MEDICAL SURGICAL NURSING

A SEMINAR ON

THYROID DISORDERS

SUBMITTED TO, SUBMITTED BY,

Mrs SINDHU C PHILIP ASHISHA.C
ASSO. PROFESSOR 1STYEAR MSC NURSING
TMM COLLEGE OF NURSING TMM COLLEGE OF NURSING
THIRUVALLA THIRUVALLA

SUBMITTED ON: 25 |01|2018

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 THYROID DISORDERS
INTRODUCTION
Thyroid disease is a medical condition that affects the function of the thyroid gland. The
symptoms of thyroid disease vary depending on the type. There are four general types:
1) hypothyroidism (low function) caused by not having enough thyroid hormones;
2) hyperthyroidism (high function) caused by having too much thyroid hormones; 3)
structural abnormalities, most commonly an enlargement of the thyroid gland; and
4) tumors which can be benign or cancerous. It is also possible to have abnormal thyroid
function tests without any clinical symptoms. Common hypothyroid symptoms include
fatigue, low energy, weight gain, inability to tolerate the cold, slow heart rate, dry skin and
constipation. Common hyperthyroid symptoms include irritability, weight loss, fast heartbeat,
heat intolerance, diarrhoea, and enlargement of the thyroid. In both hypothyroidism and
hyperthyroidism, there may be swelling of a part of the neck, which is also known as goiter.

ANATOMY AND PHYSIOLOGY OF THYROID GLAND

The thyroid gland consists of two lateral lobes connected by an isthmus. It is closely attached
to the thyroid cartilage and to the upper end of the trachea, and thus moves on swallowing. It
is often palpable in women.
Embryologically it originates from the base of the tongue and descends to the middle of the
neck. Remnants of thyroid tissue can sometimes be found at the base of the tongue (lingual
thyroid) and along the line of descent. The gland has a rich blood supply from superior and
inferior thyroid arteries.
The thyroid consist of follicles lined by cuboidal epithelioid cells. Inside is the colloid, which
is an iodinated glycoprotein, thyroglobulin, synthesised by the follicular cells. Each follicle is
surrounded by basement membrane, between which are parafollicularcells containing
calcitonin-secreting cells.

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DISORDERS OF THYROID GLANDS
 HYPOTHYROIDISM
 HYPERTHYROIDISM
 THYROIDITIS
 THYROTOXIC CRISIS
 GOITER
 MYXEDEMA

I. HYPOTHYROIDISM
DEFINITION: Deficiency of thyroid hormone results in hypothyroidism. It is called
primary (thyroprivic) when caused due to the pathology of thyroid gland and secondary
(trophoprivic) when the pituitary or hypothalamus is the cause. The disease is 6 to 8 times
common in women than men and occurs between 40-50 years of age.

ETIOLOGY
A. PRIMARY(THYROPRIVIC) HYPOTHYROIDISM
 Idiopathic primary hypothyroidism
 Goitrous- iodine deficiency, Chronic auto immune thyroiditis(Hashimotos
Disease), Hereditary defects in thyroid hormone synthesis
 Post ablation- Surgery, Radioactive iodine ablation, Radiation to head, neck
for treatment of head and neck cancers, lymphoma
 Drugs-Lithium, Contrast agents containing iodine, Anti-thyroid medications
 Transient hypothyroidism-silent thyroiditis, sub-acute thyroiditis, post
radioactive iodine therapy for Graves’ disease
 Thyroid agenesis or ectopic thyroid in children
 Infiltrative disease of thyroid: amyloidosis, sarcoidosis
 Rare causes: Thyroid hormone resistance syndrome
B. SECONDARY(TROPHOPRIVIC) HYPOTHYROIDISM
 Pituitary/ hypothalamic disorders-Tumour, haemorrhage, glaucomatous or
auto immune disease

