II)

Struma with autonomous adenoma

159
 Struma Class III

CAUSES

There are various different causes of a goiter:

 Iodine Deficiency - Iodine found in fish

products, drinking water and table salt, is
essential for the production of thyroid
hormone. If there is a lack of it, an
individual will suffer from
hypothyroidism. In an effort to produce
more thyroid hormone the thyroid gland is
over stimulated and enlarges to form an
endemic goiter. An iodine deficiency is
very common in underdeveloped countries.

 Graves’ Disease - This is an autoimmune

disorder which causes the thyroid gland to
160
 be overactive (hyperthyroidism). In Graves’
disease, antibodies produced by the
immune system stimulate the thyroid
gland which then enlarges, resulting in an
enlarged goiter, and produces excess
thyroid hormone.

 Hashimoto's Thyroiditis - Hashimoto’s

disease is also an autoimmune disorder.
The immune system destroys the thyroid
gland which results in less thyroid hormone
being produced. The pituitary gland then
stimulates the thyroid gland to produce
more thyroid hormones, causing it to
enlarge and a goiter can then develop.

 Solitary Thyroid Nodules - A single

nodule develops inside the thyroid which
causes an enlarged thyroid.

 Multinodular Goiter - In this disorder,

many nodules develop inside the thyroid
which causes an enlarged thyroid. These
nodules are usually not harmful.

 Thyroid Cancer - The cancer may be

detected as a lump or nodule in the thyroid
gland and may result in goiter formation.

161
 Inflammation - Inflammation of the
thyroid is also referred to as thyroiditis, and
it is usually associated with hypothyroidism
(underactive thyroid). There are many
causes of thyroiditis that can result in an
enlarged thyroid or goiter. Some common
symptoms of thyroiditis include mild fever
and neck pain that is worse with
swallowing.

 Pregnancy - During the first tri-mester of

pregnancy, a hormone called human
chorionic gonadotrophin (HCG) can result
in an enlarged thyroid gland. The thyroid
gland mistakenly registers HCG for TSH
(the thyroid stimulating hormone produced
by the pituitary gland) and enlarges in
response to it.

Pathophysiology:-

 Risk factor lead iodine deficiency. This

lead to decreased release of thyroid
hormones.
 By this increased TRH release from thyroid
gland
 This lead to increased cellularity of thyroid
gland.

162
  And by this thyroid gland become

RISK FACTOR (MODIFIABLE/NON-MODIFIABLE)

IODINE DEFICIENCY

DECREASED RELEASE OF THYROID HORMONES

DECREASE RELEASE OF THYROID HORMONE

INCREASED TRH INFLUENCE

INCREASED CELLULARITY OF THYROID GLAND

HYPERPLASIA OF THYROID GLANDS

MANIFESTATIONS

163
hyperplasia.

 This condition manifested by visual

swelling of neck, dysplasia, dyspnea and
acute pain.

CLINICAL MANIFESTATION

Symptoms and signs of goiter may include:

 Symptoms of hyperthyroidism or
hypothyroidism (e.g. High Blood Pressure,
Hair Loss, and Digestive Problems)
 Neck and Ear Pain
 Stress & Anxiety
 Sore Throat
 Difficulty swallowing
 Headaches
 Snoring
 Coughing
 Swelling or disfigurement of the neck
 A feeling of tightness in your throat
 Difficulty breathing

Complication

164
Complications of simple goiter are generally not
life threatening, though in rare cases goiter may
press on the windpipe, preventing breathing. As
goiter affects the production of thyroid hormones,
which are important to many aspects of
metabolism, serious complications can develop if
the disease goes untreated for long periods of
time. You can help minimize your risk of serious
complications by following the treatment plan you
and your health care professional design
specifically for you. Complications of goiter
include:

 Difficulty breathing
 Difficulty swallowing
 Hyperthyroidism (overactive thyroid)
 Hypothyroidism (underactive thyroid)
 Thyroid cancer
 Toxic nodular goiter (overproduction of
thyroid hormones)

Evaluating a Goiter

The most important part of the evaluation of a

goiter is the doctor's examination. Commonly the
doctor will evaluate a goiter using some or all of

165
the following techniques:

 Feeling the thyroid

 Blood test
 Thyroid scan
 Ultrasound

Feeling the Thyroid

By feeling the thyroid, the doctor can estimate the

size of the gland, tell whether it is growing or not,
and tell if it has any lumps in it that might be
suspicious for cancer.

Blood Test

Measurement of the levels of thyroid stimulating

hormone (TSH) and T4 in the blood stream are
important because they help the doctor determine
whether or not the goiter is making a normal
amount of thyroid hormone.

If the gland has a lump in it, the doctor may order

a thyroid scan or an ultrasound to see if there are
any masses in the thyroid that might be suspicious
for a thyroid cancer.

166
Thyroid Scan

A thyroid scan is performed by having the patient

take oral capsules that contain a harmless
radioactive tracer (which is a tiny quantity of
radioactive iodine). After four to twenty-four
hours (depending on the institution) a detector is
placed over the thyroid gland. The amount of
radioactive iodine that wound up in the thyroid
gland is measured and a picture is taken of the
distribution of radioactive iodine in the thyroid.

In a normal thyroid gland, radioactive iodine is

taken up to the same degree throughout the entire
gland. If there is an area of the thyroid that does
not take up radioactive iodine well, then it must
be further investigated. The majority of these
"cold" areas on a thyroid scan are benign, but
about 5-10% of them are thyroid cancers. Under
such circumstances an ultrasound might be
ordered.

Ultrasound

Ultrasound is a way of taking a picture of the

inside of the thyroid. Ultrasound bounces sound
waves off the thyroid and makes a picture out of

167
the returning echoes. If the ultrasound shows a
large mass that is suspicious for cancer, then the
ultrasonographer can use the ultrasound to guide a
needle into the mass to perform a fine needle
aspiration biopsy. If there are no large lumps in
the thyroid gland that are suspicious for cancer,
then no biopsy needs to be done.

Treatment

A goiter may not need treatment if it is small and

not growing. Treatment would be necessary for
the following reasons:

 Size inhibits function of parts of the neck

 Growth is fast enough to cause problems in
the near future
 Unsightly appearance

If the thyroid were large enough to press on the

swallowing tube, breathing tube, or nerve to the
voice box, this pressure might cause difficulty
swallowing, shortness of breath, or hoarseness in
the voice. It might be important to treat a goiter
that was growing in order to keep it from
eventually pressing on these important structures
and causing symptoms. Finally, if the goiter is

168
large enough to be unsightly, the patient might
want it treated for cosmetic reasons.

The best treatment for a goiter is a subtotal

thyroidectomy. This is an operation in which most
of the thyroid gland is removed. There are some
research studies suggesting that putting a patient
on a thyroid hormone pill everyday may help to
shrink goiters or keep them from growing.
However, there are other studies suggesting that
this may not work. There are also studies
suggesting that even a mild overdose of thyroid
hormone, if taken for many years, can result in
osteoporosis and may put older individuals at risk
for abnormal heart rhythms.

Nursing management

Nursing assessment:-

 Assess the condition of patient.

 Assess the size of the goiter.
 Assess the nutrition status of the patient.
 Assess vital sign for any sign of infection.
 Assess the pain level.
 Assess the level of understanding of the
patient.

169
Nursing diagnosis:-

 Disturbed body image related to visible

swelling and actual change in structure of
neck.
 Anxiety related to change in health status or
progressive growth of mass.
 Imbalance nutrition; less than body
requirement related to decreased ability to
ingest and difficulty swallowing.
 Ineffective airway clearance related to
tracheal compression or obstruction.
 Knowledge deficit related to lack of
information of disease process.

Nursing intervention:-

 explain patient to this swelling is because

of the disease condition and after taking
proper treatment it may be cure.
 Assess the patient knowledge level about
the disease condition and according to
provide health related information.
 Determine the patient’s food and fluids
preferences.consistent with the patient’s
requirements.

170
 Provide high- calorie foods and fluids
consistent with the patient’s requirements.
 Provide a quiet, calm environment at meals.
 Restrict stimulants(tea, coffee,
alcohol) ;explain rationale of requirements
and restrictions to patient.
 Encourage and pe to detrmit the patient to
eat alone if embarrassed or if otherwise
disturbed by voracious appetite.
 Monitor I.V. infusion when prescribed to
maintain fluid and electrolyte balance.
 Monitor fluid and nutritional status by
weighing the patient daily and by keeping
accurate intake and output record.
 Monitor vital signs to detect change in fluid
volume status.
 Assess skin turgor, mucous membranes,
and neck veins for signs of increased or
decreased fluid volume.
 Explain procedure to patient in an
unhurried, calm manner.
 Limit visitors; avoid stimulating
conversations or television programs.
 Reduce stressors in the environment;
reduce noise and light.
 Promote sleep and relaxation through use
of prescribed medication, massage, and

171
 relaxation exercises.
 Minimize disruption of the patient’s sleep
or rest by clustering nursing activity.
 Use safety measures to reduce risk of
trauma or falls.
 Encourage patient to verbalize concerns
and fears about illness and treatment.
 Support the patient who is undergoing
various diagnostic tests.
 Explain the purpose and requirements of
each prescribed test.
 Explain the result of tests if unclear to the
patient or if questions arise.
 Clear up misconceptions about treatment
options.
Outlook (Prognosis)

A simple goiter may disappear on its own, or may

become larger. Over time, the thyroid gland may
stop making enough thyroid hormone. This
condition is called hypothyroidism.

Less commonly, a goiter may become toxic and

produce thyroid hormone on its own. This can
cause high levels of thyroid hormone, a condition
called hyperthyroidism.

172
DISORDER OF PARATHYROID GLAND

HYPERPARATHYROIDISM

INTRODUCTION:-

The parathyroid glands are located in the neck,

near or attached to the back side of the thyroid
gland. They produce parathyroid hormone. This
hormone controls calcium, phosphorus, and
vitamin D levels in the blood and bone.

DEFINITION:-

Hyperparathyroidism is a disorder in which the

parathyroid glands in your neck produce too much
parathyroid hormone (PTH).

ETIOLOGY:-

173
One or more of the parathyroid glands may grow
larger. This leads to too much parathyroid
hormone (a condition called primary
hyperparathyroidism). Most often, the cause is
not known.

 The disease is most common in people over

age 60, but it can also occur in younger
adults. Hyperparathyroidism in childhood is
very unusual.
 Women are more likely to be affected than
men.
 Radiation to the head and neck increases
the risk.
 Rarely, the disease is caused by parathyroid
cancer.

Medical conditions that cause low blood calcium

levels or increased phosphate levels can lead to
secondary hypoparathyroidism. Common causes
include:

 Conditions that make it hard for the body to

break down phosphate
 Kidney failure
 Not enough calcium in the diet
 Too much calcium lost in the urine
174
  Vitamin D disorders (which are often seen
in children who do not get enough
nutrition, and in older adults who do not get
enough sunlight
 Problems absorbing nutrients from food
(called malabsorption)

PATHOPHISIOLOGY:-

Increase PTH level in blood

Target organ stimulate

Reaborption of calcium

Than it affect the function of kidney,

skeletal system, and GI tract

 Increased the level of PTH in blood due to

disease condition.
 Than it stimulate the target gland to
reabsorb more calcium from the blood.
 Reabsoption of calcium is increased by the
kidney, skeletal system, GI tract.
 In kidney alteration of bicarbonate and
increased reabsorption of phosphate level.
175
  In skeletal system increased the risk of
fracture, cyst, and ostopenia.
 In GI tract vitamin D is stimulated and that
lead to increases of blood calcium level.
Clinical Manifestations
 Decalcification of bones.
 Skeletal pain, backache, pain on weight-
bearing, pathologic fractures, deformities,
formation of bony cysts.
 Formation of bone—overgrowth of
osteoclasts.
 Formation of calcium-containing kidney
stones.
 Depression of neuromuscular function.
 The patient may trip, drop objects, show
general fatigue, lose memory for recent events,
experience emotional in stability, have
changes in level of consciousness, with stupor
and coma.
 Cardiac arrhythmias, hypertension, cardiac
standsill.
Complication
 Formation of renal stones, calcification of
kidney parenchyma, renal
 Ulceration of upper GI tract leading to
hemorrhage and perforation.
 Demineralization of bones, cysts, fibrosis

176
 of marrow lead to fracture, especially
vertebral bodies and ribs.
 Hypoparathyroidism after surgery.

