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I. Introduction
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 (endemic goiter 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'spopulation 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:
Scope & Delimination
This study focuses on the thyroid gland, its functions andthe disease, nontoxic multinodular goiter itself. All of these
information will be limited to what the patient manifests.
General objective
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.
S pecific Objectives
a) Inform the parents or relatives on management of carethrough health teachings.
b) Let the significant others understand such condition andgive 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.
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II. Patient¶s Profile
A. Biographical data
Name: Patient A
Gender: Female
Date of birth: March 23, 1963
Place of birth: Patar, 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 tooperation. 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 diseasesand 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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III. 13 AREA S OF A SSESSM ENT
CHAPTER 3
13 AREAS OF ASSESSMENT
1. PSYCHOSOCIAL STATUS
Patient A roots f rom Patar, Agno Pangasinan. She is 47 years of age, f emale, and married.
Based on Erik Erikson's Psychosocial Theory, the patient belongs to integrity versus despair, wherein
at this age there an acceptance of worth and uniqueness of ones own lif e and even acceptance of
death but there some negative resolution by having sense of loss and contempt f or others. She is
dependent on her f amily and currently living with them. She is a Roman Catholic and based on her
watcher, they have no religious practices that could interf ere with medical interventions. Their
f amily is in the middle classif ication in terms of socio-economic status.
2. MEN TAL AND EM OTION AL STATUS
The patient was conscious and able to response clearly to both verbal and non-verbal
stimuli. She is well oriented to f our spheres such as time, place, self and person. Patient A is able
to interact with the people around her. She is cooperative with the instructions given to her like
directions of giving medication. She can read, write and respond to any questions being asked.
Emotionally, patient shows signs of irritation regarding her condition, she was anxious regarding her
condition at the same time f earf ul.
3. ENV IRONMEN TAL STATUS
Patient A, conf ined at the ENT unit wherein she stays in a ward. It is near the nurse's
station. She is uncomf ortable within the ward, whichmade it not conducive f or her to rest. There is
also adequate lighting and ventilation. The f amily of the patient is not satisf ied with the
environment because of the inconvenient setting of the hospital. They are not able to comply with
properwaste segregation.
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4. SEN SORTY STATUS
Visual: Patient A is not wearing glasses. She has good eyesight as observed in its
ability to perceive objects. She has a good papillary response to light.
Olfactory: Nose is intact and neither inf lammation nor lesion is seen. Her nares are
patent and can determine unpleasant odors f rom pleasant one. There are no obstruction based on our
observation. She is able to determine the scent of alcohol or perf umes.
Auditory: She can hear clearly and she is able to distinguished voices of f amily, doctors,
nurses, and students.No discharges noted.
Gustatory: Patient A is able to discriminate tastes and odors.
5. M OTOR STATUS
We used Barthels Index in assessing patient motor status. The patient scores 55 out of 100.
In f eeding, the patient needs some assistance in preparing f or her f ood giving her the score of
f ive. She is able to bath independently. She can groomed herself independently like brushing
and combing. In dressing, she needs some help but can do about half unaided. She is not able to
def ecate during her f our days of stay in the hospital. Bladder is continent. Need some help, but
can do something alone with regards to toilet use. She belongs in ma jor help classif ication in
transf erring, wherein she needs one or two people to assist her but she is able to sit. In mobility
patient can walk with one person around her. We used a chair in exchange of stairs f or the
patient to be able to sit properly in her bed giving her a score of 5 wherein she needs some help.
6. N UTRITION AL STATUS
During our 8 hours shif t the patient was in DAT diet. Patient was able to consume the f oods
thatwere served.
7 . E LI M I N ATION STATUS
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The patient is able to urinate draining to yellow colored urine. During the shif t she is able to
urinate 350-750cc. The patient did not def ecate in her f our days of stay in the hospital.