CLINICAL MANIFESTATIONS
 SKIN
 Dry, scaly skin, loos of hair from scalp and body.
 Generalized oedema initially pitting, brittle nails, weight gain
 Hoarseness of voice, slowness of speech
 GASTROINTESTINAL
 Constipation
 CARDIOVASCULAR
 Decreased heart rate, blood pressure, breathlessness

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  NEUROLOGICAL
 Physical, mental slowness, lethargy, somnolence
 Delayed deep tendon reflexes
 Carpel tunnel syndrome
 RENAL
 Decreased urine output
 FEMALE REPRODUCTIVE SYSTEM
 Irregular menstrual cycle
 Galactorrhoea
PATHOPHYSIOLOGY
Thyroid hormone is secreted in response to stimulation of the thyroid gland by thyroid-
stimulating hormone (TSH) from the anterior pituitary gland. TSH is released through the
action of thyrotropin-releasing hormone. Hypothyroidism can be caused by permanent loss or
atrophy of functional thyroid tissue (primary hypothyroidism), insufficient stimulation of
normal thyroid gland by as a result of hypothalamic or pituitary disease (secondary
hypothyroidism, often accompanied by compensatory thyroid gland enlargement), or a defect
in the TSH molecule (control hypothyroidism).
Primary hypothyroidism accounts for approximately 90-95% of hypothyroidism, with a
predominantly autoimmune-mediated aetiology. TSH hypersecretion produces excessive
thyroid tissue, resulting in goitre formation. Surgical and radiation ablation account for a
large percentage of acquired cases of hypothyroidism. Congenital abnormalities,
malignancies, and infiltrative disorders including amyloidosis and sarcoidosis can also lead to
the disease. Iodine deficiency is rarely responsible for hypothyroidism in developed
countries; however, it remains the primary cause worldwide. Supra-thyroidal disorders
including hypopituitarism and hypothalamic lesions account for fewer than 10% of
cases. Rarely, peripheral resistance to thyroid hormone may occur. The congenital absence or
deficiency of thyroid tissue in cretinism, a neurodevelopmental disorder characterized by
lethargy, poor peripheral circulation, and goitre.
PHARMACOLOGICAL THERAPY
Synthetic Levothyroxine is the preferred preparation for treating hypothyroidism and
suppressing nontoxic goitres. It is customary to start slowly with a slow dose of 50mg per
day. For 3 weeks, increasing thereafter to 100 mg per day. Patient feel better within 2-3
weeks, reduction in periorbital puffiness occur quickly but the restoration of skin, hair
structure and resolutions of any effusion may take 3-6 months. It is important to measure
thyroid function every 1-2 years once the dose of thyroxin is stabilized.

II. GOITER
Enlargement of thyroid gland may be seen with both hyperthyroidism and hypothyroidism.

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ETIOLOGY
 It generally results from a lack of iodine, inflammation, or benign or malignant
tumors
 Enlargement may also appear in hyperthyroidism, especially Graves’ disease, in
which the client typically has exophthalmos as well
 Endemic goiter is caused principally by nutritional iodine deficiency. It tends to occur
in goiter “belts” geographical areas characterized by soil and water that are deficient
in iodine
 Iodine is readily available in regions with access to salt water and also through
consumption of seafood. Hence goiter typically occurs in fall and winter months and
is twice as prevalent in women as it is in men
 Goiter commonly develops in adolescents, pregnant women and nursing mothers who
live in iodine-deficient region