Diagnostic Evaluation
 Persistently elevated serum calcium
(11mg/100ml); test is performed on at least
two occasions to determine consistency of
results.
 Exclusion of other causes of hypercalcemia
—malignancy (usually bone or breast),
vitamin D excess, multiple myeloma,
sarcodosis, milk-alkali syndrome, such
drugs as thiazides, Cushing’s disease,
hyperthyroidism.
 PTH levels are increased.
 Serum calcium and alkaline phosphatase
levels are elevated and serum phosphorus
levels are decreased.
 Skeletal changes are revealed by X-ray.
 Early diagnosis typically is difficult.
 Cine computed tomography (CT) will
disclose parathyroid tumors more readily
than X-ray.
 Sestamibi scan is used to evaluate location
of the tumor prior to surgery.
Treatment

177
Treatment of hypercalcemia
 Hydration (i.v. saline and diruretics( lasix)
and ethacrynic acid (edecrin)—to increase
urinary excretion of calcium in patients not
in renal failure.
 Oral phosphate may be used as an
antihypercalcemic agent.
 Pamidronate, calcitonin, or etidronate
disodium are effective in treating
hypercalcemia by inhibiting bone
resorption.
 Dietary calcium is restricted and all drugs
might cause hypercalcemia are
discontinued.
 Dialysis may be necessary in the patients
with resistant hypercalcemia or those with
the renal failure.
 Digoxin is reduced because patient with
hypercalcemia is more sensitive to toxic
effect of those drugs.
 Monitoring of daily serum calcium, blood
urea nitrogen, potassium, and magnesium
level.
 Removal of underlying cause.
Treatment of primary hyperparathyroidism
Surgery for removal of abnormal parathyroid

178
tissue.
Nursing assessment
 Obtain review of systems and perform
multisystem examination to detect signs
and symptoms of hyperparathyroidism.
 Closely monitor patient’s input and output
and serum electrolytes, especially calcium
levels.
Nursing diagnosis
 Deficient fluid volume related to effects of
elevated serum calcium levels.
 Impaired urinary related to related to renal
calculi and calcium deposits in kidneys.
 Impaired physical monbility related to
weakness, bone pain, and pathological
fractures.
 Anxiety related to surgery.
 Risk of injury related to hypocalcemia.
Nursing interventions
Achieving fluid and electrolyte balance
 Monitor fluid intake and output.
 Provide adequate hydration—administer
water, glucose, and electrolyte orally or
I.V. as prescribed.
 Prevent or promptly treat dehydration by
reporting vomiting or other source of fluid
loss promptly.

179
  Help patient understand why and how to
avoid dietary source of calcium—daily
products, broccoli, calcium containing
antacids.
Promoting urinary elimination
 Strain all urine to observe for stones.
 Increase fluid intake to, 3,000 ml/day to
maintain hydration and prevent
precipitation of calcium and formation of
stones.
 Instruct the patient about dietary
recommendations for restriction of calcium.
 Observe the sign of UTI, hematuria and
renal colic.
 Assess renal function through serum
creatinine and BUN level.
Increasing physical mobility
 Assist patient in hygiene and activities if
bone pain is severe or if the patient
experience musculoskeletal weakness.
 Protect patient to fall or injury.
 Turns the patient cautiously and handle
extremities gently to avoid fracture.
 Administer analgesia as prescribed.
 Assess level of pain and the patient
response to analgesia.
 Encourage the patient to participate in mild

180
 exercise gradually as symptoms subside.
 Instruct and demonstrate correct body
mechanics to reduce strain, backache and
injury.
Relieving anxiety
 Encourage patient to verbalize fears and
feeling about upcoming surgery.
 Explain tests and procedure to the patient.
 Reassure the patient about skeletal recovery.
 Bone pain diminishes fairly quickly.
 Fractures are treated by orthopedic procedure.
 Prepare patient for surgery as for
thyroidectomy.
Monitoring for hypocalcemia postoperatively
 Monitor ECG to detect changes secondary to
hypercalcemia.(during moderate elevation of
serum calcium, QT interval is shortened; with
extreme hypercalcemia, widening of the T
wave is seen.)
 Monitor serum calcium level and evaluate the
sign and symptoms of hypocalcemia and onset
of tetany.
 Observe calcium level—if well below normal,
and if decline continues into the second week,
the skeletal system is absorbing calcium and
calcium administration may be necessary.
 If some significant bone involvement was

181
 noted before surgery as evidence by elevated
alkaline phosphatase level, elemental calcium
may be ordered.
Patient education and health promotion
 Instruct the patient about calcium- reducing
medications.
 Calcitonin is given subcutaneously- teach
proper technique.
 Etidronate disodium- calcium reach foods
should be avoided within 2 hours of dose;
therapeutic response may take 1- 3 months.
 Pamidronate – monitor hypercalcemia related
parameters when treat begins. Adequate intake
of calcium and vitamin D is necessary to
prevent hypocalcemia. Biphosphanates should
be used with caution in individuals with active
upper GI problems.
 Teach signs and symptoms of tetany that the
patient may be experience postoperatively and
should report to health care provider.
(numbness and tingling in extremities or
around mouth).
 Assist patient in identifying sources of
information and support available in the
community.

Prognosis

182
 The outlook depends on the type of
hyperparathyroidism.

Long-term problems that can occur when

hyperparathyroidism is not well controlled
include:

 Increased risk of bone fractures

 High blood pressure and heart disease
 Kidney stones

13. Discribe HYPOPARATHYROIDISM:- Lecture, Listen, OHP, LCD, Explain the

about discussi answe VEDIOS. pathophysio
hypoparathy INTRODUCTION:- on , ring logy of
roidism its explanat hypoparathy
etiology, The parathyroid glands help control calcium use ion& roidism
clinical and removal by the body. They do this by question
manifestatio producing parathyroid hormone, or PTH. PTH ing
n, helps control calcium, phosphorus, and vitamin D .
pathophysio levels in the blood and bone.Hypoparathyroidism
logy, occurs when the glands produce too little PTH.
diagnostic Blood calcium levels fall, and phosphorus levels
evaluation, rise.
treatment,
nursing DEFINITION:-
management Hypoparathyroidism results from a deficiency of

183
. parathyroid hormone and characterized by
hypocalcemia and neuromuscular
hyperexcitability.

ETIOLOGY:-

Risk factors for hypoparathyroidism include:

 A family history of parathyroid disorder

 Autoimmune diseases such as Addison's
disease
 Recent thyroid or neck surgery

The most common cause of hypoparathyroidism

is injury to the parathyroid glands during thyroid
and neck surgery. Rarely, hypoparathyroidism is a
side effect of radioactive iodine treatment for
hyperthyroidism.

Hypoparathyroidism may also be caused by

 Low blood magnesium levels

 Metabolic alkalosis

PATHOPHYSIOLOGY:-

Inadequate circulatory PTH

184
 Decreased bone absorption of calcium,
decreased activation of vita.D and also
decreased intestinal absorption of calcium

Hypocalcemia

hyperphosphatemia

 Because of the disease condition there is

inadequate amount of blood PTH level.
 It lead to decreased absorption of calcium
 Decreased activation of vita D
 Decreased intestinal absorption of calcium.
 Increased renal excretion of calcium.that
lead to hypocalcimia.
 And that response increased renal
absorption of phosphorus.

Clinical Manifestations
1. Tetany – general muscular hypertonia;
attempts or voluntary movement result in
tremors and spasmodic or uncoordinated
movements; fingers assume classic titanic
position.
a. Chvostek’s sign – a spasm of facial muscles
185
 that occurs when muscles or branches of
facial nerve are tapped.
b. Trousseau’s sign – carpopedal spasm
within 3 minutes after a BP cuff is inflated
20mm Hg above the patient’s systolic
pressure.
c. Laryngeal spasm.
2. Severe anxiety and apprehension.
3. Renal colic is usually present if the patient
has history of stones; preexisting stones
loosen and migrate into the ureter.

complication

Hypoparathyroidism in children may lead to poor

growth, abnormal teeth, and slow mental
development.

Too much treatment with vitamin D and calcium

can cause hypercalcemia (high blood calcium)
and may sometimes interfere with kidney
function.

Hypoparathyroidism increases your risk of:

 Addison's disease
 Cataracts
 Parkinson's disease

186
  Pernicious anemia

Diagnostic Evaluation
1. Phosphorus level in blood is elevated.
2. Decrease in serum calcium level to a low
level (7.5 mg/100 mL or less).
3. PTH levels are low in most cases; may be
normal or elevated in
pseudohypoparathyroidism.
An ECG may show abnormal heart rhythms.

A urine test may be done to determine how much

calcium is being removed from the body.

Management
I.V. Calcium Administration
1. A syringe and an ampule of a calcium
solution (calcium chloride, calcium
gluceptate, calcium gluconate) are to be
kept at the bedside at all times.
2. Most rapidly effective calcium solution is
ionized calcium chloride (10%).
3. For rapid use to relieve severe tetany,
infusion carried out every 10 minutes.
a. All I.V. calcium preparations are
administered slowly. It is highly
irritating, stings, and causes
thrombosis; patient experiences

187
 unpleasant burning flush of skin and
tongue.
b. Typical doses are as follows:
i. Calcium Chloride – 500 mg to 1g (5
to 10 mL) as indicated by serum
calcium; administer at rate of less
than 1mL/minute of 10% solution.
ii. Calcium gluconate – 500 mg to 2 g
(10 to 20 mL) at a rate of less than
0.5 mL/minute of a 10% solution.
iii. Calcium gluceptate – 1 to 2g (5 to 10
mL) at a rate of less than 1
mL/minute.
4. A slow drip of I.V. saline containing
calcium gluconate is given until control of
tetany is ensured; then I.M. or oral
administration of calcium is prescribed.
5. Later, vitamin D is added to calcium intake
– increases absorption of calcium and also
induces a high level of calcium in the
bloodstream. Thiazide diuretics may also
be added because of their calcium-retaining
effect on the kidney; doses of calcium and
vitamin D may be lowered.
6. Administration of I.V. calcium seems to
cause rapid relief of anxiety.
Other Measures

188
1. Treat kidney stones.
2. Monitor patient for hypercalciuria. Periodic
24 hours urinary calcium determinations
are recommended.
3. Monitor blood calcium level periodically;
variations in vitamin D may effect calcium
levels.

Nursing Assessment
1. Perform multisystem assessment, focusing
on neuromuscular system.
2. Closely monitor patient’s input and output
and serum electrolytes, especially calcium
level.
3. Assess anxiety.
Nursing Diagnosis
 Imbalanced Nutrition : Less Than Body
Requirements for calcium.
 Anxiety related to disease condition as
manifested by verbalizes by the client.
 Safe care deficit regarding to care of
complication.
 Irregular body movement related to disease
condition as manifested by uncoordinated
movement.

Nursing Interventions

189
Maintaining Normal Serum Calcium Levels
 Assess neuromuscular status frequently in
patients with hypoparathyroidism and in
those at risk for hypocalcemia (patients in
the immediate postoperative period after
thyroidectomy, parathyroidectomy, radical
neck dissection).
 Check for Trousseau’s and Chvostek’s
signs and notify health care provider if tests
results are positive.
 Assess respiratory status frequently in acute
hypocalcemia and postoperatively.
 Monitor serum calcium and phosphorus
levels.
 Promote high-calcium diet if prescribed –
dairy products, green, leafy vegetables.
 Instruct the patient about signs and
symptoms of hypo and hypercalcemia that
should be reported.
 Use caution in administering other drugs to
the patient with hypocalcemia.
 The hypocalcemia patient is sensitive to
digoxin (Lanoxin); as hypocalcemia is
reversed, the patient may rapidly develop
digitalis toxicity.
 Cimetidine (Tagamet) interferes with
normal parathyroid function, especially

190
 with renal failures, which increases the risk
of hypocalcemia.

Relieving anxiety
 Encourage patient to verbalize fears and
feeling about upcoming surgery.
 Explain tests and procedure to the patient.
 Reassure the patient about skeletal recovery.
 Bone pain diminishes fairly quickly.
 Fractures are treated by orthopedic procedure.
 Prepare patient for surgery as for
thyroidectomy.

Patient Education and Health Maintenance

1. Explain to the patient and family the
function of PTH and the roles of vitamin D
and calcium in maintaining good health.
2. Discuss the importance of each medication
prescribed for the control of hypocalcemia
including vitamin D , calcium, and thiazide
diuretic.
a. Take medications as prescribed.
b. Do not substitute with over-the-
counter preparations without the
advice and supervision of the health
care provider.
3. Provide the patient with a written list about

191
 hypercalcemia and hypocalcemia and
advice the patient to contract the health care
provider immediately should signs of either
condition develop.
4. Advise the patient to wear a Medic Alert
braceler.
5. Explain the need for periodic medical
follow-up for life.
Outcome-Based Evaluation (Prognosis)

The outcome is likely to be good if the diagnosis

is made early. However, changes in the teeth,
cataracts, and brain calcifications cannot be
reversed.
14. DISORDERS OF THE ADRENAL GLANDS

The adrenal medulla, or inner portion of the

gland, is not necessary to maintain life, but
enables a person to cope with stress. It secretes
two hormones:
 Epinephrine (adrenalin) acts on alpha and
beta receptors to increase contractility and
excitability of heart muscle, leading to
increased cardiac output; facilitates blood
flow to muscles, bran and viscera; enhances
blood sugar by stimulating conversion of
glycogen to glucose in liver; and inhibits
smooth muscle contraction.
192
  Norepinephrine (noradrenaline) acts
primarily on alpha receptors to increase
peripheral vascular resistance leading to
increases in diastolic and systolic BP.
 The adrenal cortex, or outer portion of the
gland, is essential to life. It secretes
adrenocortical hormones – synthesize from
cholesterol.
 Glucocorticoids (cortisone and
hydrocortisone) enhance protein catabolism
and inhibit protein synthesis; antagonize
action of insulin and increase blood sugar;
increase synthesis of glucose by liver;
influence defense mechanism of body and
its reaction to stress; and influence
emotional reaction.
 Mineralocorticoids (aldosterone and
desoxycorticosterone) regulate reabsorption
of sodium; regulate excretion of postassium
by renal tubules.
 Adrenosterones (adrenal androgens) exert
minimal effect on sex characteristics and
function.

Adrenal disorder:-
1. Adrenal cortex:-
 Cushing syndrome.

