Case Study Caballes

Ê Ê
We the group of NPD-2 chose this case because we wanted to

elaborate what we already know about the condition and want to
have a more comprehensive elucidation of the case.
Multinodular goiter is a structurally and functionally

heterogeneous thyroid enlargement, most often caused by iodine
deficiency (g gg by which it is a thyroid enlargement
that occurs in more than 10% of a population) or by medication,
malnutrition, inherited defects in thyroid hormone synthesis,
and growth stimulating antibodies. With increasing age thyroid
function may become more autonomous and subclinical
Hyperthyroidism or overt hyperthyroidism may develop.
Multinodularity is consistent with a benign nodular disease,
especially when all nodules have a similar consistency.
Iodine comes from ingestion of food. Iodine content of the

soil determines the iodine content of plants and animals. Iodine
is washed from the soil by water and is eventually washed out to
the oceans. In general, areas with mountain ranges or heavy
rainfall and flooding are iodine deficient. Iodine deficiency
occurs in populations that depend on locally grown food and rely
on vegetable protein rather than on animal or fish protein.
Indications for the treatment of nontoxic multinodular

goiter are: compression of the trachea or esophagus, venous-
outflow obstruction, growth of the goiter, neck discomfort,
cosmetic issues. Therapeutic options are: surgery (bilateral
subtotal thyroidectomy) which is the standard therapy for
patients with nontoxic multinodular goiter. If only one lobe is
enlarged, unilateral lobectomy and isthmectomy may suffice. The
surgical mortality rate associated with bilateral thyroid
operations in patients with nontoxic multinodular goiter is less
than 1%.
Studies have shown that iodine supplementation can

eliminate cretinism and is highly effective in the prevention of
endemic goiter. When urinary iodide falls below 25 micrograms
per gram of creatinine, a palpable goiter occurs in 40-90% of
the population, hypothyroidism occurs in 30-50% of the
population, and cretinism occurs in 1-10% of the population.
More than 2.2 billion people worldwide have some form of

iodine deficiency disorder. Twenty-nine percent of the world's
population lives in a region that has iodine deficiency
(primarily in Asia, Latin American, central Africa, and regions
of Europe). Of those at risk, 655 million were known to have
goiter. In the iodine-deficient regions of the world, goiter is
more common than in the United States. The prevalence of goiter
can be estimated based on the iodine intake of the population.
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As reported by the World Health Organization (WHO), the
United Nations Children's Fund (UNICEF), and the International
Council for the Control of Iodine Deficiency Disorders (ICCIDD),
the absence of iodine deficiency (ie, median urine iodine >100
mg/dL) is associated with a goiter prevalence of less than 5%;
mild iodine deficiency (ie, median urine iodine 50-99 mg/dL),
with a goiter prevalence of 5-20%; moderate iodine deficiency
(ie, median urine iodine 20-49 mg/dL), with a goiter prevalence
of 20-30%; and severe iodine deficiency (ie, median urine iodine
20-49 mg/dL), with a goiter prevalence of greater than 30%.
From the above information, the group came up with:

This study focuses on the thyroid gland, its functions and

the disease, nontoxic multinodular goiter itself. All of these
information will be limited to what the patient manifests.

Within the hospital duty, the student nurses would be able

to obtain necessary information and assess the case of the
patient they chose to present by interviewing and review of
systems through physician¶s finding as well as group¶s
assessment. They would also be able to be effectively provided
quality nursing care and health teachings based on patient¶s
identified problems.

a)Inform the parents or relatives on management of care

through health teachings.
b)Let the significant others understand such condition and
give appropriate action or response with regards to it.
c)Assess over-all condition of the patient in terms of
[cephalo-caudal or head to toe assessment] and or through
review of systems.
d)Increase the level of awareness of the significant others
regarding the importance and significance of health
practices to improve the well-being of the patient.
6
ÊÊ

A.Biographical data
Name: Patient A
Gender: Female
Date of birth: March 23, 1963
Place of birth: ñ Agno, Pangasinan
Age: 47 y/o
Religion: Roman Catholic
Nationality: Filipino
Date admitted: August 2, 2010
Chief complaint: Anterior neck mass
Principal Diagnosis: Nontoxic Multinodular Goiter
Principal Operation Procedure: Thyroidectomy, Total lobectomy,