PATHOPHYSIOLOGY

Dietary insufficiency of iodine intake

OR Suppressed production of thyroid
hormones

Thyroid enlarges to compensate

for hormonal deficiency

TSH stimulates the thyroid to

secrete more T4 when blood T4
levels are low

Thyroid gland enlarges and

compresses the structures in
neck and chest

Respiratory problems and

dysphagia

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 DIAGNOSTIC EVALUATION
 History collection
 Physical examination
 Blood tests-T3,T4, TSH
 Needle Biopsy
CLINICAL MANIFESTATION
 Asymptomatic
 Most goiters are painless. However, an inflamed thyroid can be painful
 A large thyroid may press on the trachea or even the oesophagus behind the trachea.
This may cause difficulty with breathing
MEDICAL MANAGEMENT
o When enlargement is a compensatory reaction to iodine deficiency and consequent
suppression of T4 secretion, the client can be treated with preparations of iodine and
thyroid hormones
o Either a strong solution (Lugol’s solution) or the solution of potassium iodide (SSKI)
drops can be administered.
o Iodine reduces the size and the vascularity of the enlarged gland
o The client may switch to iodized salt.
o Dietary goitrogens (E.g. turnips, soya beans, green leafy vegetables carrots and
peanuts)
SURGICAL MANAGEMENT
Surgery is indicated for a goiter that is very large, does not respond to treatment, or is putting
too much pressure on other structure in neck

III. MYXAEDEMA
DEFINITION: It is a clinical syndrome in which the deficiency or absence of thyroid
hormone slows bodily metabolic processes. It refers to the thickened, non pitting edematous
changes to the soft tissues of the patients in a markedly hypothyroid state.
CLINICAL MANIFESTATIONS
 Lethargy
 Generalized weakness
 Brittle or thinning hair
 Menstrual irregularity
 Menorrhagia
 Forgetfulness
 Fullness in throat
 Deep, husky voice secondary to mucopolysaccharide infiltration of the vocal cords
 Weight gain
 Headache
 Constipation
 Emotional lability

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  Depression
 Blurred vision
TREATMENT
 Oxygen
 L- Thyroxine
 Liothyronine
 Hydrocortisone

IV. HYPERTHYROIDISM
DEFINITION: Hyperthyroidism is the hyperactivity of the thyroid gland with sustained
increase in the synthesis and release of thyroid hormones. Hyperthyroidism occurs in
frequency in persons 20 to 40 years old. The most common form of hyperthyroidism is
graves’disease.
ETIOLOGY:
 Toxic nodular goiter
 Thyroiditis
 Exogenous iodine excess
 Pituitary Tumors
 Thyroid cancer
PATHOPHYSIOLOGY

Due to etiological factors

Diffuse thyroid enlargement and

excessive thyroid hormone
secretion

Develops antibodies to the TSH

receptor

Antibodies attach to the receptors

and stimulate thyroid gland to
release T4, T3 or both

Excessive release leads to

clinical manifestations
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MANAGEMENT: There is no standard choice for treating Graves’ hyperthyroidism. Beta
blockers may be used to inhibit the sympathetic nervous system symptoms of rapid heart rate
and nausea until such time as anti-thyroid treatments start to take effect.
PHARMACOLOGICAL MANAGEMENT
ANTI THYROID DRUGS
The main antithyroid drugs are carbimazole, methimazole, and Propylthiouracil/PTU.
These drugs block the binding of iodine and coupling of iodotyrosines. The most dangerous
side-effect is Agranulocytosis (1/250, more in PTU); this is an idiosyncratic reaction which
does not stop on cessation of the drug.
SURGICAL MANAGEMENT
This modality is suitable for young patients and pregnant patients. The indications for surgery
are a large goitre (especially when compressing the trachea). Suspicious nodules or suspected
cancer (to pathologically examine the thyroid) and patients with ophthalmopathy
surgical procedure: As operating on a frankly hyperthyroid patient is dangerous, prior to
thyroidectomy preoperative treatment with antithyroid drugs is given to render the patient
"euthyroid" (ie normothyroid). Preoperative administration of (not radioactive) iodine,
usually by Lugol's Iodine solution decreases intraoperative blood loss during thyroidectomy
in patients with Grave's disease. However, it appears ineffective in patients who are already
euthyroid due to treatment with anti-thyroid to drugs and T4.
Partial or total removal of the thyroid gland (subtotal thyroidectomy vs total thyroidectomy).
A total removal excludes the difficulty in determining how much thyroid tissue must be
removed more aggressive surgery has a higher likelihood of inducing hypothyroidism.
Less aggressive surgery has a higher likelihood of recurrent hyperthyroidism. Around 10-
15% of patients who had a subtotal thyroidectomy will develop underactive thyroids many
years after their operation. This is not counting those who develop underactive thyroids
immediately after the operation (within 6 weeks). Thyroid remnants smaller than 4 grams are
associated with postoperative hypothyroidism in 27 to 99 percent of patients. Patients who
have thyroid remnants of 7 to 8 become euthyroid, but may have subclinical hyperthyroidism.
In addition, 9 to 12 percent develop recurrent overt hyperthyroidism.
As repeat surgery is associated with a high risk of complications, further permanent treatment
should be with radioiodine thyroid hormone.