193
  Addison disease.
2. Adrenal medulla:-
 Primary aldosteronism.
 Phenochromocytoma.

Discribe CUSHING’S SYNDROME Lecture, Listen, OHP, LCD, Explain the

about discussi answe VEDIOS. treatment
cushing INTRODUCTION on , ring measure of
syndrome Cushing’s syndrome is a condition in which explanat cushing
its etiology, the plasma cortisol levels are elevated, causing ion& disorder.
clinical signs and symptoms of hypercortisolism question
manifestatio ing
n, DEFINITION.
pathophysio
logy, Cushing syndrome is a disorder that occurs when
diagnostic body is exposed to high levels of the hormone
evaluation, cortisol. It may also occur if take too much
treatment, cortisol or other steroid hormones.
nursing
management Etiology
.
. people develop Cushing syndrome because their
bodies produce too much cortisol, a hormone
normally made in the adrenal gland. Causes of too

194
much cortisol are:

 Cushing's disease, when the pituitary gland

makes too much of the hormone ACTH.
ACTH then signals the adrenal glands to
produce cortisol. Tumor of the pituitary
gland may cause this condition.
 Tumor of the adrenal gland
 Tumor elsewhere in the body that produces
cortisol
 Tumors elsewhere in the body that produce
ACTH (such as the pancreas, lung, and
thyroid)

Pathophysiology

When stimulated by ACTH, the adrenal gland

secretes cortisol and other steroid hormones.
ACTH is produced by the pituitary gland and
released into the petrosal venous sinuses in
response to stimulation by corticotropin-releasing
hormone (CRH) from the hypothalamus . ACTH
is released in a diurnal pattern that is independent
of circulating cortisol levels: peak release occurs
just before awakening, and ACTH levels then
decline throughout the day. Control of CRH and
ACTH release is maintained through negative

195
feedback by cortisol at the hypothalamic and
pituitary levels. N euronal input at the
hypothalamic level can also stimulate CRH
release.

196
Hypothalamic-pituitary-adrenal axis. (CRH =
corticotropin-releasing hormone; ACTH =
adrenocorticotropin hormone)

Although the adenomas of Cushing's disease

secrete excessive amounts of ACTH, they
generally retain some negative feedback
responsiveness to high doses of glucocorticoids.
Ectopic sources of ACTH, usually in the form of
extracranial neoplasms, are generally not
responsive to negative feedback with high doses
of glucocorticoids. However, some overlap exists
in the response to negative feedback between
pituitary and ectopic sources of excessive ACTH.

197
Increases the hormones level in circulation

increased increased sex

glucocarticoid increased
hormone
mineralocarticoid
increased * increased water
virilization in female
metabolism of gynecomastia and
and mineral
testicular atropy and
fat, meabolism
change in libido.
carbohydrates, * emotional
unstability
protien.

198
Clinical Manifestations

Most people with Cushing syndrome will have:

 Upper body obesity (above the waist) and

thin arms and legs
 Round, red, full face (moon face)
 Slow growth rate in children

Skin changes that are often seen:

 Acne or skin infections

 Purple marks (1/2 inch or more wide)
called striae on the skin of the abdomen,
thighs, and breasts
 Thin skin with easy bruising

Muscle and bone changes include:

 Backache, which occurs with routine

activities
 Bone pain or tenderness
 Collection of fat between the shoulders
(buffalo hump)
 Rib and spine fractures (caused by thinning
of the bones)
199
  Weak muscles

Women with Cushing syndrome often have:

 Excess hair growth on the face, neck, chest,

abdomen, and thighs
 Menstrual cycle that becomes irregular or
stops

Men may have:

 Decreased or no desire for sex

 Impotence

Other symptoms that may occur with this disease:

 Mental changes, such as depression,

anxiety, or changes in behavior
 Fatigue
 Headache
 Increased thirst and urination

Complications

 Diabetes
 Enlargement of pituitary tumor
 Fractures due to osteoporosis
 High blood pressure
 Kidney stones
200
  Serious infections

Diagnostic Evaluation

1.Excessive plasma cortisol levels.

2.Decreased serum potassium level.
3.Decreased serum potassium level.
4.Reduced eosinophils.
5.Elevated urinary 17-hydroxycorticoids and
17-ketogenic steroids.
6. Elevation of plasma ACTH in patients with
pituitary tumors.
7. Low plasma ACTH levels with adrenal
tumor.
8. Loss of diurnal variation of cortisol
secretion.
9. X-rays of the skull detect erosion of the
sella turcica by a pituitary tumor.
10.Overnight DST, possibly with cortisol
secretion measurement.
a. Unsuppressed cortisol level in
Cushing’s syndrome caused by adrenal
tumors.
b. Suppressed cortisol level in Cushing’s
disease caused by pituitary tumor.
11.CT scan and ultrasonography detect
location of tumor.
Management
201
Surgical and Radiation
Tumor (adrenal or pituitary) is removed or treated
with irradiation.
1. The most recent development in the
management of pituitary Cushing’s
syndrome in adults is transsphenoidal
adenomectomy or hypophysectomy
(pituitary removal) (see page 886).
2. Transfrontal craniotomy may be necessary
when pituitary tumor has enlarged beyond
sella turcica (see page 484).
3. Hyperplasia of adrenals – bilateral
adrenalectomy.
Replacement Therapy Postoperatively

1. Adrenalectomy patients require a lifelong

replacement therapy with the following:
a. A glucocorticoid – cortisone (Cortef).
b. A mineralocorticoid – fludrocortisones
(Florinef).
2. After pituitary irradiation or
hypophysectomy, patient may require
adrenal replacement, plus thyroid, posterior
pituitary, and gonadal replacement therapy.
3. After transsphenoidal adenomectomy,
patient requires hydrocortisone replacement

202
 therapy for periods of 12 to 18 months and
additional hormones if excessive loss of
pituitary function has occurred.
4. Protein anabolic steroids may be given to
facilitate protein replacement; potassium
replacement is usually required.

Medical Treatment -
If patients cannot undergo surgery, cortisol
synthesis-inhibiting medications may be used.
1. Mitrotane, an agent toxic to the adrenal
cortex (DDT de-rivative)-known as medical
adrenalectomy. Nausea, vomiting, diarrhea,
somnolence, and depression may occur
with use of this drug.
2. Metryrapone (Metopirone) to control
steroid hypersecretion in patients who do
not respond to mitotane therapy.
3. Aminoglutethimide (Cytadren) blocks
cholesterol con-version to pregnenolone,
effectively blocking cortisol production.
Adverse effects include GI disturbances,
somnolence, and skin rashes.

Nursing Assessment –
1. Observe patient for signs and symptoms of

203
 cushing’s dis-case.
2. Perform multisystem physical examination.
3. Monitor intake and output, daily weights,
and serum electrolytes.
Nursing Diagnoses –
 Impaired skin Integrity related to altered
healing, thin and fragile skin, and edema.
 Dressing, Grooming, Toileting Self-care
Deficit related to muscle wasting,
osteoporosis, and fatigue.
 Disturbed Body Image related to altered
physical appearance and emotional
instability.
 Anxiety related to surgery.
 Risk for Injury related to surgical
procedure.
Nursing Interventions -
Maintaining Skin Integrity
 Assess skin frequently to detect reddened
areas, break-down or tearing of skin,
excoriation, infection, or edema.
 Handle skin and extremities gently to
prevent trauma; protect from falls by use of
side rails.
 Avoid use of adhesive tape to reduce risk of
trauma to skin on its removal.
 Encourage patient to turn in bed frequently

204
 or to ambulate to reduce pressure on bony
prominences and areas of edema.
 Use meticulous skin care to reduce injury
and breakdown.
 Provide foods low in sodium to minimize
edema formation.
 Assess intake and output and daily weight
to evaluate fluid retention.
Encouraging active Participation in Self-Care
–
1. Assist patient with ambulation and hygiene
when weak and fatigued.
2. Assist patient in planning schedule to
permit exercise and rest.
3. Encourage patient to rest when fatigued.
4. Encourage gradual resumption of activities
as the patient gains strength.
5. Identify for patient the signs and symptoms
indicating excessive exertion.
6. Instruct patient in correct body mechanics
to avoid pain or injury during activities.
7. Use assistive devices during ambulation to
prevent falls and fractures.
8. Encourage foods high in potassium
(bananas, orange juice, tomatoes), and
administer weakness related to
hypokalemia.

205
Strengthening Body Image –
1. Encourage the patient to verbalize concern
about illness, changes in appearance, and
altered role functions.
2. Identify situations that are disturbing to
patient and explore with patient ways to
avoid or modify those situations.
3. Be alert for evidence of depression: in some
instances this has progressed to suicide;
alert health care provider of mood changes,
sleep disturbance, changes in activity level,
change in appetite, or loss of interest in
visitors or other experiences.
4. Refer for counseling, if indicated.
5. Explain to patient who has be benings
adenoma or hyperplasia that, with proper
treatment, evidence of masculinization can
be reversed.
Reducing Anxiety –
1. Answer questions about surgery and
encourage thorough discussion with health
care provider if patient is not well
informed.
2. Describe nursing care to expect
postoperative period.
3. Prepare the patient for abdominal surgery
or hypophysectomy as indicated.

206
Providing Postoperative Care –
1. Provide routine postoperative care for
patient with abdominal surgery (see page
637) or hypophysectory (see page 887).
2. Monitor closely for infection because
glucocorticoid administration interferes
with immune function; maintain aseptic
technique, clean environment, and good
had washing.
3. Monitor thyroid functions test and provide
hormone replacement therapy as ordered
after hypophysectomy.
4. Monitor DI caused by ADH deficiency
after hypophysectomy.
Patient Education and Health Maintenance –
1. Instruct patient on lifetime hormone
replacement therapy and the need to follow
up at regular intervals to determine if
dosage is appropriate or to detect adverse
effects.
2. Instruct patient in proper skin care and in
the prompt reporting of trauma or infection
for medical treatment.
3. Teach patient to monitor urine or blood
glucose or to report for blood glucose tests
as directed to detect hyper-glycemia.
4. Help patient prevent hyperglycemia and

207
 obesity by teaching about a low-calorie,
low-concentrated carbohydrate and fat diet
and to increase activity as tolerated.
5. Encourage diet high in calcium (dairy
products, broccoli) and weight-bearing
activity to prevent osteoporosis caused by
glucocorticoid replacement.
6. Assist patient in identifying sources of
information and support available in the
community.
PROGNOSIS:-

Removing the tumor may lead to full recovery,

but there is a chance that the condition will return.

Survival for people with ectopic tumors depends

on the tumor type. Untreated, Cushing syndrome
can be life-threatening.

15. Discribe ADRENOCORTICAL INSUFFICIENCY – Lecture, Listen, OHP, LCD, Explain the
about discussi answe VEDIOS. symptoms
addison’s Addison's disease on , ring. of Addison
disesese its explanat disease.
etiology, introduction ion&
clinical question

208
manifestatio ing
n, Addison’s disease (also chronic adrenal
pathophysio insufficiency, hypocortisolism, and
logy, hypoadrenalism) is a rare, chronic endocrine
diagnostic disorder in which the adrenal glands do not
evaluation, produce sufficient steroid hormones
treatment, (glucocorticoids and often mineralocorticoids). It
nursing is characterised by a number of relatively
management nonspecific symptoms, such as abdominal pain
. and weakness, but under certain circumstances,
Lecture, these may progress to Addisonian crisis, a severe
discussion , illness which may include very low blood
explanation pressure and coma
&
questioning Definition
OHP, LCD,
VEDIOS. Addison's disease is a disorder that occurs when
Listen, the adrenal glands do not produce enough of their
answering. hormones.

Etiology

The adrenal glands are small hormone-releasing

organs located on top of each kidney. They are
made up of the outer portion (called the cortex)
and the inner portion (called the medulla).

209
The cortex produces three types of hormones:

 The glucocorticoid hormones (such as

cortisol) maintain sugar (glucose) control,
decrease (suppress) immune response, and
help the body respond to stress.
 The mineralocorticoid hormones (such as
aldosterone) regulate sodium and potassium
balance.
 The sex hormones, androgens (male) and
estrogens (female), affect sexual
development and sex drive.

Addison's disease results from damage to the

adrenal cortex. The damage causes the cortex to
produce less of its hormones.

This damage may be caused by the following:

 The immune system mistakenly attacking

the gland (autoimmune disease)
 Infections such as tuberculosis, HIV, or
fungal infections
 Hemorrhage, blood loss
 Tumors
 Use of blood-thinning drugs

210
 (anticoagulants)

Risk factors for the autoimmune type of Addison's

disease include other autoimmune diseases:

 Chronic thyroiditis
 Dermatis herpetiformis
 Graves' disease
 Hypoparathyroidism
 Hypopituitarism
 Myasthenia gravis
 Pernicious anemia
 Testicular dysfunction
 Type I diabetes
 Vitiligo

Certain genetic defects may cause these

conditions.

Pathophysiology

 Addison's disease is a chronic condition

that results from partial or complete adrenal
destructon. ACTH acts primarily to
regulate the adrenal release of
glucocorticoids, primarily cortisol;
mineralocorticoids including aldosterone;
and sex steroids that supplement those

211
 produced by the gonads. ACTH secretion is
controlled by corticotropin releasing
hormone from the hypothalamus and by
negative feedback control by the
glucocorticoids.
 Cortisol deficiency causes decreased liver
gluconeogenesis. Glucose levels of patients
on insulin may be dangerously low.
 Aldosterone deficiency causes increased
renal sodium loss and enhances potassium
reabsorption. Sodium excretion causes a
reduction in water volume that leads to
hypotension.
 Androgen deficiency may result in
decreased hair growth in axillary and pubic
areas, loss of erectile function,or decreased
libido.