VIII. FLUID AND ELECTROLYTE STATUS
The patient has an IVF of D5LRS 1L inf using well on the lef t hand. She has consumed two bottles of
above IVF during our shif t. Patient A claims that she consumes 5-7 glasses of water a day. Her lips are
slightly dry and there are no f urther signs of dehydration.
IX. CIRCULATORY STATUS
The patient's pulse rate ranges f rom 78-84 bpm. Her blood pressure is withn the range of normal, with a
systole ranging f rom 110-120mmHg and a diastole ranging f rom 70-90mmHg.
X. TEMPERATURE STATUS
The room has proper ventilation.Her body temperature s ranging f rom 36.4-37.2 degrees Celsius.
XI. INTEGUMENTARY STATUS
The patient's skin tone is f air and has no history of any skin allergies. Nails are trimmed and clean prior
to operation. Her hair is evenly distributed. There is no unpleasant odor noted f rom the patent. There
are no signs of inf ecton such as f ungal inf ections. With discontinuity of skin integrity due to the
operation perf ormed to her, Thyroidectomy. but upon assessment to the operative site, there were no
redness and no swelling and therewere no signs of bleeding, dry sutured wound noted.
XII. RESPIRATORY STATUS
Patient's airway is patent. Patient breaths 17-21 cycles per minute regular. There is no diff iculty of
breathing and does not use respiratorymuscle when breathing.
XIII. COMFORT AND REST STATUS
Patent X sleeps around 5-6 hours and does take a nap in the af ternoon. She claims that she is irritated
sometimes because of the changing of weather. Weakness is noted f rom the patient particularly when
trying to sit, stand andwalk due to the discomf ort and pain f elt on the operative site. Painwas described
by the patient as continuous pricking and burning pain aggravated by sudden movements of the neck,
when sitting, walking and standing. she rated pain as 4/10 in the pain scale of 10 as the highest and 1 as
the lowest. Aside f rom verbalizing what she f elt, we also noted that she grimaces and with guarding
behavior on the operative site.
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IV. L ABORATORY FINDINGS AND INTERPRETATION
Laboratory Result
1.) CHEST PA>No Active lung Infiltrate.
>Heart is not enlarged by C-T ratio.
>Lung Vascular is within normal.
>Hemidiaphagms and sulci are unremarkable.
>Bones are not unusual.
*Remarks: Negative Chest.
2.) NECK ULTRASOUND
Clinical diagnosis:Hyperthyrodism
>the right thyroid lobe is enlarged with a homogenous mass with central hyroechoic area
measuring 3.65 x 3.03
>No significant vascular flow on color flow studies
>The left lobe is normal.
>The trachea is midline.
>Major neck vessels are unremarkable.
y IMPRESION
>Complex thyroid mass, right
3.) POST OPERATIVE DIAGNOSIS:
Anterior neck mass, R/O malignancy
>Operation Performed: FNAB>Specimen: anterior neck mass aspirate
>CYTHOPHATOLOGIC DIAGNOSIS
>Suspicious for malignant cells
Comment : A papillary carcinoma cannot be entirely ruled out: suggest open biopsy.
>Gross Description : The specimen consist of four (4) smears that are taken for study.
>Microscopic Pathology . The cytology smears show individually scattered and
several cluster of fallicuiar cells exhibiting faint nuclear groovesand inclusions with
interspersed acute and chronic inflammatory cells set against a hemorrihagic
background .
4.Method: Direct Chemiluminescence
TEST RESULT REFERENCE INTERPRETATION
TSH, 3rd
Generation 1.74 0.35-5.50 u/U/mL Normal
FREE T4 1.19 0.89-1.76ng/dL Normal
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5. HEMATOLOGY : AUG. 02-2010
DETERMINATION RESULT NORMALVALUES INTERPRETATION
HEMOGLOBIN 144-147 120-160 g/L Normal
HEMATOCRIT 0.43-0.44 0.37-0.47 Vol% Normal
LEUCOCYTES
(WBC)
7.8-8.4 5-10X10 g/L Normal
NEUTROPHILS 0.60-0.65 0.50-0.70 Normal
LYMPHOCYTES 00.35-0.40 0.20-0.40 Normal
PLATELET 309-404 150-440X10 g/L Normal
Clotting time 4¶10´ 2-7 mins. Normal
Bleeding time 3¶50´ 1-6 mins. Normal
All the CBC result is normal that indicates no pathogens are present in the blood.