V. THYROIDITIS
DEFINITION: Thyroiditis is an inflammation (not an infection) of the thyroid gland.
TYPES:
 HASHIMOTO’S THYROIDITIS
 DE QUERVAIN’S THYROIDITIS
 SILENT THYROIDITIS

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 HASHIMOTO'S THYROIDITIS
Hashimoto's thyroiditis, also called autoimmune or chronic lymphocytic thyroiditis, is the
most common type of thyroiditis. It is named after the Japanese physician, Hakaru
Hashimoto, who first described it in 1912. Hashimoto's thyroiditis is the most common cause
of hypothyroidism. The thyroid gland is always enlarged in Hashimoto's thyroiditis, although
only one side may be enlarged enough to feel. During the course of this disease, the cells of
the thyroid becomes inefficient in converting iodine into thyroid hormone and "compensate"
by enlarging
The radioactive iodine uptake may be paradoxically high while the patient is hypothyroid
because the gland retains the ability to take-up or "trap" iodine even after it has lost its ability
to produce thyroid hormone.

As the disease progresses, the TSH (Thyroid stimulating hormone) increases since the
pituitary is trying to induce the thyroid to make more hormone, the T4 (a different thyroid
hormone) falls since the thyroid can't make it, and the patient becomes hypothyroid. This
sequence of events can occur over a relatively short span of a few weeks or may take several
years.
 Treatment should begin with thyroid hormone replacement. This prevents or corrects the
hypothyroidism, and it also generally keeps the gland from getting larger.
 In most cases, the thyroid gland will decrease in size once thyroid hormone replacement is
started.
 Thyroid antibodies are present in 95% of patients with Hashimoto's thyroiditis and serve as a
useful "marker" in identifying the disease without thyroid biopsy or surgery.
 Thyroid antibodies may remain for years after the disease has been adequately treated and the
patient is on thyroid hormone replacement

DE QUERVAIN'S THYROIDITIS
De Quervain's thyroiditis (also called subacute or granulomatous thyroiditis) was first
described in 1904 and is much less common than Hashimoto's thyroiditis. The thyroid gland
generally swells rapidly and is very painful and tender.
The gland discharges thyroid hormone into the blood and the patients become hyperthyroid;
however, the gland quits taking up iodine (radioactive iodine uptake is very low), and the
hyperthyroidism generally resolves over the next several weeks.
 Patients frequently become ill with fever and prefer to be in bed.
 Thyroid antibodies are not present in the blood, but the sedimentation rate (which measures
inflammation) is very high.
 Although this type of thyroiditis resembles an infection within the thyroid gland, no
infectious agent has ever been identified, and antibiotics are of no use.
 Treatment is usually bed rest and aspirin to reduce inflammation.
 Occasionally cortisone (steroids, which reduce inflammation) and thyroid hormone (to "rest"
the thyroid gland) may be used in prolonged cases.
 Nearly all patients recover, and the thyroid gland returns to normal after several weeks or
months.

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 A few patients will become hypothyroid once the inflammation settles down and therefore
will need to stay on thyroid hormone replacement indefinitely.
 Recurrences are uncommon.