212
Clinical Manifestations –

The symptoms of adrenal insufficiency usually

begin gradually. The most common symptoms are

 chronic, worsening fatigue

 muscle weakness
 loss of appetite
 weight loss

Other symptoms can include

 nausea
 vomiting
213
  diarrhea
 low blood pressure that falls further when
standing, causing dizziness or fainting
 irritability and depression
 a craving for salty foods due to salt loss
 hypoglycemia, or low blood glucose
 headache
 sweating
 in women, irregular or absent menstrual
periods

Hyperpigmentation, or darkening of the skin, can

occur in Addison's disease but not in secondary
adrenal insufficiency. This darkening is most
visible on scars; skin folds; pressure points such
as the elbows, knees, knuckles, and toes; lips; and
mucous membranes such as the lining of the
cheek.

Because the symptoms progress slowly, they are

often ignored until a stressful event like an illness
or accident causes them to worsen. Sudden,
severe worsening of symptoms is called an
Addisonian crisis, or acute adrenal insufficiency.
In most cases, symptoms of adrenal insufficiency
become serious enough that people seek medical
treatment before a crisis occurs. However,
sometimes symptoms first appear during an
214
Addisonian crisis.

Symptoms of an Addisonian or "adrenal" crisis

include

 sudden, penetrating pain in the lower back,

abdomen, or legs
 severe vomiting and diarrhea
 dehydration
 low blood pressure
 loss of consciousness

If not treated, an Addisonian crisis can be fatal.

1. Hyponatremia and hyperkalemia

2. Water loss, dehydration, and hypovolemia
3. Muscular weakness, fatigue, weight loss.
4. GI problems – anorexia, nausea, vomiting,
diarrhea, constipation, abdominal pain.
5. Hypotension, hypoglycemian, low basal
metabolic rate, increased insulin sensitivity.
6. Mental changes- depression, irritability,
anxiety, apprehension caused by
hypoglycemia and hypovolemia.
7. Normal responses to stress lacking.
8. Hyperpigmentation.

215
Possible Complications

Complications can occur if you take too little or

too much adrenal hormone supplement.

Complications also may result from the following

related illnesses:

 Diabetes
 Hashimoto's thyroiditis (chronic thyroiditis)
 Hypoparathyroidism
 Ovarian hypofunction or testicular failure
 Pernicious anemia
 Thyrotoxicosis

Diagnostic Evaluation –
 In its early stages, adrenal insufficiency can
be difficult to diagnose. A review of a
patient’s medical history and symptoms
may lead a doctor to suspect Addison’s
disease.

 A diagnosis of adrenal insufficiency is

confirmed through laboratory tests. The
aim of these tests is first to determine
whether levels of cortisol are insufficient
and then to establish the cause. Radiologic

216
 exams of the adrenal and pituitary glands
also are useful in helping to establish the
cause.
 ACTH Stimulation Test

 The ACTH stimulation test is the most

commonly used test for diagnosing adrenal
insufficiency. In this test, blood cortisol,
urine cortisol, or both are measured before
and after a synthetic form of ACTH is
given by injection. The normal response
after an ACTH injection is a rise in blood
and urine cortisol levels. People with
Addison's disease or long-standing
secondary adrenal insufficiency have little
or no increase in cortisol levels.
 Both low- and high-dose ACTH stimulation
tests may be used depending on the
suspected cause of adrenal insufficiency.
For example, if secondary adrenal
insufficiency is mild or of recent onset, the
adrenal glands may still respond to ACTH
because they have not yet atrophied. Some
studies suggest a low dose-1 microgram-
may be more effective in detecting
secondary adrenal insufficiency because the

217
 low dose is still enough to raise cortisol
levels in healthy people but not in people
with mild or recent secondary adrenal
insufficiency.
 CRH Stimulation Test

 When the response to the ACTH test is

abnormal, a CRH stimulation test can help
determine the cause of adrenal
insufficiency. In this test, synthetic CRH is
injected intravenously and blood cortisol is
measured before and 30, 60, 90, and 120
minutes after the injection. People with
Addison’s disease respond by producing
high levels of ACTH but no cortisol.
People with secondary adrenal
insufficiency have absent or delayed ACTH
responses. CRH will not stimulate ACTH
secretion if the pituitary is damaged, so an
absent ACTH response points to the
pituitary as the cause. A delayed ACTH
response points to the hypothalamus as the
cause.
 Diagnosis during an Emergency

 In patients suspected of having an

218
 Addisonian crisis, health professionals must
begin treatment with injections of salt,
glucose-containing fluids, and
glucocorticoid hormones immediately.
Although a reliable diagnosis is not
possible during crisis treatment,
measurement of blood ACTH and cortisol
during the crisis-before glucocorticoids are
given-is enough to make a preliminary
diagnosis. Low blood sodium, low blood
glucose, and high blood potassium are also
usually present at the time of an adrenal
crisis. Once the crisis is controlled, an
ACTH stimulation test can be performed to
obtain the specific diagnosis. More
complex laboratory tests are sometimes
used if the diagnosis remains unclear.
 Other Tests

 Once a diagnosis of Addison's disease is

made, radiologic studies such as an x ray or
an ultrasound of the abdomen may be taken
to see if the adrenals have any signs of
calcium deposits. Calcium deposits may
indicate bleeding in the adrenal gland or
TB, for which a tuberculin skin test also

219
 may be used. Blood tests can detect
antibodies associated with autoimmune
Addison's disease.
 If secondary adrenal insufficiency is
diagnosed, doctors may use different
imaging tools to reveal the size and shape
of the pituitary gland. The most common is
the computerized tomography (CT) scan,
which produces a series of x-ray pictures
giving cross-sectional images. A magnetic
resonance imaging (MRI) scan may also be
used to produce a three-dimensional image
of this region. The function of the pituitary
and its ability to produce other hormones
also are assessed with blood tests.

Treatment

Treatment with replacement corticosteroids will

control the symptoms of this disease. However,
you will usually need to take these drugs for life.
People often receive a combination of
glucocorticoids (cortisone or hydrocortisone) and
mineralocorticoids (fludrocortisone).

Never skip doses of your medication for this

condition, because life-threatening reactions may

220
occur.

The health care provider may increase the

medication dose because of:

 Infection
 Injury
 Stress
 Surgery

During an extreme form of adrenal insufficiency,

called adrenal crisis, you must inject
hydrocortisone immediately. Supportive treatment
for low blood pressure is usually needed as well.

Some people with Addison's disease are taught to

give themselves an emergency injection of
hydrocortisone during stressful situations. It is
important for you to always carry a medical
identification card that states the type of
medication and the proper dose you need in case
of an emergency. Your health care provider
may also tell you to always wear a Medic-Alert
tag (such as a bracelet) alerting health care
professionals that you have this condition in case
of emergency.

221
Nursing Assessment -

1. Obtain recent or past history of

corticosteroid therapy, including length of
treatment, dosage, and compliance.
2. Review history for sources of stress, such
as surgical procedures, infection, or
development of other illness.
3. Perform through physical examination for
manifestations of adrenocortical
insufficiency or contributing factors.
Nursing Diagnoses –
 Deficient fluid volume related to renal
losses of sodium and water
 Risk for injury related to ineffective stress
response
 Activity intolerance related to decreased
cortisol production and fatigue.
Nursing Interventions
Achieving Normal Fluid and Electrolyte
Balance -
1. Assess fluid intake and output and serial
daily weights.
2. Monitor vital signs frequently; a drop in BP
may suggest an impending crisis.
3. Monitor results of serum sodium and
potassium.
222
 4. Assess skin turgor and muscous
membrances for dehydration.
5. Encourage diet high in sodium and fluid
content; administer or teach self-
administration of potassium supplements, if
prescribed.
6. Administer or teach self-administration of
prescribed glucocortiocoids and mineral
ocorticoids; document response.
7. Adminsiter I.V. infusions of sodium, water,
and glucose as indicated.
Protecting well-being –
1. Minimize stressful situations.
2. Protect patient from infection.
a. Control patient’s contracts so the
infectious organisms are not transmitted.
b. Protect patient from drafts, dampness,
exposure to cold.
c. Prevent overexertion.
d. Use meticulous hand washing and
asepsis.
3. Assess comfort and emotional status of
patient.
a. Control the temperature of the room to
avoid sharp deviations in patient’s
temperature.
b. Maintain a quiet, peaceful environment;

223
 avoid loud talking and noisy radios.
Increasing Activity Tolerance –
1. Assist the patient with ADLs.
2. Provide for periods of rest and activity to
avoid overexertion.
3. Provide for high-calorie, high protein diet.
Patient Edcuation and Health Maintenance -
1. Instruct the patient about the necessary for
long-term therapy for adrenocortical
insufficiency and medical follow-up visits.
a. Inform the patient that therapy must be
continued throughout his life span.
b. Emphasize the importance of taking
more hormones when under stress.
c. Suggest that the patient carry an
identification card that indicates the type
of medication being taken and health
care provider’s telephone number.
2. Instruct the patient about manifestation of
excessive use of medications and reportable
symptoms.
3. Identify actions to take to avoid factors that
may precipitate addisonian crisis (infection,
extremes of temperature, trauma).
4. Assist patient in identifying sources of
information and support available in the
community (see Box 24-1, page 891).

224
 Evaluation : Expected Outcomes –

The prognosis for any patient with adrenal

insufficiency will depend on the underlying cause.
In those patients in whom the prognosis is not
affected by the underlying pathology, replacement
therapy should result in a return to health with a
normal life expectancy. However, a Norwegian
study found an excess of mortality in patients
diagnosed with Addison's disease at a young age,
associated with acute adrenal failure, infection
and sudden death.

16. Discribe PRIMARY ALDOSTERONISM Lecture, Listen, OHP, LCD, Give the
about discussi answe VEDIOS. definition of
acromegaly INTRODUCTION on , ring. Addison
its etiology, aldosteronism, also known as primary explanat disease.
clinical hyperaldosteronism, is characterized by the ion&
manifestatio overproduction of the mineralocorticoid hormone question
n, aldosterone by the adrenal glands, when not a ing
pathophysio result of excessive renin secretion. Aldosterone
logy, causes increase in sodium and water retention and
diagnostic potassium excretion in the kidneys, leading to
evaluation, arterial hypertension (high blood pressure). An
treatment, increase in the production of mineralocorticoid
nursing from the adrenal gland is evident. It is amongst
225
management the most common causes of secondary
. hypertension, renal disease being the most
common.

DEFINITION:-

Primary aldosteronism refers to excessive

secretion of aldosterone by the adrenal cortex.
Secondary aldosteronism occurs frequently and
result from the presence of exogenous conditions,
that stimulate the renin-angiostenism-aldosterone
system which include:-
 Cardiac failure
 ,idiopathic cyclic edema.
 Liver disease.
 Nephrosis.
 Hypovolmia.

Etiology
The syndrome is due to:

 Most commonly Adrenal Adenoma (Conn's

Syndrome) (66%)
 Bilateral idiopathic adrenal hyperplasia
(30%)
 Primary (unilateral) adrenal hyperplasia—
2% of cases
 Aldosterone-producing adrenocortical

226
 carcinoma—<1% of cases
 Familial Hyperaldosteronism (FH)
 Glucocorticoid-remediable aldosteronism
(FH type I)—<1% of cases
 FH type II (APA or IHA)—<2% of cases
 Ectopic aldosterone-producing adenoma or
carcinoma—< 0.1% of cases

Recent studies indicate that the prevalence of

aldosteronism due to bilateral idiopathic
adrenal hyperplasia (IAH) is higher than had
previously been believed, for as many as 75% of
aldosteronism cases.

Pathophisiology:-

Excessive aldosterone secreted by adrenal

gland

Stimulate the reabsorption of sodium by the

kidney

Decreased potassium and hydrogen level

227
 Lead to water retention

Hypertension
 There is increased level of aldosterone in
circulation.
 This lead to increase sodium level
decreased potassium level and also
hydrogen level in circulation.
 And by this water retention is occurs and
secondary BP is arise.
Clinical Manifestations
1. Hypertension (1% to 2% of cases of
hypertension are a result of primary
aldosteronism, which usually can be
treated successfully by surgical removal
of the adenoma)
2. A profound decline in blood levels of
potassium (hypokalemia) and hydrogen
ions (alkalosis) results in muscle
weakness and inability of kidneys to
acidify or concentrate urine, leading to
excess volume of urine (polyuria).
3. A decline in hydrogen ions (alkalosis)
results in tetany, paresthesia.
4. An elevation in blood sodium
(hypernatremia) results in excessive

228
 thirst (polydipsia) and arterial
hypertension.

 Weakness
 Cardiac arrhythmias
 Muscle cramps
 Excess thirst or urination

Complications

Primary aldosteronism can lead to high blood

pressure and low potassium levels. These
complications in turn can lead to other problems.

Problems related to high blood pressure

Persistently elevated blood pressure can lead to
problems with your heart and kidneys, including:

 Heart attack
 Heart failure
 Left ventricular hypertrophy —
enlargement of the muscle that makes up
the wall of the left ventricle, your heart's
main pumping chamber
 Stroke

229
  Kidney disease or kidney failure
 Premature death

High blood pressure caused by primary

aldosteronism carries a higher risk of
cardiovascular complications than do other types
of high blood pressure. This excess risk is due to
the high aldosterone levels, which can cause heart
and blood vessel damage independently of
complications related to high blood pressure.