Right, Subtotal Lobectomy, Left with
Isthmusectomy
B. Patient¶s History
B.1. Present Medical History
The condition of the patient started five months prior to

admission, when the patient noticed a gradually enlarging mass on
the anterior neck area. The mass was movable, non-tender and
soft. There was no noted dysphagia or dyspnea. Patient sought
consultation at Baguio General Hospital and was diagnosed to have
goiter. Three months prior to admission, the patient went for
consultation again at Baguio General Hospital and was scheduled
for thyroidectomy last July 23, 2010 however, operation was
deferred because patient had high blood pressure prior to
operation. She was given amlodipine as her maintenance
medication.
B.2. Past Medical History
Patient is known hypertensive for 1 year and currently

taking in amlodipine as her maintenance medication. Patient has
no diabetes, asthma, allergy to food and drugs.
B.3. Family History
According to the patient they have no hereditary diseases

and or any allergies on both maternal and paternal traces.
B.4. Social and environmental History
Patient does not smoke cigarette. She does not drink

alcoholic beverages.
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In vertebrate anatomy, the $% & or simply, the
$%, is one of the largest endocrine glands in the body, and
is not to be confused with the "parathyroid glands" (a
completely different set of glands). The thyroid gland is found
in the neck, inferior to (below) the thyroid cartilage (also
known as the 'Adam's Apple') and at approximately the same level
as the cricoid cartilage. The thyroid controls how quickly the
body uses energy, makes proteins, and controls how sensitive the
body should be to other hormones.
The thyroid gland participates in these processes by

producing thyroid hormones, principally triiodothyronine (T3) and
thyroxine (T4). These hormones regulate the rate of metabolism
and affect the growth and rate of function of many other systems
in the body. T3 and T4 are synthesized utilizing both iodine as
well as tyrosine. The thyroid gland also produces a hormone
called 'calcitonin', which plays a role in calcium homeostasis.
The thyroid gland is controlled by the hypothalamus and

pituitary (specifically, the anterior pituitary). The thyroid
gland gets its name from the Greek word for "shield", after the
shape of the related thyroid cartilage. The most common problems
of the thyroid gland consist of an over-active thyroid gland,
referred to as 'hyperthyroidism', and an under-active thyroid
gland, referred to as 'hypothyroidism
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The thyroid gland is a butterfly-shape organ and is

composed of two cone-like lobes or wings, ©
g g (right
lobe) and ©
g (left lobe), connected via the isthmus.
The organ is situated on the anterior side of the neck, lying
against and around the larynx and trachea, reaching posteriorly
the oesophagus and carotid sheath. It starts cranially at the
oblique line on the thyroid cartilage (just below the laryngeal
prominence, or 'Adam's Apple'), and extends inferiorly to
approximately the fifth or sixth tracheal ring. It is difficult
to demarcate the gland's upper and lower border with vertebral
levels because it moves position in relation to these during
swallowing.
The thyroid gland is covered by a fibrous sheath, the

©© ©g g, composed of an internal and
external layer. The external layer is anteriorly continuous with
the © g g©gg © and
posteriorolaterally continuous with the carotid sheath. The
gland is covered anteriorly with infrahyoid muscles and
laterally with the sternocleidomastoid muscle. On the posterior
side, the gland is fixed to the cricoid and tracheal cartilage
and cricopharyngeus muscle by a thickening of the fascia to form
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the posterior suspensory ligament of Berry. In variable extent,
Lalouette's Pyramid, a pyramidal extension of the thyroid lobe,
is present at the most anterior side of the lobe. In this
region, the recurrent laryngeal nerve and the inferior thyroid
artery pass next to or in the ligament and tubercle.
Between the two layers of the capsule and on the posterior

side of the lobes there are on each side two parathyroid glands.
The thyroid isthmus is variable in presence and size, and

can encompass a cranially extending pyramid lobe (©

© or g ©), remnant of the
thyroglossal duct. The thyroid is one of the larger endocrine
glands, weighing 2-3 grams in neonates and 18-60 grams in
adults, and is increased in pregnancy.
The thyroid is supplied with arterial blood from the