SILENT THYROIDITIS
Silent thyroiditis is the third and least common type of thyroiditis. It was not recognized until
the 1970s, although it probably existed and was treated as Graves' disease before that.
This type of thyroiditis resembles in part Hashimoto's thyroiditis and in part De Quervain's
thyroiditis. The blood thyroid test is high and the radioactive iodine uptake is low (like De
Quervain's thyroiditis), but there is no pain and needle biopsy resembles Hashimoto's
thyroiditis. The majority of patients have been young women following pregnancy.
The disease usually needs no treatment, and 80% of patients show complete recovery and
return of the thyroid gland to normal after 3 months. Symptoms are similar to Graves' disease
except milder. The thyroid gland is only slightly enlarged and exophthalmos (development of
"bug eyes") does not occur.
Treatment is usually bed rest with beta blockers to control palpitations (drugs to prevent
rapid heart rates). Radioactive iodine, surgery, or antithyroid medication is never needed. A
few patients have become permanently hypothyroid and needed to be placed on thyroid
hormone.

VI. THYROID CARCINOMA

CLASSIFICATION
Thyroid cancers can be classified according to their histopathological characteristics. The
following variants can be distinguished (distribution over various subtypes may show
regional variation):

 Papillary thyroid cancer (75% to 85% of cases) – often in young females – excellent
prognosis. May occur in women with familial adenomatous polyposis and in patients
with Cowden syndrome.
 Non-invasive follicular thyroid neoplasm with papillary-like nuclear features is
considered an indolent tumor of limited biologic potential.
 Follicular thyroid cancer (10% to 20% of cases) – occasionally seen in patients with
Cowden syndrome
 Medullary thyroid cancer (5%to 8% of cases) – cancer of the para-follicular cells, often
part of multiple endocrine neoplasia type 2
 Poorly differentiated thyroid cancer
 Anaplastic thyroid cancer (less than 5% of cases) is not responsive to treatment and can
cause pressure symptoms.
 Others
 Thyroid lymphoma
 Squamous cell thyroid carcinoma
 Sarcoma of thyroid

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The follicular and papillary types together can be classified as "differentiated thyroid cancer".
These types have a more favourable prognosis than the medullary and undifferentiated types.

 Papillary micro carcinoma is a subset of papillary thyroid cancer defined as measuring

less as or equal to 1 cm. Management strategies for incidental papillary micro carcinoma
on ultrasound (and confirmed on FNAB) range from total thyroidectomy with radioactive
iodine ablation to observation alone. Harach et al. suggest using the term "occult
papillary tumour" to avoid giving patients distress over having cancer. It was Woolner et
al. who first arbitrarily coined the term "occult papillary carcinoma" in 1960, to describe
papillary carcinomas ≤ 1.5 cm in diameter.

STAGING

Stage M1 thyroid cancer Stage N1a thyroid cancer Stage N1b thyroid cancer

StageT1a thyroid cancer Stage T1b thyroid cancer Stage T2 thyroid cancer

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 Stage T3 thyroid cancer Stage T4a thyroid cancer

Stage T4b thyroid cancer

CLINICAL MANIFESTATIONS
Thyroid carcinoma most commonly manifests as a painless, palpable, solitary thyroid nodule.
Patients or clinicians discover most of these nodules during routine palpation of the neck.
Signs and symptoms associated with malignancy in thyroid nodules include the following:
 Solitary nodules: Most likely to be malignant in patients older than 60 years and in
patients younger than 30 years
 Increased rate of malignancy in males
 Nodular growth
 Rapid growth: Ominous sign
 Usually painless (nontender to palpation); sudden onset of pain more strongly
associated with benign disease (e.g., haemorrhage into a benign cyst, subacute viral
thyroiditis)
 Hard and fixed nodules