Problems related to low potassium levels

Some, but not all, people with primary
aldosteronism have low potassium levels
(hypokalemia). Mild hypokalemia may not cause
any symptoms, but very low levels of potassium
can lead to:

 Weakness
 Cardiac arrhythmias
 Muscle cramps
 Excess thirst or urination

Diagnostic Evaluation
1. Suspected in all hypertensive patients
with spontaneous hypokalemia; also if
hypokalemia develops concurrently with
start of diuretics and remains after

230
 diuretics are discontinued.
2. Salt loading used as screening test –
ingestion of at least 200 mEq/day
(approximately 12g salt) for 4 days does
not influence the serum potassium level
without aldosteronism, but will cause a
decrease of serum potassium to less than
3.5mEq/L in a patient with
aldosteronism.
3. CT scanning to determine and localize
cortical adenoma.
Management
1. Removal of adrenal tumor – unilateral
adrenalectomy.
2. Management of underlying cause of
secondary aldosteronism.
3. Spironolactone (Aldactone) to treat both
hypertension and potassium-depleted
stages; therapy is needed 4 to 6 weeks
before the full effect on BP is seen.
a. Adverse effects include reduced
testosterone in men (decreased libido,
impotence, gynecomastia) and GI
discomfort.
b. Amiloride (Midamor) may be used
instead in sexually active men or in
cases of GI intolerance.

231
 c. Sodim restriction is necessary – no
saline infusions, low-sodium diet.
d. Potassium supplementation is usually
necessary, based on severity of
deficit.
4. Addition of antihypertensive agent –
thiazide diuretic such as triamterene
(Dyrenium).
Nursing Assessment
1. Obtain history of symptoms, such as
muscle weakness, paresthesia, thirst, and
polyuria.
2. Perform multisystem physical
examination.
3. Evaluate BP.
4. Monitor input and output of fluid.
5. Assess patient understanding level and
knowledge regarding to disease
management.

Nursing Diagnosis
 Excess fluid Volume related to sodium
retention.
 Hypertension related to hypernatremia.
 Imbalance nutrition; less than body
requirement related to disease condition.
 Anxiety related to progession of disease

232
 and continues persistant weakness.
Maintaining Normal Fluid and Sodium
Balance
1. Monitor fluid intake and output, daily
weight, ECG changes for hypokalemia.
2. Teach low-sodium diet, administration of
potassium supplements, as ordered;
evaluate serum sodium and potassium
results.
3. Monitor BP; administer or teach self-
administration of antihypertensives as
ordered.
4. Assess for dependent edema; encourage
activity, frequent repositioning, and
elevation of feet periodically.
Maintaining normal blood pressure:-
 Monitor BP in regular interval.
 Instructly maintain the output input level of the
patient.
 Dietary sodium intake is restricted.
 Antihypertensive drugs are given as prescribed
by the doctor.

Maintaining Skin Integrity

1. Assess skin frequently to detect reddened
areas, break-down or tearing of skin,
excoriation, infection, or edema.

233
2. Handle skin and extremities gently to
prevent trauma; protect from falls by use of
side rails.
3. Avoid use of adhesive tape to reduce risk of
trauma to skin on its removal.
4. Encourage patient to turn in bed frequently
or to ambulate to reduce pressure on bony
prominences and areas of edema.
5. Use meticulous skin care to reduce injury
and breakdown.
6. Provide foods low in sodium to minimize
edema formation.
7. Assess intake and output and daily weight
to evaluate fluid retention.

Patient Education and Health Maintenance

1. Instruct patient about the nature of illness,
the necessary treatment, and the need for
continued medical care after discharge.
2. Instruct patient on the importance of
following prescribed medical treatments.
a. For medical management, patient must
remain on spironolactone (Aldactone)
for life.
b. Patient should report significant adverse
effects that interfere with sexual
performance and quality of life.

234
 c. Glucocorticoid administration may be
temporary after subtotal or unilateral
adrenalectomy, chronic for bilateral
adrenalectomy; dose may need to be
increased during times of illness or
stress.
3. Teach patient and family members how to
take BP readings, if indicated.

PROGNOSIS:-
The prognosis is generally excellent with early
diagnosis and Streatment. Surgical
removal of an adrenal tumor or an
adrenalectomy results in complete
resolution of symptoms and return to
normal blood pressure in about 70% of
cases. However, blood pressure often does
not return to normal immediately
following surgery but rather changes
gradually over 1 to 4 months.
Adrenalectomy, when performed
laparoscopically, is reported to have a
lower operative morbidity and shorter
hospital stay than the traditional open
surgical technique.

17. Discribe PHEOCHROMOCYTOMA – Lecture, Listen, OHP, LCD, What are the

235
about discussi answe VEDIOS. etiological
pheochromo INTRODUCTION:- on , ring. factor of
cytoma its explanat phechromoc
etiology, Pheochromocytomas are a type of tumor of the ion& ytoma.
clinical adrenal glands that can release high levels of question
manifestatio epinephrine and norepinephrine. As the name ing
n, implies, the “ad-renal” glands are located near the
pathophysio "renal" area. In other words, the adrenal glands
logy, are small glands that are located near the top of
diagnostic the kidneys. One adrenal gland sits on top of each
evaluation, of the two kidneys.
treatment,
nursing DEFINITION:-
management
. Pheochromocytoma is a catecholamine-
secreting neoplasm associated with hyperfunction
of the adrenal medulla. It may appear wherever
chromaffin cells are located; however, most found
in the adrenal meduall.

ETIOLOGY:-

.
1. Pheochromocytoma can occur at any age,
but is most common between the ages of 30
and 60; it is uncommon in people older
than age 65.
2. Most pheochromocytoma tumors are

236
 benign; 10% are malignant with metastasis.
3. Tumours located in the adrenal medulla
produce both in-creased epinephrine and
norepinephrine, those located outside the
adrenal gland tend to produce epinephrine
only.
4. May occur as component of multiple
endocrine neoplasia II, an autosomal-
dominant syndrome characterized by
pheochromocytoma, thyroid cancer,
characterized by pheochromocytoma,
thyroid cancer, hyperparathyroidism, and
Cushing’s syndrome with excess ACTH.
5. withdrawal from drugs (such as suddenly
stopping certain blood pressure
medications); panic attacks, and spinal cord
injuries are among the many conditions that
can also lead to some of the symptoms seen
in pheochromocytomas.

Pathophysiology:-
Pheochromocytomas of the adrenal medulla
release excessive amounts of catecholamines both
epinephrines and norepinephrine. A tumor of the
sympathetic nervous system in turn releases
excessive amounts of norepinephrine.the
hormones release may be constant or episodic

237
producing constant or episodic clinical
manifestation. a paroxysm or crisis may be
precipated by any lifting, straining, bending or
exercise that increases intra-abdominal pressure
or moves abdominalcontents.

Clinical Manifestations –
1. Variation in signs and symptoms depends
on the predominance of norepinephrine or
epinephrine secretion and on whether
secretion is continuous or intermittent.
2. Excess secretion of norepinephrine and
epinephrine produces hypertension,
hypermetabolism, and hyperglycemia.
3. Hypertension may be paroxysmal
(intermittent) or persistent (chronic).
a. Chronic form mimics essential
hypertension; however,
antihypertensives are not effective.
b. Headaches and vision disturbances are
common.
4. The hypermetabolic and hyperglycemic
effects produce excessive perspiration,
tremor, pallor or face flushing,
nervousness, elevated blood glucose levels,
polyuria, nausea vomiting, diarrhea,
abdominal pain, and parestheia.

238
 5. Emotional changes, including psychotic
behavious, may occur.
6. Symptoms may be triggered by allergic
reactions, physical exertion, emotional
upset, or may occur without identifiable
stimulus.
Diagnostic Evaluation –
1. VMA and metanephrine (metabolites of
epinephrine and norepinephrine) are
elevated in 24-hour urine sample.
2. Epinephrine and norepinephrine in urine
and blood are elevated while patient is
symptomatic.
3. CT scan and magnetic resonance imaging
(MRI) of the adrenal glands or of the entire
abdomen are done to identify tumor.
4. Clonidine suppression test is used to
distinguish essential hypertension from
pheochromocytoma.
Management –
Medical Control of BP and Preparation for
Surgery
1. Alpha-adrenergic blocking agents, such as
phentolamine (Regitine) or
phenoxybenzamine (Dibenzyline), inhibit
the effects of catecholamines on BP.
a. Effective control of BP and blood

239
 volume may take 1 or 2 weeks.
b. Surgery is delayed until BP is controlled
and blood volume has been expanded.
2. Catecholamine synthesis inhibitors, such as
metyrosine (Demser), may be used
preoperatively or for long-term
management of inoperable tumors.
a. Adverse effects include sedation and
crystalluria.
Surgery –
Unilateral or bilateral adrenalectomy or
other tumor removal.
Complications –
Metastasis of tumor.
Nursing Assessment –
1. Obtain history of signs and symptoms
patient has been experiencing.
2. Assess for predisposing factors that may be
triggering signs and symptoms (i.e.
physical exertion, emotional upset,
allergies)
3. Perform thorough physical examination to
determine effects of hypertension.

Nursing diagnosis:-

240
 3. Hypertension related to diseases
condition secondary to excess
secretion of epinephrine and non-
epinephrine as evidence by by BP-
150/100 mm of hg.
4. Dehydration related to disease
condition secondary to
hypermetabolic and
hyperglycemiclan effect as
manifested by polyurea.
5. Imbalance nutrient; less than body
requirement related disease
progession as manifested by
persistent vomiting.
6. Anxiety related to the systemic
effects of epinephrine and
nonepinephrine.
7. Ineffective tissue perfusion related to
hypotension during the postoperative
period.

Nursing Interventions –
1. Maintain normal BP:-
 Monitor vital sign time to time.
 Encourage client to verbalize his feeling
that help him to reduce blood pressure.
 Dietary intake of sodium will be restricts.
 Antihypertensive drug are provided as

241
 prescribed
.
Improve nutritional status:-
 Take history about dietary hadits,life style,
cultural, background,activity level ans food
preference.
 An appropriate caloric intake allows the
patient.
 The patient is encouraged to eat full meals
and snacks as prescribed per the diabetes
diet.
 Arrangements are made with the dietitian
for extra snacks before increased physical
activity.

Reducing Anxiety
1. Remain with the patient during acute
episodes of hypertension.
2. Ensure bed rest and elevate the head of bed
45 degrees during severe hypertension.
3. Carry out tasks and procedures in clam,
unhurried manner when with the patient.
4. Instruct the patient about use relaxation
exercises.
5. Reduce environmental stressors by
providing clam, quiet environment, Restrict
visitors.

242
 6. Eliminate stimulants (coffee, tea, cola)
from the diet.
7. Reduce events that precipitate episodes of
severe hypertension-palpation of the tumor,
physical exertion, emotional upset.
8. Administer sedatives as prescribed to
promote relaxation and rest.
9. Monitor for orthostatic hypotension after
administration of phentolamine (Regitine)
10.Encourage oral fluids and maintain I.V.
infusion preoperatively to ensure adequate
volume expansion going into surgery.
Maintaining Tissue Perfusion Postoperatively
–
1. Monitor vital signs, ECG, arterial BP,
neurologic status and urine output closely
postoperatively.
2. Assess for and report complications of
hypertension, hypotension, and
hyperglycemia.
3. Maintain adequate hydration with I.V.
infusion to prevent hypotension. (Because
reduction of catecholamines immediately
postoperatively causes vasodilation and
enlargement of vascular space, hypotension
may occur.)
4. Monitor intake and output and laboratory

243
 results for BUN, creatinine, and glucose.
Patient Education and Health Maintenance -
1. Instruct the patient how and when to take
medications warn patients who take
metyrosine (Demser) of sedation and need
to avoid taking other CNS depressants and
participating in activities that require
alertness; need to increase fluid intake to at
least 2,000 mL/day to prevent kidney
stones.
2. Inform patient regarding the need for
continued follow-up for;
a. Recurrence of pheochromocytoma.
b. Assessment of any residual renal or
cardiovascular injury related to
preoperative hypertension.
c. Documentation that catechoamines
levels are normal 1 to 3 months
postoperatively (by 24-hou urine tests).
3. Help patient identify sources of information
and support available in the community .
Expectations (prognosis)

Most patients who have noncancerous tumors that

are removed with surgery are still alive after 5
years. The tumors come back in less than 10% of
these patients. Levels of the hormones

244
 norepinephrine and epinephrine return to normal
after surgery.

18. Explain GLUCOSE HEMOSTASIS DISORDER Lecture, Listen, OHP, LCD, What are the
about DM discussi answe VEDIOS. management
its etiology, Diabetes Mellitus on , ring. of DM.
clinical explanat
manifestatio .INTRODUCTION:- ion&
n, Diabetes Mellitus affects about 17 million people, question
pathophysio 5.9 million of whom are undiagnosed. In ing
logy, the united States, approximately 800,000
diagnostic new cases of diabetes are diagnosed yearly.
evaluation, In the United States, diabetes is the leading
treatment, case of nontraumatic amputations,
nursing blindness amoung working age adults and
management end stage renal disease. Diabetes is the
. third leading cause of death by disease,
primarily because of the high rate of
cardiovascular disease (M.I. stroke and
peripheral vascular disease) among people

245
 with diabetes.

Definition of Diabetes Mellitus :-

D.M. is a group of metabolic disease
characterized by elevated levels of glucose in the
blood (hyperglycemia) resulting from defects in
insulin secretion, insulin action or both.