superior thyroid artery, a branch of the external carotid
artery, and the inferior thyroid artery, a branch of the
thyrocervical trunk, and sometimes by the thyroid ima artery,
branching directly from the brachiocephalic trunk. The venous
blood is drained via superior thyroid veins, draining in the
internal jugular vein, and via inferior thyroid veins, draining
via the ©g g in the left brachiocephalic
vein.
Lymphatic drainage passes frequently the lateral deep

cervical lymph nodes and the pre- and parathracheal lymph nodes.
The gland is supplied by parasympathetic nerve input from the
superior laryngeal nerve and the recurrent laryngeal nerve.
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In the fetus, at 3±4 weeks of gestation, the thyroid gland

appears as an epithelial proliferation in the floor of the
pharynx at the base of the tongue between the tuberculum impar
and the copula linguae at a point latter indicated by the
foramen cecum. The thyroid then descends in front of the
pharyngeal gut as a bilobed diverticulum through the
thyroglossal duct. Over the next few weeks, it migrates to the
base of the neck. During migration, the thyroid remains
connected to the tongue by a narrow canal, the thyroglossal
duct.
Thyrotropin-releasing hormone (TRH) and thyroid-stimulating

hormone (TSH) start being secreted from the fetal hypothalamus
and pituitary at 18-20 weeks of gestation, and fetal production
of thyroxine (T4) reach a clinically significant level at 18±20
weeks. Fetal triiodothyronine (T3) remains low (less than
15 ng/dL) until 30 weeks of gestation, and increases to 50 ng/dL
at term. Fetal self-sufficiency of thyroid hormones protects the
fetus against e.g. brain development abnormalities caused by
maternal hypothyroidism. However, preterm births can suffer
neurodevelopmental disorders due to lack of maternal thyroid
hormones due their own thyroid being insufficiently developed to
meet their postnatal needs.
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The portion of the thyroid containing the parafollicular C
cells, those responsible for the production of calcitonin, are
derived from the 4th pharyngeal pouch endoderm. This is first
seen as the ultimobranchial body, which joins the primordial
thyroid gland during its descent to its final location in the
anterior neck.
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At the microscopic level, there are three primary features

of the thyroid:

The thyroid is composed of spherical
follicles that selectively absorb iodine
(as iodide ions, I-) from the blood for
production of thyroid hormones. Twenty-
five percent of all the body's iodide
ions are in the thyroid gland. Inside
Follicles
the follicles, colloid serve as a
reservoir of materials for thyroid
hormone production and, to a lesser
extent, act as a reservoir for the
hormones themselves. Colloid is rich in
a protein called thyroglobulin.
The follicles are surrounded by a single
layer of thyroid epithelial cells, which
secrete T3 and T4. When the gland is not
Thyroid epithelial cells secreting T3/T4 (inactive), the
(or "follicular cells") epithelial cells range from low columnar
to cuboidal cells. When active, the
epithelial cells become tall columnar
cells.
Scattered among follicular cells and in
spaces between the spherical follicles
Parafollicular cells
are another type of thyroid cell,
(or "C cells")
parafollicular cells, which secrete
calcitonin.
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The primary function of the thyroid is production of the

hormones triiodothyronine (T3), thyroxine (T4), and calcitonin.
Up to 80% of the T4 is converted to T3 by peripheral organs such
as the liver, kidney and spleen. T3 is several times more
powerful than T4, which is largely a prohormone, perhaps fouror
even ten times more active.
'

The system of the thyroid hormones T3 and T4.
Thyroxine (T4) is synthesised by the follicular cells from free

tyrosine and on the tyrosine residues of the protein called
thyroglobulin (Tg). Iodine is captured with the "iodine trap" by
the hydrogen peroxide generated by the enzyme thyroid peroxidase
(TPO) and linked to the 3' and 5' sites of the benzene ring of
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the tyrosine residues on Tg, and on free tyrosine. Upon
stimulation by the thyroid-stimulating hormone (TSH), the
follicular cells reabsorb Tg and cleave the iodinated tyrosines
from Tg in lysosomes, forming T4 and T3 (in T3, one iodine atom
is absent compared to T4), and releasing them into the blood.
Deiodinase enzymes convert T4 to T3. Thyroid hormones that are
secreted from the gland is about 80-90% T4 and about 10-20% T3.
Cells of the brain are a major target for the thyroid