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DIAGNOSITIC EVALUATION: The key to the workup of the solitary thyroid
nodule is to differentiate malignant from benign disease and, thus, to determine which
patients require intervention and which patients may be monitored serially.
 History Taking,
 Physical Examination,
 Laboratory Evaluation, And
 Fine-Needle Aspiration Biopsy (FNAB) are the mainstays in the evaluation of thyroid
nodules. Imaging studies can be adjuncts in select cases.
Examination in patients suspected of thyroid cancer includes the following:
 Thorough head and neck examination, including thyroid gland and cervical soft tissues
 Indirect laryngoscopy
Firm cervical masses are highly suggestive of regional lymph node metastases. Vocal fold
paralysis implies involvement of the recurrent laryngeal nerve.
Procedures
FNAB is the most important diagnostic tool in evaluating thyroid nodules and should be the
first intervention. The following are the 4 possible results from this procedure:
 Benign disease
 Malignant disease
 Indeterminate for diagnosis
 Nondiagnostic
Up to 50% of repeated biopsies result in a definitive diagnosis. Patients whose findings are
indeterminate or nondiagnostic despite repeat biopsy can undergo surgery for lobectomy for
tissue diagnosis. Nondiagnostic cases can also be monitored clinically, and radioiodine scans
can be useful for determining the functional status of the nodule, because most hyper
functioning nodules are benign.
Laboratory testing
The following laboratory studies may be used to assess patients with suspected thyroid
cancer:
 Serum thyroid-stimulating hormone concentration: Sensitive for
hyperthyroidism/hypothyroidism and for evaluation of solitary thyroid nodules
 Serum calcitonin/Penta gastrin-stimulated calcitonin levels: Elevated levels highly
suggestive of medullary thyroid carcinoma
 Polymerase chain reaction (PCR) assay for germline mutations in the RET proto-
oncogene: For diagnosis of familial medullary thyroid carcinoma
Imaging studies
The following imaging studies may be used to evaluate patients with suspected thyroid
cancer:
 Neck ultrasonography: Most common modality to evaluate thyroid disease; however,
limited usefulness for distinguishing between malignant and benign nodules
 Thyroid radioiodine imaging: To determine functional status of a nodule but cannot
exclude carcinoma
 Neck computed tomography (CT) scanning or magnetic resonance imaging (avoid
iodinated contrast agents): To evaluate soft-tissue extension of large or suspicious
thyroid masses into the neck, trachea, or oesophagus, and to assess metastases to the
cervical lymph nodes; no role in routine management of solitary thyroid nodules

MANAGEMENT: Malignant diagnoses require surgical intervention. Papillary thyroid

carcinoma and medullary thyroid carcinoma are often positively identified on the basis of

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FNAB results alone. Cervical metastases discovered preoperatively or intraoperatively should
be removed by means of lymphatic dissection of the respective cervical compartment
(selective neck dissection) while sparing the non-lymphatic structures.

Well-Differentiated Neoplasms
Patients with follicular neoplasm, as determined with FNAB results, should undergo surgery
for thyroid lobectomy for tissue diagnosis. The extent of surgical therapy for well-
differentiated neoplasms is controversial. Primary treatment for papillary and follicular
carcinoma is surgical excision whenever possible. Total thyroidectomy has been the mainstay
for treating well-differentiated thyroid carcinoma. Modifications to total thyroidectomy
include subtotal thyroidectomy to reduce the risk of recurrent laryngeal nerve injury and
hypoparathyroidism
Hürthle Cell Carcinomas

For patients with Hürthle cell carcinomas based on initial FNAB findings, most surgeons
advocate an aggressive approach with lobectomy and isthmectomy, followed by completion
thyroidectomy with confirmation on final pathologic result. For tumors larger than 5 cm or
for palpable lymphatic metastases, total thyroidectomy (including neck dissection for
palpable lymph nodes) is often performed during the initial operation.