Causes of Diabetes Mellitus :-

 Genetic :- by Mutation, Mutation is a
permanent charges in the genetic structure
due to which the offspring differ from
parent in a characteristic.
 (ii) Immunologic – Autoantibodies
against islet cells and endogenous insulin.
 (iii) Environment factors like virus etc.
 (iv) Obesity.
 (V) Heredity :- if parents or other
members of family whom related the
family with gen, if they have suffer. With
diabetes mellitus. The children may be
suffer from the disease.
Classification of Diabetes :-
Major Classification of diabetes are :-
(1) Type I diabetes
(2) Type II diabetes
(3) Gastational diabetes
(4) Diabetes associated with other
246
 conditions or syndrome.
1) Type I Diabetes (Insulin-dependent
diabetes mellitus) (5-10% of all diabetes)
Type –I diabetes mellitus is characterized by
destruction of pancreatic beta cells. That why
secreation of endogenous insulin is “O” OR little
amount of need.
 On set age, but usually young (<30 year)
 Usually thin at diagnosis; with resent
weight loss.
 Etiology includes genetic, immunological
or environmental factors (virus)
 Often have islet cell antibodies.
 Often have antibiodies to insulin even
before treatments.
 Little or no endogenous insulin.
 Need insulin to preserve life.
 Ketosis prome when insulin absent.
 Acute complication of hyperglycemia;
diabetic ketoacidosis.
Pathophysiology :-
There is no endogenous insulin or little
amount of insulin present in blood stream. After
need increase blood glucose level because of lack
of insulin and by increase production of glucose
by the liver. The condition create hyperglycemia.

247
248
Sign & Symptoms :-
Polyuria, polydipsia, polyphagia, and
glucosuria.
 Fatigue and weakness, weight loss.
 Blurred Vision, Headche.
 Sign of Behydratian.
 Aceton breath, poor appetite, Nausea
 Vomiting Abd. Pain. Respiration.
2) Type II Diabetes OR Non insulin –
dependent diabetes mellitus (90% - 95% of all
diabetes; obese 80% type 20% of type)
The two main problems related to insulin in
type -2 diabetes are insulin resistance and
impaired insulin secretion.
 Onset any age, usually oven 30 years.
 Usually obese at diagnosis.
 Causes include obesity, heredity or

249
 environmental factors.
 No islet cell antibodies.
 Decrease in endogenous insulin or
increased with insulin resistance .
 If dietary modification and exercise are
successful than oral antidiabetic agents may
improve B.G.L.
 Kelosis rare, except in stress or infection.
 Accute complication; hyperglyosmolar
nonketotic syndrome.
Pathophysiology:-
1. Impaired insulin secreation by pancereas.
2. Gastrointestinal absorption of glucose.
3. Increased hepatic glucose production in
liver.
4. In muscle decreased insulin stimulated
glucose uptake (absorption).
They all lead to Hyperglycemia.

250
251
Sign And Symptoms :-
 Fatigue, palyuria, polyphagia.
 Slow wound heading.
 Sudden vision changes.
 Type – 2 diabetes result from a slow
progressive glucose intolerance and result
in long term complication for many year.
3) Diabetes Mellitus associated with other
conditions OR Syndrome:-
Accompanied by conditions known or
suspected to cause the disease; pancreatic disease,
hormonal adnormalities, mediation, such as
conticosteroids and estrogen containing
preparation.
4) Gestational diabetes :- Onset during
pregnancy, usually in second or third trimester.
Due to hormones secreted by the placenta, which
inhibit the action of insulin. Above- normal sick
for perinatal complication especially macrosomia
(Abnormally large babies). Treated with diet and
if needed, insulin to strictly maintain blood
glucose levels. Occurs in about 2 to 5% of all
pregnancies.

CLINICAL MANIFESTATIONS:-
252
The classic symptoms of untreated diabetes are
loss of weight, polyuria (frequent urination),
polydipsia (increased thirst) and polyphagia
(increased hunger). Symptoms may develop
rapidly (weeks or months) in type 1 diabetes,
while they usually develop much more slowly and
may be subtle or absent in type 2 diabetes.

Prolonged high blood glucose can cause glucose

absorption in the lens of the eye, which leads to
changes in its shape, resulting in vision changes.
Blurred vision is a common complaint leading to
a diabetes diagnosis; type 1 should always be
suspected in cases of rapid vision change, whereas
with type 2 change is generally more gradual, but
should still be suspected A number of skin rashes
that can occur in diabetes are collectively known
as diabetic dermadromes.

Complication of Diabetes :-
Complication associated with both types of
diabetes are classified acute or chronic.
Acute complications occurs from short term
imbalance in blood glucose and include :-
 Hypoglycemia

253
  DKA
 HHNS
Chronic complication generally
occurs 10 to 20 years after the onset of
diabetes mellitus. They include :-
Macrovascular (Large Vessel) : affects
coronary, peripheral vascular and cerebral
vascular circulations.
Microvascular (Small Vessel) disease :- affect
the eyes (retinopathy) and kidneys (nephropathy)
control blood glucose level to delay on avoid
onset of both complication (macro & micro)
Neuropathic disease :- Affects sensory motor
and autonomic nerves and contributes to such
problems as impotence and foot ulcers.
Foot And Leg Problem :-
Complication of diabetes that contribute to
the increased risk of food infection includes
Neauropathy :-
(1) Sensory neuropathy leads to loss of pain
and pressure sensation.
(2) Autonomic neuropathy leads to loss of
pain and pressure sensation.
(3) Autonomic neuropathy led to increased
lead to increased dryness and fissuring
of skin.
(4) Motor neuropathy result in muscular

254
 atropy, which may lead to changes in
the shape of foot.
Peripheral vascular disease –
Poor circulation of lower extremities
contributes to poor would heading and the
development of gangers.
Immuno compromise :-
Hyperglycemia impairs the ability of
specialized leukocytes to destroy bacteria. Thus in
poorly controlled diabetes, there is a lowered
resistance to certain infections
Normal Blood Glucose Levels:-
Fasting - 60 -110mg/dlL
Post prandial -65-140mg/dL
Renal threshold - 180 to200mg/dL

Diagnostic Evaluation :-
Blood investigation – High blood glucose level :
FBG levels 126 mg/dL or more OR RBG level
more than 200mg/dL or more than one occasion.
Urine Investigation – That may use sevior
condition OR chronic diabetes because until blood
sugar level more than renal threshold may not
appearance in orine. We can do urine
investigation.
- For sugar
- Albumin

255
 - Ketone body.
Prevention – For obese pt (type-2); weight loss is
the key to treatment and the major preventive
factor for the development of diabetes.

Management –

Goals-To normalize insulin activity.

-To reduce B.G.L.
-To Prevent Complication
-To Provide better Health.
There are five components of diabetes
management.
(1) Nutritional Management -
Goals :-
 We should be advice pt for sugar free diet.
 Providing all the essential food constitivent
(eg. Vitamins, mineral) necessary for
optimal nutrition.
 Meeting energy meals.
 Achieving maintaining a reasonable weight.
 Decreasing serum lipid levels, if elevated to
reduce the risk for macrovascular disease.
Caloric Requirement :-
Carbohydrate - 50% -60%
Fat - 20% - 30%
Protein - 10% - 20%
256
  The Food Guide Pyramid chart –

 Consumpation of Alcohol.
 Add sweaters.
 Aviod smoking.
(2) Exercise - Exercise is extremely
important because of :-
 Its effects on lowering blood glucose.
 Its effects or reducing cardiovascular risk
factors.
 Improves circulation and muscle tone.
 Exercise is useful in losing weight, easily
stress and maintaining a feeling of well –
being.
 Cholestrol , Triglyceride level.

257
  We should Encourage the pls for exercise.
 Warn pt about postexcercise.
 Discuss testing BGI before, during and
after exercise.
 Encourage regular daily exercise.
 Advise all pts with diabetes to discuss an
exercise program with their physician.
(3) Monitoring:-
Glucose monitoring self laboratory.
 Self monitoring of blood glucose level
(SMBG)
SMBG allows allows adjustment in the
treatment regimen for optimal blood
glucose level and motivates patients to
continue treatment.
 Assessing Glycosylated Hemoglobin :-
If the Pt’s glycosylated nemoglobin
level is high but BGL test normal, a special
blood test that reflects average BGL over a
period of about 2 to 3 months is performed.
Depending on the result, determine the
presence of error in methods of SMBG.
 Testing Urine for Ketone:-
Urine testing is for pts who cannot
OR will not perform blood glucose testing.
Provide instruction in the urine testing
procedure for the pt with type 1 diabetes

258
 who has glucosuria or unexplained elevated
blood glucose levels (more than 250mg/dL)
and for patient who are ill or pregnant.

(5) Pharmacologic Therapy :-

When exercise and nutrition
management not manatainance the level of
glucose in type II case or type I case then
we must give to pt in insulin neither orally
or inject able.
Species (source):-
In past all insulin were obtained from becf
(low) and pork (pig) pancreas “Human insulin”
are now widely available.
Human insulines are producted by
recombinant DNA technology and have largely
replaced insulin. They are not antigenic.
Alternative method of Insulin Delivery :-
 Insulin pens
 Jet Injections
 Insulin pumps.
Oral Antidiabetic Agents:-
(1) First Generation sulfonylurea’s:-
- Acetohexamide
- Chlorpropamide
- Tolazamide
Categories of Insulin (Injectable):-

259
(2) Second Generation sulfonylurease –
- Glipizide
- Glyburide
- Glimepiride
(3) Biguarides - Metformin
- Glucophage
(4) Alpha Glucosidage inhibitors:-
- Acarbose
- Miglitol
(5) Non – Sulfonylurea insulin –
Secretogogues
- Repagliride
- Neteglide
(6) Thiazolidinediones -
Pioglitazone
-

260
 Rosiglitazone.
Education :-
Diabetes mellitus is a chronic illness that
requires a lifetime of special self management
bahaviour. We should be advise to patient about :-
 Healthy eating.
 Being active
 Monitoring (self)
 Taking Medicines
 Problem solving
 Reducing risks
 Healthy coping (Co-operating)
,
Nursing Diagnosis :-
(1) Risk for fluid volume deficit related to
polyuria and dehydration.
(2) Imbalanced nutrition related to imbalance
of insulin, food, and physical activity.
(3) Deficient knowledge about diabetes self
care skills/information.
(4) Anxiety related to loss of control, fear of
inability to manage diabetes, mis
information related to diabetes fear of
diabetes complications.
(5) Activity intolerance related to poor glucose
control
(6) Risk for impaired skin integrity related to

261
 decreased sensation and circulation to
lower extremities.
(7) Ineffective coping related to chronic
disease and complex self care regimen.
Nursing intervention

Improve nutritional status:-

 Take history about dietary hadits,life style,
cultural, background,activity level ans food
preference.
 An appropriate caloric intake allows the
patient.
 The patient is encouraged to eat full meals
and snacks as prescribed per the diabetes
diet.
 Arrangements are made with the dietitian
for extra snacks before increased physical
activity.
Improved knowledge about diabetes self care
skills:-
 Patient teaching about the major strategy
used to prepare the patient for self care.
 Special equipment may be provide for
instruction on diabetes survival skill such
as magnifying glass and injection device.
 Low- literacy information in other
languages can be obtained from the ADA.

262
  Family is also taught so that they can assist
in diabetes management.
Improving activity tolerance:-
 Advice patient to assess blood glucose level
before and after strenuous exenrcise.
 Instruct patient to plan exercises on a
regular basis each day.
 Encourage patient to eat a carbohydrate
snack before excising to avoid
hypoglycemia.
 Counsel patient to inject insulin into the
abdominal site on days when arms or legs
are exercised.

reduce anxiety:-
 Provide emotional support and sets aside
time to take with the patient.
 Try to ruleout, any misconception
regarding diabetes.
 Encourage patient to perform the skills.
 Positive reinforcement is given for the self
care behaviors attempted.
PATIENT EDUCATION AND HEALTH
MAINTENANCE:-
 Ongoing education of patient to include
advanced skills and rationales for
treatment, prevention, and management of

263
 complications.
 Educational focus- lifestyle management
issues, to include sick-day management,
exercise adjustments, travel preparation,
foot care guidelines, intensive insulin
management, and dietary considerations for
diniing out.
 For additional information and support,
refer to drugs manufacturers.


PROGNOSIS:-

Uncontrolled diabetes is a leading cause of

blindness, end-stage renal disease, and limb
amputations. It also doubles the risks of heart
disease and increases the risk of stroke. Eye
problems including cataracts, glaucoma, and
diabetic retinopathy also are more common in
diabetics.

Diabetic peripheral neuropathy is a condition

where nerve endings, particularly in the legs and
feet, become less sensitive. Diabetic foot ulcers
are a particular problem since the patient does not
feel the pain of a blister, callous, or other minor
injury. Poor blood circulation in the legs and feet

264
 contribute to delayed wound healing. The
inability to sense pain along with the
complications of delayed wound healing can
result in minor injuries, blisters, or callouses
becoming infected and difficult to treat. In cases
of severe infection, the infected tissue begins to
break down and rot away. The most serious
consequence of this condition is the need for
amputation of toes, feet, or legs due to severe
infection.

Heart disease and kidney disease are common

complications of diabetes. Long-term
complications may include the need for kidney
dialysis or a kidney transplant due to kidney
failure.

Babies born to diabetic mothers have an increased

risk of birth defects and distress at birth.

19. Discribe SEX HORMONES DISORDER Lecture, Listen, OHP, LCD, Can you
about discussi answe VEDIOS. define about

265
klinefelter KLINEFELTER SYNDROME on , ring. klinefelter
syndrome explanat syndrome
its etiology, Introduction ion&
clinical Humans have 46 chromosomes. Chromosomes question
manifestatio contain all of your genes and DNA, the building ing
n, blocks of the body. The two sex chromosomes
pathophysio determine if you become a boy or a girl. Females
logy, normally have two XX chromosomes. Males
diagnostic normally have an X and a Y chromosome.
evaluation, Klinefelter syndrome is the presence of an extra X
treatment, chromosome in a male.
nursing
management Definition
. Klinefelter syndrome is one of a group of sex
chromosome problems. It results in males who
have at least one extra X chromosome. Usually,
this occurs due to one extra X. This would be
written as XXY.
Etiology
The cause of the sex chromosome disorder is a
defect of meiosis during gametogenesis, meiotic
defects of the zygote cause Klinefelter's syndrome
with mosaic karyotype.