hormones T3 and T4. Thyroid hormones play a particularly crucial
role in brain maturation during fetal development. A transport
protein that seems to be important for T4 transport across the
blood-brain barrier (OATP1C1) has been identified.[18] A second
transport protein (MCT8) is important for T3 transport across
brain cell membranes.[18]
Non-genomic actions of T4 are those that are not initiated

by liganding of the hormone to intranuclear thyroid receptor.
These may begin at the plasma membrane or within cytoplasm.
Plasma membrane-initiated actions begin at a receptor on the
integrin alphaV beta3 that activates ERK1/2. This binding
culminates in local membrane actions on ion transport systems
such as the Na(+)/H(+) exchanger or complex cellular events
including cell proliferation. These integrins are concentrated
on cells of the vasculature and on some types of tumor cells,
which in part explains the proangiogenic effects of
iodothyronines and proliferative actions of thyroid hormone on
some cancers including gliomas. T4 also acts on the
mitochondrial genome via imported isoforms of nuclear thyroid
receptors to affect several mitochondrial transcription factors.
Regulation of actin polymerization by T4 is critical to cell
migration in neurons and glial cells and is important to brain
development.
T3 can activate phosphatidylinositol 3-kinase by a

mechanism that may be cytoplasmic in origin or may begin at
integrin alpha V beta3.
In the blood, T4 and T3 are partially bound to thyroxine-

binding globulin (TBG), transthyretin, and albumin. Only a very
small fraction of the circulating hormone is free (unbound) - T4
0.03% and T3 0.3%. Only the free fraction has hormonal activity.
As with the steroid hormones and retinoic acid, thyroid hormones
cross the cell membrane and bind to intracellular receptors (Į1,
Į2, ȕ1 and ȕ2), which act alone, in pairs or together with the
retinoid X-receptor as transcription factors to modulate DNA
transcription[1].
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The production of thyroxine and triiodothyronine is

regulated by thyroid-stimulating hormone (TSH), released by the
anterior pituitary. The thyroid and thyrotropes form a negative
feedback loop: TSH production is suppressed when the T4 levels
are high, and vice versa. The TSH production itself is modulated
by thyrotropin-releasing hormone (TRH), which is produced by the
hypothalamus and secreted at an increased rate in situations
such as cold (in which an accelerated metabolism would generate
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more heat). TSH production is blunted by somatostatin (SRIH),
rising levels of glucocorticoids and sex hormones (estrogen and
testosterone), and excessively high blood iodide concentration.
An additional hormone produced by the thyroid contributes

to the regulation of blood calcium levels. Parafollicular cells
produce calcitonin in response to hypercalcemia. Calcitonin
stimulates movement of calcium into bone, in opposition to the
effects of parathyroid hormone (PTH). However, calcitonin seems
far less essential than PTH, as calcium metabolism remains
clinically normal after removal of the thyroid (thyroidectomy),
but not the parathyroids.
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N/A - thyroid
Radioiodine scan (gamma camera) N/A
contrasted images
Free thyroxine fraction FT4F 0.03-0.005%
Serum thyroxine T4 4.6-12.0 ug/dl
Thyroid hormone binding ratio THBR 0.9-1.1
Free Thyroxine index FT4I 4-11
Free Triiodothyronine l FT3 230-619 pg/d
Free T3 Index FT3I 80-180
12-20 ug/dl T4 +1.8
Thyroxine-binding globulin TBG
ugm
9-30 uIU/ml at 20-30
TRH stimulation test Peak TSH
min
Serum thyroglobulin l Tg 0-30 ng/m
Thyroid microsomal antibody
TMAb Varies with method
titer
Thyroglobulin antibody titer TgAb Varies with method
À uU/ml = microunit per milliliter

À ng/dl = nanograms per deciliter
À ug, ugm = micrograms
À pg/d = picograms per day
À uIU/ml = micro international unit per milliliter
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In areas of the world where iodine is lacking in the diet

the thyroid gland can become considerably enlarged, a condition
called 'endemic goitre'. Pregnant women who have diet which is
severely deficient of iodine can give birth to infants who can
present with thyroid hormone deficiency, manifesting in problems
of physical growth and development as well as brain development
(a condition referred to as 'endemic cretinism'), and is one
cause of congenital hypothyroidism. In many developed countries
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newborns are routinely tested for congenital hypothyroidism as
part of newborn screening. Children with congenital
hypothyroidism are treated supplementally with levothyroxine,
which facilitates normal growth and development.
Thyroxine is critical to the regulation of metabolism and