Medullary Thyroid Carcinomas and Familial Medullary Thyroid Carcinomas

Sporadic medullary thyroid carcinomas and familial medullary thyroid carcinomas are treated
with total thyroidectomy and lymphatic dissection of the anterior compartment of the neck. If
the vasculature of the parathyroid gland is disrupted, auto transplantation of the parathyroid
gland into the sternocleidomastoid muscle or the non-dominant forearm is performed. In
children with multiple endocrine neoplasia (MEN) type 2A and MEN 2B syndromes,
prophylactic thyroidectomy and central-compartment lymph-node dissection is performed.
Anaplastic thyroid carcinoma, primary thyroid lymphoma, thyroid sarcoma

Total or subtotal thyroidectomy is performed for anaplastic thyroid carcinoma when the
extent of the tumor permits it. Tracheotomy is needed in cases with airway compromise due
to tracheal invasion.
Stage IE lymphomas may be treated with total thyroidectomy followed by postoperative
radiation therapy. Surgical excision should not be performed if local infiltration into
surrounding tissues is evident. Stage IIE lymphomas are treated with combined chemotherapy
and radiation therapy. Doxorubicin or CHOP (ie, cyclophosphamide, hydroxydaunomycin,
Oncovin [vincristine], prednisone) is the commonly used chemotherapeutic regimen.
The treatment for thyroid sarcomas is total thyroidectomy. Radiation therapy may be used in
an adjunctive setting.

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Post-surgical Management
After total thyroidectomy, patients undergo radioiodine scanning to detect regional or distant
metastatic disease, followed by radio ablation of any residual disease found. In addition,
patients are given thyroid replacement therapy with T4 or triiodothyronine (T3).

In patients with anaplastic thyroid carcinoma, chemotherapy and radiation therapy are
typically administered in combination. Postoperative external-beam irradiation is effective in
improving local control; this may also be used as primary treatment in unresectable cases.
Chemotherapy (most commonly doxorubicin) is added for palliation.

NURSING MANAGEMENT FOR THYROID DISORDERS

Risk for Decreased Cardiac Output: At risk for inadequate blood pumped by the heart to
meet metabolic demands of the body.

Risk factors may include

 Uncontrolled hyperthyroidism, hypermetabolic state

 Increasing cardiac workload
 Changes in venous return and systemic vascular resistance
 Alterations in rate, rhythm, conduction

Desired Outcomes

Maintain adequate cardiac output for tissue needs as evidenced by stable vital signs, palpable
peripheral pulses, good capillary refill, usual mentation, and absence of dysrhythmias.

Nursing Interventions

 Monitor BP lying, sitting, and standing, if able. Note widened pulse pressure.
 Monitor central venous pressure (CVP), if available.
 Assess pulse and heart rate while patient is sleeping.
 Auscultate heart sounds, note extra heart sounds, development of gallops and systolic
murmurs.
 Observe signs and symptoms of severe thirst, dry mucous membranes, weak or
thready pulse, poor capillary refill, decreased urinary output, and hypotension

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Risk for Deficient Fluid Volume: At risk for experiencing vascular, cellular, or
intracellular dehydration.

Common Risk Factors

 Increase in sodium and water excretion with potassium retention

 GI disturbances (e.g., nausea, vomiting, diarrhoea, which can be manifestations of
Addison’s disease).

Common Expected Outcomes

 Patient experiences adequate fluid volume and electrolyte balance as evidenced

by urine output greater than 30 mL/hr, normotensive blood pressure (BP), heart
rate (HR) less than 100 beats/min, consistent weight, and normal skin turgor.

Nursing Interventions Rationale

The patient will have dry skin and mucous

Assess skin turgor and mucous membranes for
membranes. Tenting of the skin will occur.
signs of dehydration.
The tongue may have longitudinal furrows.

A BP drop of more than 15 mm Hg when

changing from supine to sitting position,
Assess vital signs, especially noting BP and HR for
with a concurrent elevation of 15 beats per
orthostatic changes.
min in HR, indicates reduced circulating
fluids.