Klinefelter's syndrome results in a sclerosis of the

seminiferous tubules, missing or severely
damaged spermatogenesis and hyperplasia of

266
Leydig cells.

Pathophysiology

XXY syndrome

The extra X chromosome is retained because of a

nondisjunction event during meiosis I
(gametogenesis). Nondisjunction occurs when
homologous chromosomes, in this case the X and
Y sex chromosomes, fail to separate, producing a
sperm with an X and a Y chromosome. Fertilizing
a normal (X) egg produces an XXY offspring.
The XXY chromosome arrangement is one of the
most common genetic variations from the XY
karyotype, occurring in about 1 in 500 live male
births.

Another mechanism for retaining the extra X

267
chromosome is through a nondisjunction event
during meiosis II in the female. Nondisjunction
will occur when sister chromatids on the sex
chromosome, in this case an X and an X, fail to
separate. An XX egg is produced which, when
fertilized with a Y sperm, yields XXY offspring.

In mammals with more than one X chromosome,

the genes on all but one X chromosome are not
expressed; this is known as X inactivation. This
happens in XXY males as well as normal XX
females. A few genes located in the
pseudoautosomal regions, however, have
corresponding genes on the Y chromosome and
are capable of being expressed. These triploid
genes in XXY males may be responsible for
symptoms associated with Klinefelter's syndrome.

It is currently thought that rare X-linked recessive

conditions occur even less frequently in XXY
males than in normal XY males. Since these
conditions are transmitted by genes on the X
chromosome, people with two X chromosomes
are typically only carriers rather than affected by
these X-linked recessive conditions.

268
Clinical manifestation

A person with typical untreated

(surgery/hormones) Klinefelter
46,XY/47,XXY mosaic, diagnosed at
age 19. Scar from biopsy may be visible
on left nipple.
There are many variances within the XXY
population, just as within the 46,XY population.
While it is possible to characterise XXY males
with certain body types and physical
characteristics, that in itself should not be the
method of identification as to whether or not
someone has XXY. The only reliable method of

269
identification is karyotype testing. The degree to
which XXY males are affected, both physically
and developmentally, differs widely from person
to person.

Physical
As babies and children, XXY males may have
weaker muscles and reduced strength. As they
grow older, they tend to become taller than
average. They may have less muscle control and
coordination than other boys their age.
During puberty, the physical traits of the
syndrome become more evident; because these
boys do not produce as much testosterone as other
boys, they have a less muscular body, less facial
and body hair, and broader hips. As teens, XXY
males may have larger breasts, weaker bones, and
a lower energy level than other boys.
By adulthood, XXY males look similar to males
without the condition, although they are often
taller. In adults, possible characteristics vary
widely and include little to no signs of
affectedness, a lanky, youthful build and facial
appearance, or a rounded body type with some
degree of gynecomastia (increased breast tissue).
Gynecomastia is present to some extent in about a
third of affected individuals, a slightly higher

270
percentage than in the XY population. About 10%
of XXY males have gynecomastia noticeable
enough that they may choose to have cosmetic
surgery.
Affected males are often infertile, or may have
reduced fertility. Advanced reproductive
assistance is sometimes possible.[10]
The term hypogonadism in XXY symptoms is
often misinterpreted to mean "small testicles" or
"small penis". In fact, it means decreased
testicular hormone/endocrine function. Because of
this (primary) hypogonadism, individuals will
often have a low serum testosterone level but high
serum follicle-stimulating hormone (FSH) and
luteinizing hormone (LH) levels. Despite this
misunderstanding of the term, however, it is true
that XXY men may also have microorchidism
(i.e. small testicles).
XXY males are also more likely than other men to
have certain health problems, which typically
affect females, such as autoimmune disorders,
breast cancer, vein diseases, and osteoporosis. In
contrast to these potentially increased risks, it is
currently thought that rare X-linked recessive
conditions occur less frequently in XXY males
than in normal XY males, since these conditions
are transmitted by genes on the X chromosome,

271
and people with two X chromosomes are typically
only carriers rather than affected by these X-
linked recessive conditions.

Cognitive and developmental

Some degree of language learning or reading
impairment may be present, and
neuropsychological testing often reveals deficits
in executive functions, although these deficits can
often be overcome through early intervention.
There may also be delays in motor development
which can be addressed through occupational
therapy. XXY males may sit up, crawl, and walk
later than other infants; they may also struggle in
school, both academically and with sports.

Complication
Enlarged teeth with a thinning surface is very
common in Klinefelter syndrome. This is called
taurodontism. It can be diagnosed by dental x-
rays.
Klinefelter syndrome also increases your risk of:
 Attention deficient hyperactivity disorder
 Autoimmune disorders such as lupus,
rheumatoid arthritis, and Sjogren syndrome
 Breast cancer in men
 Depression

272
  Learning disabilities, including dyslexia,
which affects reading
 A rare type of tumor called an extragonadal
germ cell tumor
 Lung disease
 Osteoporosis
 Varicose veins

Diagnostic evaluation
About 10% of Klinefelter cases are found by
prenatal diagnosis. The first clinical features may
appear in early childhood or, more frequently,
during puberty, such as lack of secondary sexual
characters and aspermatogenesis, while tall stature
as a symptom can be hard to diagnose during
puberty. Despite the presence of small testes, only
a quarter of the affected males are recognized as
having Klinefelter syndrome at puberty and 25%
received their diagnosis in late adulthood: about
64% affected individuals are not recognized as
such. Often the diagnosis is made accidentally as
a result of examinations and medical visits for
reasons not linked to the condition.
The standard diagnostic method is the analysis of
the chromosomes' karyotype on lymphocytes. In
the past, the observation of the Barr body was
common practice as well. To confirm the

273
mosaicism, it is also possible to analyze the
karyotype using dermal fibroblasts or testicular
tissue.
Other methods may be: research of high serum
levels of gonadotropins (follicle-stimulating
hormone and luteinizing hormone), presence of
azoospermia, determination of the sex chromatin,
and prenatally via chorionic villus sampling or
amniocentesis. A 2002 literature review of
elective abortion rates found that approximately
58% of pregnancies in the United States with a
diagnosis of Klinefelter syndrome were
terminated.

Management
The genetic variation is irreversible. Testosterone
treatment should begin at puberty. This treatment
can normalize body proportions and promote
development of normal secondary sex
characteristics but does not treat infertility,
gynecomastia and small testes. Often individuals
that have noticeable breast tissue or
hypogonadism experience depression and/or
social anxiety because they are outside of social
norms. This is academically referred to as
psychosocial morbidity. At least one study
indicates that planned and timed support should

274
be provided for young men with Klinefelter
syndrome to ameliorate current poor psychosocial
outcomes.
By 2010 over 100 successful pregnancies have
been reported using IVF technology with
surgically removed sperm material from men with
Klinefelter syndrome.
Nursing management
Nursing assessment:-
 Assess the level of knowledge about
diseases.
 Assess the mental as well as the physical
growth.
 Assess the level of understanding the
condition.
 Assess the growth pattern of body.
 Family assessment is also important.
Nursing diagnosis:-
 Disturbed body image related to the disease
condition secondary to low level of
testosterone as manifested by growth of
breast.
 Disturbed personal identity related to
disease condition as evidence by female
like features.
 Hopelessness related to the present
condition of patient as manifested by

275
 verbalization.
 Risk for injury related to disease condition.
 Anxiety related to outcome of the disease
as evidence by verbalization.
Nursing intervention:-
 Assess the body changes of the patient.
Give psychological support.
 Assess the anxiety level of the patient
Explain the patient about progressive
features of the disorder
Divert the attention of the patient by
talking.
 Explain the patient about progressive
features of the disorder.
Clarify patient’s doubts and questions
regarding disorder.
 Provide comfortable position to the
patient.
Provide calm and quiet environment.
 Provide high- calorie foods and fluids
consistent with the patient’s
requirements.
 Provide a quiet, calm environment at
meals.
 Restrict stimulants(tea, coffee,
alcohol) ;explain rationale of
requirements and restrictions to patient.

276
  Encourage and pe to detrmit the patient
to eat alone if embarrassed or if
otherwise disturbed by voracious
appetite
 Reduce stressors in the environment;
reduce noise and light.
 Promote sleep and relaxation through
use of prescribed medication, massage,
and relaxation exercises.
 Minimize disruption of the patient’s
sleep or rest by clustering nursing
activity.
 Use safety measures to reduce risk of
trauma or falls.
 Encourage patient to verbalize concerns
and fears about illness and treatment.
 Support the patient who is undergoing
various diagnostic tests.
 Explain the purpose and requirements of
each prescribed test.
 Explain the result of tests if unclear to
the patient or if questions arise.
 Clear up misconceptions about
treatment options.

Prognosis
Children with a XXY form differ little from

277
 healthy children. Although they can face
problems during adolescence, often emotional and
behavioural, and difficulties at school, most of
them can achieve full independence from their
families in adulthood. Some manage to obtain an
university education and a normal, healthy life.
The results of a study carried out on 87 Australian
adults with the syndrome shows that those who
have had a diagnosis and appropriate treatment
from a very young age had a significant benefit
with respect to those who had been diagnosed in
adulthood.
20. Discribe INTRODUCTION:- Lecture, Listen, OHP, LCD, Explain
about turner discussi answe VEDIOS. treatment of
syndrome Turner syndrome or Ullrich–Turner syndrome on , ring. turner
its etiology, , 45,X, encompasses several conditions in human explanat syndrome.
clinical females, of which monosomy X is most common. ion&
manifestatio It is a chromosomal abnormality in which all or question
n, part of one of the sex chromosomes is absent . ing
pathophysio Normal females have two X chromosomes, but in
logy, Turner syndrome, one of those sex chromosomes
diagnostic is missing or has other abnormalities. In some
evaluation, cases, the chromosome is missing in some cells
treatment, but not others, a condition referred to as
nursing mosaicism or "Turner mosaicism".
management
.

278
Girl with Turner syndrome before and immediately after
her operation for neck-webbing which is a characteristic
clinical feature of patients with the syndrome.

DEFINITION:-

Turner syndrome is a genetic condition in which a

female does not have the usual pair of two X
chromosomes.

 Monosomy. The complete absence of an X

chromosome generally occurs because of
an error in the father's sperm or in the
mother's egg. This results in every cell in
the body having only one X chromosome

279
 — a condition called monosomy.
 Mosaicism. In some cases, an error occurs
in cell division during early stages of fetal
development. This results in some cells in
the body having two complete copies of the
X chromosome. Other cells have only one
copy of the X chromosome, or they have
one complete and one altered copy. This
condition is called mosaicism.
 Y chromosome material. In a small
percentage of cases of Turner syndrome,
some cells have one copy of the X
chromosome and other cells have one copy
of the X chromosome and some Y
chromosome material. These individuals
develop biologically as girls, but the
presence of Y chromosome material
increases the risk of developing a type of
cancer called gonadoblastoma.

ETIOLOGY:-

1. Risk factors for Turner syndrome are

not well known
2. Genetic mosaicism (46,XX/45,X) is
most often implicated, alongside
nondisjunction (45,X) and partial

280
 monosomy (46,XX).
Nondisjunctions increase with
maternal age, such as for Down
syndrome, but that effect is not clear
for Turner syndrome.
3. It is also unknown if there is a
genetic predisposition present that
causes the abnormality, though most
researchers and doctors treating
Turners women agree that this is
highly unlikely. In 75% of cases, the
inactivated X chromosome is of
paternal origin.
4. There is currently no known cause
for Turner syndrome, though there
are several theories surrounding the
subject. The only solid fact that is
known today is that during
conception part or all of the second
sex chromosome is not transferred to
the fetus. In other words, these
females do not have Barr bodies,
which are those X chromosomes
inactivated by the cell.

pathophysiology

Turner syndrome is caused by a reduced

281
complement of genes that are typically expressed
from both X chromosomes in females. Normally
one X chromosome is randomly inactivated
during the first week of life (when there are fewer
than 200 embryonic cells); therefore, it may seem
paradoxical that having a single X chromosome
would cause clinical consequences. However, not
all genes from the second chromosome are
inactivated in Turner syndrome. Some genes
escape X-inactivation via a process initiated by
the X-inactivation-specific transcript (XIST) gene
that is transcribed exclusively from the inactive
genes. The loss of these noninactivated X genes
causes the phenotypic manifestations
characteristic of Turner syndrome, such as short
stature.

CLINICAL MANIFESTATION:-

Common symptoms of Turner syndrome

include:

 Short stature
 Lymphedema (swelling) of the hands and
feet
 Broad chest (shield chest) and widely
spaced nipples

282
  Low hairline
 Low-set ears
 Reproductive sterility

Lymphedema, puffy legs of a newborn with

Turner syndrome

 Rudimentary ovaries gonadal streak

(underdeveloped gonadal structures that
283
 later become fibrosed)
 Amenorrhoea, or the absence of a
menstrual period
 Increased weight, obesity
 Shield shaped thorax of heart
 Shortened metacarpal IV
 Small fingernails
 Characteristic facial features
 Webbed neck from cystic hygroma in
infancy
 Coarctation of the aorta
 Bicuspid aortic valve
 Poor breast development
 Horseshoe kidney
 Visual impairments sclera, cornea,
glaucoma, etc.
 Ear infections and hearing loss
 High waist-to-hip ratio (the hips are not
much bigger than the waist)
 Attention Deficit/Hyperactivity Disorder or
ADHD (problems with concentration,
memory, attention with hyperactivity seen
mostly in childhood and adolescence)
 Nonverbal Learning Disabilit y (problems
with math, social skills and spatial
relations)

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Other features may include a small lower jaw
(micrognathia), cubitus valgus[8] (turned-in
elbows), soft upturned nails, palmar crease, and
drooping eyelids. Less common are pigmented
moles, hearing loss, and a high-arch palate
(narrow maxilla). Turner syndrome manifests
itself differently in each female affected by the
condition, and no two individuals will share the
same features.