growth throughout the animal kingdom. Among amphibians, for
example, administering a thyroid-blocking agent such as
propylthiouracil (PTU) can prevent tadpoles from metamorphosing
into frogs; in contrast, administering thyroxine will trigger
metamorphosis.
Because the thyroid concentrates this element, it also

concentrates various radioactive isotopes of iodine produced by
nuclear fission. In the event of large accidental releases of
such material into the environment, the uptake of radioactive
iodine isotopes by the thyroid can, in theory, be blocked by
saturating the uptake mechanism with a large surplus of non-
radioactive iodine, taken in the form of potassium iodide
tablets. One consequence of the Chernobyl disaster was an
increase in thyroid cancers in children in the years following
the accident.
The use of iodised salt is an efficient way to add iodine

to the diet. It has eliminated endemic cretinism in most
developed countries, and some governments have made the
iodination of flour, cooking oil, and salt mandatory. Potassium
iodide and sodium iodide are typically used forms of
supplemental iodine.
As with most substances, either too much or too little can

cause problems. Recent studies on some populations are showing
that excess iodine intake could cause an inceased prevelence of
autoimmune thyroid disease resulting in permanent
hypothyroidism.
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Ê ##"Êº"
Simple nontoxic goiter, which may be diffuse or nodular, is noncancerous hypertrophy of the thyroid without
hyperthyroidism, hypothyroidism, or inflammation. Except in severe iodine deficiency, thyroid function is normal and
patients are asymptomatic except for an obviously enlarged, nontender thyroid. Diagnosis is clinical and with
determination of normal thyroid function. Treatment is directed at the underlying cause, but partial surgical removal
may be required for very large goiters.

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Some thyroid glands have multiple nodules, referred to as multinodular goiters; this is generally a benign
condition. Multinodular goiters are most common in post-menopausal women, and although it seems
illogical, goiters can be seen in both hypothyroidism and hyperthyroidism.
There are two types of goiters: endemic and sporadic. Endemic goiters occur specifically in geographic
areas known as "goiter belts," which are areas with soil and water deficient in iodine. Generally, these are
areas without access to salt water and seafood; historically, in the U.S. the Midwest and Great Lakes
regions have been considered "goiter belts." Coastal areas have a much lower incidence of goiters.
Sporadic goiters are not associated with specific geographical locations. They are thought to be caused
by one of three factors [11] :
À £bnormal iodine metabolism, probably of genetic origin

À Êngestion of large amounts of goitrogens from food sources, such as cabbage, soybeans, peanuts, peaches,
peas, strawberries, radishes, rutabagas, and spinach
À Êngestion of pharmaceutical goitrogens, such as glucocorticoids, dopamine, lithium, rifampin, adrenergic
antagonists, methimazole, and thiocarbanides
Êf goiters are diagnosed, this is an excellent opportunity for patient education regarding iodine
consumption. £dults generally require a minimum of 150 mcg of iodine daily, but pregnant and
breastfeeding women require an additional 100 mcg daily. Êodized salt contains 1 part iodine to 100,000
parts of salt. The average £merican ingests 6.2 grams of salt a day; this equates to 474 mcg of iodine if
the salt is iodized [11] .
Ê 3
The thyroid gland is controlled by thyroid-stimulating
hormone (TSH; also known as thyrotropin), secreted from the
pituitary gland, which in turn is influenced by the thyrotropin-
releasing hormone (TRH) from the hypothalamus. TSH permits
growth, cellular differentiation, and thyroid hormone production
and secretion by the thyroid gland. Thyrotropin acts on TSH
receptors located on the thyroid gland. Serum thyroid hormones
levothyroxine and triiodothyronine feed back to the pituitary,
regulating TSH production. Interference with this TRH-TSH
thyroid hormone axis causes changes in the function and
structure of the thyroid gland. Stimulation of the TSH receptors
of the thyroid by TSH, TSH-receptor antibodies, or TSH receptor
agonists, such as chorionic gonadotropin, may result in a
diffuse goiter. When a small group of thyroid cells,
inflammatory cells, or malignant cells metastatic to the thyroid
is involved, a thyroid nodule may develop.
A deficiency in thyroid hormone synthesis or intake leads