Urine volume will decrease, urine specific

Assess colour, concentration, and amount of urine. gravity will increase, and colour will be
darker.

Rapid weight loss will occur with fluid

Assess trends in weight.
volume deficit.

Assess for fatigue, sensory deficits, These are signs of hyperkalaemia.

or muscle weakness, which may progress to Aldosterone deficiency leads to potassium
paralysis. retention by the kidneys.

Assess electrocardiogram rhythm, as available, for Signs of hyperkalaemia are sharp peaked T
signs of hyperkalaemia. wave and widened QRS complex.

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 Nursing Interventions Rationale

Abnormal laboratory findings

include hyperkalaemia (related to
aldosterone deficiency and decreased renal
perfusion), hyponatremia (related to
Assess additional indicated laboratory tests.
decreased aldosterone and impaired free
water clearance), and increase in blood urea
nitrogen (related to decreased
glomerular filtration from hypotension).

Observe for petechiae. Patient bruises easily.

As sodium loss increases, extracellular fluid

volume decreases. These interventions are
Encourage oral fluids as the patient tolerates. necessary to prevent fluid volume deficit
because the kidneys are unable to
conserve sodium

Risk for Imbalanced Nutrition: Less Than Body Requirements: Intake of nutrients
insufficient to meet metabolic needs.

Common Risk Factors

 Decreased gastrointestinal (GI) enzymes, causing loss of appetite and decreased

oral intake tolerance
 Decreased gastric acid production
 Nausea, vomiting, diarrhoea

Common Expected Outcomes

 Patient’s nutritional status is optimized as evidenced by maintenance of weight

and adequate dietary intake.

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 Nursing Intervention
Assess appetite and for the presence of nausea,
vomiting, or diarrhoea.
Monitor trends in weight.
Assess foods that patient can tolerate.
Monitor serum glucose levels.
Assess for salt cravings.
Ask the dietician to provide high-protein, low-
carbohydrate, high-sodium diet.
Keep a late-morning snack available.
Suggest need for frequent small meals.
Encourage rest periods after eating.
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Rationale
Cortisol deficiency can impair GI function,
causing anorexia, nausea, and vomiting
This provides documentation of weight loss
trends. Weight loss is a common
manifestation of adrenal insufficiency.
Appetite may increase with preferred and
tolerable foods.
Patients with adrenal insufficiency are likely
to experience hypoglycaemia. It may require
adjustment of insulin dosage.
Aldosterone deficiency causes increased renal
excretion of sodium.
The patient tires because of inadequate
production of hepatic glucagon; the
recommended diet
prevents fatigue, hypoglycaemia,
and hyponatremia. The patient with primary
Addison’s disease needs to increase salt
intake 5 g if any activity causes an increase in
diaphoresis (activities in warm weather).
In case the patient becomes hypoglycaemic
Inadequate caloric intake in meals may
precipitate hypoglycaemia. Promotion of oral
intake maintains adequate blood glucose
levels and nutrition.
This is important to facilitate digestion.
 CONCLUSION
Through the hormones it produces, the thyroid gland influences almost all of the
metabolic processes in your body. Thyroid disorders can range from a small,
harmless goitre (enlarged gland) that needs no treatment to life-threatening cancer.
The most common thyroid problems involve abnormal production of thyroid
hormones. Too much thyroid hormone results in a condition known
as hyperthyroidism. Insufficient hormone production leads to hypothyroidism.
Although the effects can be unpleasant or uncomfortable, most thyroid
problems can be managed well if properly diagnosed and treated.

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 BIBLIOGRAPHY
 Dirksen.H.L. Lewis Medical Surgical Nursing assessment of clinical
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NET REFERENCE

 https://www. Medicinenet.com
 https://medlineplus.gov>thyroid disease
 https://en.m.wikipedia.org
 https:www.webmd.com

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