COMPLICATION:-

 Abnormal aortic valve or narrowing of the

aorta in an infant, and widening of the
aorta in an adult
 Arthritis
 Cataracts
 Diabetes
 Hashimoto's thyroiditis
 Heart defects
 High blood pressure
 Kidney problems
 Middle ear infections
 Obesity
 Scoliosis (in adolescence)

DIAGNOSTIC EVALUATION:-

285
Prenatal

Turner syndrome may be diagnosed by

amniocentesis or chorionic villus sampling during
pregnancy.

Often, fetuses with Turner syndrome can be

identified by abnormal ultrasound findings (i.e.,
heart defect, kidney abnormality, cystic hygroma,
ascites).

An increased risk of Turner Syndrome may also

be indicated by abnormal triple or quadruple
maternal serum screen. The fetuses diagnosed
through positive maternal serum screening are
more often found to have a mosaic karyotype than
those diagnosed based on ultrasonographic
abnormalities, and conversely those with mosaic
karyotypes are less likely to have associated
ultrasound abnormalities.

Although the recurrence risk is not increased,

genetic counseling is often recommended for
families who have had a pregnancy or child with
Turner syndrome.

286
Postnatal

Turner Syndrome can be diagnosed postnatally at

any age. Often, it is diagnosed at birth because of
heart problems, an unusually wide neck or
swelling of the hands and feet. However, it is also
common for it to go undiagnosed for several
years, typically until the girl reaches the age of
puberty/adolescence and she fails to develop
properly (the changes associated with puberty do
not occur). In childhood, a short stature can be
indicative of Turner syndrome.

A test, called a karyotype or a chromosome

analysis, analyzes the chromosomal composition
of the individual. This is the test of choice to
diagnose Turner syndrome.

Treatment

As a chromosomal condition, there is no cure for

Turner syndrome. However, much can be done to
minimize the symptoms. For example:

 Growth hormone, either alone or with a low

dose of androgen, will increase growth and
probably final adult height. Growth

287
 hormone is approved by the U.S. Food and
Drug Administration for treatment of
Turner syndrome and is covered by many
insurance plans. There is evidence that this
is effective, even in toddlers.

 Estrogen replacement therapy such as the

birth control pill, has been used since the
condition was described in 1938 to promote
development of secondary sexual
characteristics. Estrogens are crucial for
maintaining good bone integrity,
cardiovascular health and tissue health.
Women with Turner Syndrome who do not
have spontaneous puberty and who are not
treated with estrogen are at high risk for
osteoporosis and heart conditions.

 Modern reproductive technologies have

also been used to help women with Turner
syndrome become pregnant if they desire.
For example, a donor egg can be used to
create an embryo, which is carried by the
Turner syndrome woman.

 Uterine maturity is positively associated

with years of estrogen use, history of

288
 spontaneous menarche, and negatively
associated with the lack of current hormone
replacement therapy.

Nursing assessment:-
 Assess the level of knowledge about
diseases.
 Assess the mental as well as the physical
growth.
 Assess the level of understanding the
condition.
 Assess the growth pattern of body.
 Family assessment is also important.

Nursing diagnosis:-
 Disturbed body image related to the disease
condition secondary to low level of
estrogen as manifested by poor growth of
breast.
 Disturbed personal identity related to
disease condition as evidence by less
female like features.
 Hopelessness related to the present
condition of patient as manifested by
verbalization.
 Risk for hypertension related to disease
condition as evidence by increased body
289
 weight.
 Risk for infection related to disease
condition.
 Anxiety related to outcome of the disease
as evidence by verbalization

Nursing intervention:-
 Assess the body changes of the patient.
Give psychological support.
 Assess the anxiety level of the patient
Explain the patient about progressive
features of the disorder
Divert the attention of the patient by
talking.
 Explain the patient about progressive
features of the disorder.
Clarify patient’s doubts and questions
regarding disorder.
 Provide comfortable position to the
patient.
Provide calm and quiet environment.
 Provide high- calorie foods and fluids
consistent with the patient’s
requirements.
 Provide a quiet, calm environment at
meals.

290
 Restrict stimulants(tea, coffee,
alcohol) ;explain rationale of
requirements and restrictions to patient.
 Encourage and pe to detrmit the patient
to eat alone if embarrassed or if
otherwise disturbed by voracious
appetite
 Reduce stressors in the environment;
reduce noise and light.
 Promote sleep and relaxation through
use of prescribed medication, massage,
and relaxation exercises.
 Minimize disruption of the patient’s
sleep or rest by clustering nursing
activity.
 Use safety measures to reduce risk of
trauma or falls.
 Encourage patient to verbalize concerns
and fears about illness and treatment.
 Support the patient who is undergoing
various diagnostic tests.
 Explain the purpose and requirements of
each prescribed test.
 Explain the result of tests if unclear to
the patient or if questions arise.
 Clear up misconceptions about
treatment options.

291
 Expectations (prognosis)

Those with Turner syndrome can have a normal

life when carefully monitored by their doctor.

21. Discribe Introduction Lecture, Listen, OHP, LCD, Enlist the

about discussi answe VEDIOS. symptoms
acromegaly Kallmann syndrome is a congenital endocrine on , ring. of kallmann
its etiology, disorder that adversely affects the development of explanat syndrome.
clinical sexual organs in both males and females. Get ion&
manifestatio detailed information about the condition, question
n, including its causes, symptoms, diagnosis, and ing
pathophysio treatment methods.
logy,
diagnostic Definition
evaluation,
treatment, This hormonal condition is characterized by
nursing delayed, incomplete or absent puberty. It is
management simply abbreviated as KS.
.
Causes

It is caused by a lack of secretion of the gonadal

stimulating pituitary hormones: follicle
stimulating hormone (FSH) and luteinizing

292
hormone (LH).

Normally, the hypothalamus in the brain releases

gonadotropin-releasing hormone (GnRH). This
hormone stimulates the pituitary gland to release
other hormones, including FSH and
LH. These hormones tell the female ovaries and
male testes to release hormones that lead to
normal sexual development in puberty. Any
change in this hormone release chain causes a
lack of sex hormones and prevents normal sexual
maturity.

Failure of the hypothalamus is usually a result of

Kallmann syndrome. Kallmann syndrome is an
inherited form of hypogonadotropic
hypogonadism that can occur with a loss of smell

Kallmann syndrome Pathophysiology

KS is caused by genetic mutations in AL1,

FGFR1, PROKR2, and PROK2. These genes
have a crucial role in the migration of olfactory
and GnRH neurons in the fetal brain. Anomalies
in the genes disrupt an individual’s sense of smell
and interfere with the normal sexual development.
The additional features of KS have been ascribed

293
to the impact of various other genetic and
environmental factors by several medical
scientists. KS follows an X-linked recessive
pattern of inheritance and can be passed from one
generation to another. The KAL1 gene is located
on the X chromosome, one of the two sex
chromosomes present in each cell. As males carry
a single X chromosome, one altered copy of the
gene in each cell is sufficient to cause the
disorder. However, mutation in the two copies of
KAL1 gene is a prerequisite for causing KS in
females, owing to the presence of two X
chromosomes in them. Thus, males are more
likely to develop the X-linked recessive disorder
than females.

Clinical manifestation

A simple constitutional delay of puberty could

often be confused with KS, owing to the absence
of reproductive features. The condition normally
has the following clinical manifestations:

 Presence of small penis in males

 Failure of testicular development in males
called Cryptorchidism
 Decreased libido and erectile dysfunction in

294
 males
 Absence of a menstrual period in females
 Incomplete development of secondary
sexual characteristics in both genders
 Infertility
 Osteoporosis
 Total absence of sense of smell (known as
Anosmia)
 Hyposmia, or partial impairment of sense
of smell
 Fatigue
 Shortness of breath
 Palpitations
 Bluish discoloration of the skin called
cyanosis
 Fainting
 Loss of muscle tone
 Sensorineural hearing loss
 Epilepsy
 Impairment in motor or sensory function of
the lower extremities
 Color blindness
 Decreased vaginal lubrication in females
 Craniofacial anomalies
 Abnormal ocular movements
 Dental defects
 Bimanual synkinesis

295
  Excessive bone growth
 Congenital absence or severe malformation
of one or both kidneys

Complications

 Delayed puberty
 Infertility
 Low self-esteem due to late start of puberty
(emotional support may be helpful)

Diagnostic evaluation

During a physical examination, clinicians can

easily suspect the possibility of KS as signs like
delayed puberty and impaired sense are
symptomatic of this disorder. The family medical
history is crucial to track the ailment as it may
provide some information about the genetic
makeup of the affected individuals. Some medical
tests and exams for the diagnosis of KS include:

Blood test

In KS-affected patients, a simple hematology test

reveals a problem in the hypothalamus or the
pituitary gland by showing the following features:

296
  Low levels of LH and FSH in males as well
as in females
 Low serum testosterone in males
 Reduced levels of serum estrogen in
females
 Decreased pituitary hormones in both
genders

Genetic screening

The highly-specialized technique can identify

mutations in the KAL 1 gene and the other genes
involved in this disorder.

X-ray

A bone age study can be conducted using the X-

ray technique to evaluate how an individual’s
bones are maturing. A delayed growth or puberty
is obvious when the test reveals a bone age lesser
than the chronological or actual age of the
patients.

Magnetic resonance imaging

Damaged olfactory neurons in the nose and

deformity in the pituitary gland or hypothalamus

297
can be confirmed with the help of MRI findings.

Smell test

Commercially available testing kits, containing a

variety of odorous chemicals are placed beneath
the nostrils of the patients. These various sources
of smell are then made to be identified. The
inability of the patients to perceive the odors
signifies some kind of malformation in the
olfactory system.

Treatment

The condition can be treated through therapeutic

procedures like:

Hormone replacement therapy

The estrogen or combination estrogen

/progesterone treatment is performed to raise the
levels of the sex hormones in females and can be
given in pill, patch, or gel form. Estrogen signals
the start of a menstrual cycle. It is also responsible
for causing development of the sex organs,
including breast tissue. Progesterone regulates the
estrogen level, and plays an important role in

298
fertility by building up the endometrial lining and
shedding it during menstruation when no
pregnancy occurs. Testosterone replacement
therapy can be prescribed as an intramuscular
injection or in the form of capsules, patches or
gels on the skin. Testosterone is needed to form
and maintain the male sex organs as well as
promote secondary male sex characteristics. It
even facilitation the muscle growth as well as
bone development and maintenance.

Fertility treatments

Health specialists can advice the patients to go for

in vitro fertilization (IVF) or intake of fertility
drugs like clomiphene, gonadotropins or
bromocriptine to stimulate the production, and
release of eggs and sperms. Administration of
human chorionic gonadotrophin (hCG) can evoke
testosterone production in males and ovulation
induction in females.

Additional medical therapies are also used to treat

the other symptoms, including osteoporosis.

299
If you are worried about delayed puberty, and
have a family history of Kallmann syndrome, get
quickly in touch with a healthcare provider. Early
detection and quick treatment can restore normal
pubertal development and fertility.

Nursing assessment:-
 Assess the level of knowledge about
diseases.
 Assess the mental as well as the physical
growth.
 Assess the level of understanding the
condition.
 Assess the growth pattern of body.
 Family assessment is also important.

Nursing diagnosis:-

 Risk for fracture related to osteoporosis.

 Fatigue related to disease condition as
manifested by low energy level.
 Disturbed body image related to the disease
condition.
 Disturbed personal identity related to
disease condition as evidence by features.
 Hopelessness related to the present
condition of patient as manifested by

300
 verbalization.
 Risk for injury related to disease condition.
 Anxiety related to outcome of the disease
as evidence by verbalization

Nursing intervention:-

 Calcium supplement and calcium reach

diet should be provided to the patient.
 Give psychological support.
 Assess the anxiety level of the patient
Explain the patient about progressive
features of the disorder
Divert the attention of the patient by
talking.
 Explain the patient about progressive
features of the disorder.
Clarify patient’s doubts and questions
regarding disorder.
 Provide comfortable position to the
patient.
Provide calm and quiet environment.
 Provide high- calorie foods and fluids
consistent with the patient’s
requirements.
 Provide a quiet, calm environment at
meals.
 Restrict stimulants(tea, coffee,
301
 alcohol) ;explain rationale of
requirements and restrictions to patient.
 Encourage and pe to detrmit the patient
to eat alone if embarrassed or if
otherwise disturbed by voracious
appetite
 Reduce stressors in the environment;
reduce noise and light.
 Promote sleep and relaxation through
use of prescribed medication, massage,
and relaxation exercises.
 Minimize disruption of the patient’s
sleep or rest by clustering nursing
activity.
 Use safety measures to reduce risk of
trauma or falls.
 Encourage patient to verbalize concerns
and fears about illness and treatment.
 Support the patient who is undergoing
various diagnostic tests.
 Explain the purpose and requirements of
each prescribed test.
 Explain the result of tests if unclear to
the patient or if questions arise.
 Clear up misconceptions about
treatment options.

302
Outlook (Prognosis)

With the right hormone treatment, the person can

go through puberty, and fertility may be restored.

303