to increased TSH production. Increased TSH causes increased
cellularity and hyperplasia of the thyroid gland in an attempt
to normalize thyroid hormone levels. If this process is
sustained, a goiter is established. Causes of thyroid hormone
deficiency include inborn errors of thyroid hormone synthesis,
iodine deficiency,1 and goitrogens.
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Goiter may result from a number of TSH receptor agonists.
TSH receptor stimulators include TSH receptor antibodies,
pituitary resistance to thyroid hormone, adenomas of the
hypothalamus or pituitary gland, and tumors producing human
chorionic gonadotropin.
#Ê Ê
Age (over 40 y/o), gender (female), and

goitrogens(like cabbage).
Iodine deficiency
Decreased production of thyroid

hormones: thyroxine (')
and triiodothyronine ( )
Stimulates hypothalamus to release

thyrotropin releasing hormone
(TRH)
Stimulate anterior pituitary gland

to release thyroid stimulating
hormone (TSH)
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Compensated increase hormonal
production (T3 and T4)
Hyperplasia of
local follicles
Enlarged thyroid/ nodular

goiter
Compression of the Subtotal

trachea and esophagus thyroidectomy
Difficulty Difficulty
swallowing breathing
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3 The primary $ &3 The following
ÀKakaopera ko defense of the 3 ÀMonitor vital ÀServe as the objective was
lang kahapon body against ÀAfter 30 signs. baseline data met during the
sa lalamunan infection is the minutes of for untoward shift:
ko´ skin. So, any proper nursing changes of the ÀThe patient
break in the interventions patient¶s was able to
3 continuity of the patient status. verbalize
ÀWith intact this organ will will be able ÀAssess for ÀTo determine understanding
dressing on increase the to verbalize characteristic sign of of individual
the wound. risk of understanding s of wound. inflammation risk factors
infection. of individual or presence of as evidenced
ÀWound is
Like in the case risk factors infection. by justifying
characterized
of our patient, as evidenced $
3 if her
as not
she had by justifying activities
swollen, not ÀMaintain ÀTo eliminate
undergone a if her will prevent
erythematous, sterile pathogenic
surgical activities infection.
no signs of technique for microorganisms
procedure. The will prevent
bleeding and all , thus reduce
surgical infection.
dry. procedures. cross-
incision is
ÀWith contamination.
considered to be
temperature of discontinuity on ÀAdminister ÀTo prevent and

36.8oC. the skin and it prophylactic kill

serving as the antibiotics as pathogenic

portal of entry ordered. organisms.

for
& microorganism. 3
º& The following
&3 ÀInstruct on ÀTo minimize
3 objective was
ÀRisk for proper hygiene pathogenic partially met
ÀWithin 24
infection especially on microorganisms because the
hours of
related to hand washing. , universal patient was
proper nursing
inadequate precaution to discharge at the
interventions
primary avoid second day of
the patient
6
defense. will be able infection the rotation:
to demonstrate ÀEncourage to ÀTo promote
lifestyle include wound healing. ÀThe patient
changes to protein and partially
prevent or Vitamin C rich demonstrated
reduce the food in the lifestyle
risk of diet. changes to
infection as prevent or
evidenced by reduce the
practicing risk of
proper infection as
hygiene. evidenced by
practicing
proper
hygiene.
u
ÊÊÊ - - "
DRUG NAME CLASSIFICATION ACTION INDICATION ADVERSE REACTION NURSING

CONSIDERATION
GENERIC NAME: Nonsteroidal Thought to To relieve CNS: dizziness, Patients

CELECOXIB Anti- inhibit signs and headache, allergic to or
inflammatory prostaglandin symptoms of insomnia with a history
BRAND NAME: drugs synthesis, osteoarthritis CV: peripheral of
CELEBREX impeding To relieve edema anaphylactic
cyclooxygenase-2 signs and EENT: reactions to
(COX-2), to symptoms of pharyngitis, sulfonamides,
400mg OD produce anti- rheumatoid rhinitis, aspirin, or
inflammatory, arthritis sinusitis other NSAIDs
analgesic, and Acute pain and GI: abdominal may be
anti pyretic primarily pain, diarrhea, allergic to
effects. dysmenorrhea dyspepsia, this drug.
flatulence, watch for
nausea signs and
SKIN: rash symptoms of
overt
bleeding.
- NSAIDs such
as celecoxib
can cause
fluid
retention;
monitor
patient with
hypertension,
edema, or
heart failure.
uc
GENERIC NAME: Anti-anginals Inhibits calcium Chronic stable CNS: headache, Monitor
AMLODIPINE drug ion influx angina, fatigue, patient
across cardiac vasospasm dizziness, light carefully.
BRAND NAME: and smooth- angina headedness, Some patients,
NORVASC muscle cells, Hypertension paresthesia especially
thus decreasing CV: edema, those with
10mg per tab. 1 myocardial flushing, severe
tab OD contractility palpitations obstructive
and oxygen GI: nausea, coronary
demand; also abdominal pain artery
dilates coronary GU: sexual disease, have
artery difficulties developed
Musculoskeletal: increased
muscle pain frequency,
Respiratory: duration, or
dyspnea severity of
SKIN: rash, angina or
pruritus acute MI after
initiation of
calcium
channel
blocker
therapy.
Monitor blood
pressure
frequently
during
initiation of
therapy.
Because drug-
induced
vasodilation
has a gradual
u6
onset, acute
hypotension is
rare.
GENERIC NAME: Anti-ulcer drugs Blocks proton Healing of CNS: headache Consider
RABEPRAZONE pump activity erosive or additional
and gastric acid ulcerative courses of
BRAND NAME: secretion by gastroesophage therapy if
ACIPHEX inhibiting al reflux duodenal ulcer
gastric disease (GERD) or GERD isn¶t
20mg 1 tab OD hydrogen- Healing of healed after
potassium duodenal first course
adenosine ulcers of therapy.
triphosphatase Symptomatic If H. pylori
at secretory GERD, eradication is
surface of including unsuccessful,
gastric parietal daytime and do
cells. nighttime susceptibility
heartburn testing. If
H. pylori patient is
eradication, resistant to
to reduce the clarithromycin
risk of or
duodenal ulcer susceptibility
recurrence testing isn¶t
possible,
expect to
start therapy
using a
different
antimicrobial.
uu
GENERIC NAME: Vitamin B- A coenzyme that Megaloblastic CNS: Nausea Determine
MECOBALAMINE complex stimulates anemia GI: diarrhea reticulocyte
metabolic SKIN: skin rash count,
BRAND NAME: function and is hematocrit,
METHYCOBAL needed for cell vitamin B12,
replication , iron, and
hematopoiesis, folate levels
500mg 1 tab TID and before
nucleoprotein beginning
and myelin therapy
synthesis Obtain a
sensitivity
test history
before
administration
GENERIC NAME: Macrolide URTI, LRTI, Skin CNS: dizziness, Monitor

ROXITHROMYCIN and soft tissue headache patient¶s
infections GI: GI vital signs as
BRAND NAME: disturbances the therapy
RULID begins
Watch out for
allergic
300mg 1 cap OD reaction

uG
Ê6 º-Ê
A goiter, also called a bronchocele, is a swelling in the
thyroid gland, which can lead to a swelling of the neck or
larynx (voice box). Goitre usually occurs when the thyroid gland
is not functioning properly. In general, goiter(goiter)
unassociated with any hormonal abnormalities will not cause any
symptoms aside from the presence of anterior neck mass. However,
for particularly large masses, compression of the local
structures may result in difficulty in breathing or swallowing.
In those presenting with these symptoms, malignancy must be
considered. Thyroidectomy was performed to relieve obstruction.
Discharge may be delayed if the living situation is high risk or
if non adherence is likely. Consulting with social service
workers in the hospital or community health nursing agency is
important to ensure that the client is discharged to the
appropriate environment with supervision.
u0
6 Ê
Recommendations are formulated with the aid of the
aforementioned conditions and conclusions, and these basically,
consist of comments and suggestions of the group facilitate
supportive care for the patient and to prevent further
complications. As we continually update our scientific basis and
as we integrate more and more precise treatment modalities,
intensive management, the risk for long term complications from
thyroidectomy can be reduced.
$ #

À Nursing management does not only involve proper
administration of drugs and doing paper work but it also
comprises bedside care, providing comfort and promoting
rest. The staff should continue the strict and honest
monitoring of the patient¶s status.
À The hospital is the primary health care provider; they are
expected to meet client¶s individual needs in order to
achieve optimum health, treat illness and prevent future
infirmities. It is expected that they will continue
rendering health care to patients in its best as well as
letting the nursing student handle cases as thyroidectomy,
not only for them to be exposed but also to provide the
nursing interventions that are applicable for the wellness
of the patient.
uÿ
$ &
À The student nurses play an important role in caring for
their patients. Students should know their patients well.
Detailed and truthful assessment should be learned and
enhanced so that every problem of the patient is identified
and attended to. Therapeutic communication promotes rapport
between the nurse and the patient that facilitates
information extraction. A compassionate and empathetic
counseling is more effective.
À Students should have the initiative and the effort to study
and be familiar with the patient¶s case as well as the
drugs. It is essential to read and understand the chart,
doctor¶s orders and the special considerations given to the
patient. They should be vigilant in reporting any
abnormalities and in providing needed care to the patients.
À It is suggested that the student take time out to do extra
research or additional readings not only to learn but also
to be able to share the right and needed information with
others.
$ -%
À The university should continue its good work in promoting
and delivering quality education to the nursing students.
This will strengthen the nursing student¶s capabilities,
skills and knowledge uplifting the standard of nursing
u
education in this particular institution, as well as
providing available resources to enhance the exposure that
may help the students apply what they have learned in the
medical field.
u
6Ê Ê
u

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Ê  Ê

We the group of NPD-2 chose this case because we wanted to

Multinodular goiter is a structurally and functionally

Iodine comes from ingestion of food. Iodine content of the

Indications for the treatment of nontoxic multinodular

Studies have shown that iodine supplementation can

More than 2.2 billion people worldwide have some form of

From the above information, the group came up with:

This study focuses on the thyroid gland, its functions and

   

Within the hospital duty, the student nurses would be able

a)Inform the parents or relatives on management of care

Date of birth: March 23, 1963

Place of birth: ñ Agno, Pangasinan

Religion: Roman Catholic

Date admitted: August 2, 2010

Chief complaint: Anterior neck mass

Principal Diagnosis: Nontoxic Multinodular Goiter

Principal Operation Procedure: Thyroidectomy, Total lobectomy,

B. Patient¶s History

B.1. Present Medical History

The condition of the patient started five months prior to

B.2. Past Medical History

Patient is known hypertensive for 1 year and currently

B.3. Family History

According to the patient they have no hereditary diseases

B.4. Social and environmental History

Patient does not smoke cigarette. She does not drink

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  ñ       

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       G 

       

               

ñ     

ñ       0ÿ        

The thyroid gland participates in these processes by

The thyroid gland is controlled by the hypothalamus and

The thyroid gland is a butterfly-shape organ and is

The thyroid gland is covered by a fibrous sheath, the

Between the two layers of the capsule and on the posterior

The thyroid isthmus is variable in presence and size, and

The thyroid is supplied with arterial blood from the

Lymphatic drainage passes frequently the lateral deep

In the fetus, at 3±4 weeks of gestation, the thyroid gland

Thyrotropin-releasing hormone (TRH) and thyroid-stimulating

At the microscopic level, there are three primary features

The primary function of the thyroid is production of the

The system of the thyroid hormones T3 and T4.

Thyroxine (T4) is synthesised by the follicular cells from free

Cells of the brain are a major target for the thyroid

Non-genomic actions of T4 are those that are not initiated

T3 can activate phosphatidylinositol 3-kinase by a

In the blood, T4 and T3 are partially bound to thyroxine-

  ' &

The production of thyroxine and triiodothyronine is

An additional hormone produced by the thyroid contributes

$%  %  (  & 

Ê Ê

a)Inform the parents or relatives on management of care

B. Patient¶s History

ÊÊÊ c

ñ ñ ñ

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$% % ( &

&

À uU/ml = microunit per milliliter

&

À £bnormal iodine metabolism, probably of genetic origin

-Ê º 4Êº5

GENERIC NAME: Nonsteroidal Thought to To relieve CNS: dizziness, Patients

GENERIC NAME: Macrolide URTI, LRTI, Skin CNS: dizziness, Monitor

À Nursing management does not only involve proper

À The hospital is the primary health care provider; they are

À The student nurses play an important role in caring for

À Students should have the initiative and the effort to study