6. URINALYSIS: Aug. 02,2010
PHYSICAL & CHEMICAL MICROSCOPIC
COLOR- light yellow PUS CELL- 0-3/HPF
APPEARANCE- slightly turbid RBC- 0-2/HPF
REACTION- acidic MUCUS THREADS- few
Sp.Grams- 1.015 EPITHELIAL CELLS- few
ALBUMIN- (-) AMORPHOUS/PHOSPHATES- few
SUGAR-(-)
URINALYSIS: July 20,2010
PHYSICAL & CHEMICAL MICROSCOPIC
COLOR- light yellow PUS CELL- 1-3/HPF
APPEARANCE- turbid RBC- 0-2/HPF
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REACTION- acidic MUCUS THREADS- few
Sp.Grams- 1.015 EPITHELIAL CELLS- few
ALBUMIN- (-) AMORPHOUS/PHOSPHATES- few
SUGAR-(-)
The urinalysis result interprets as light yellow, turbid in appearance and acidic reaction that
indicates normal result. No signs of bateria present in the urine.
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V. ANATO M Y AND PHYSIOLOGY
Thyroid
In vertebrate anatomy, the thyroid gland or simply, thethyroid , 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 byproducing 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 theshape 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
Anatomy
The thyroid gland is a butterfly-shape organ and is
composed of two cone-like lobes or wings, lobus dexter (right
lobe) and lobus sinister (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
capsula g landulae thyroidea, composed of an internal and
external layer. The external layer is anteriorly continuous withthe lamina pretrachealis fasciae cervicalis 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 (lobus
pyramidalis or processus pyramidalis), 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 plexus thyroideus impar 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 thesuperior laryngeal nerve and the recurrent laryngeal nerve.
Embryological development
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 thebase 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 thefetus 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.
Histology
At the microscopic level, there are three primary features
of the thyroid:
Feature Description
Follicles
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
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.
Thyroid epithelial cells
(or "follicular cells")
The follicles are surrounded by a single
layer of thyroid epithelial cells, which
secrete T3 and T4. When the gland is notsecreting T3/T4 (inactive), the
epithelial cells range from low columnar
to cuboidal cells. When active, the
epithelial cells become tall columnar
cells.
Parafollicular cells
(or "C cells")
Scattered among follicular cells and in
spaces between the spherical follicles
are another type of thyroid cell,
parafollicular cells, which secrete
calcitonin.
Physiology
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.
T3 and T4 production and action
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 thyroidreceptors 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 verysmall 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 (1,
2, 1 and 2), which act alone, in pairs or together with the
retinoid X-receptor as transcription factors to modulate DNA
transcription[1].
T3 and T4 regulation
The production of thyroxine and triiodothyronine isregulated 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.
Thyroid function laboratory tests - Normal ranges
Test Abbreviation Normal Ranges
Serum thyrotropin/Thyroid-stimulating hormone TSH 0.5-6 uU/ml
Free Thyroxine FT4 0.7-1.8 ng/dl
Serum Triiodothyronine T3 80-180 ng/dl
Radioactive Iodine-123 uptake RAIU 10-30%
Radioiodine scan (gamma camera) N/AN/A - thyroid
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
Thyroxine-binding globulin TBG12-20 ug/dl T4 +1.8
ugm
TRH stimulation test Peak TSH9-30 uIU/ml at 20-30
min
Serum thyroglobulin l Tg 0-30 ng/m
Thyroid microsomal antibody
titerTMAb Varies with method
Thyroglobulin antibody titer TgAb Varies with method
y uU/ml = microunit per milliliter
y ng/dl = nanograms per deciliter
y ug, ugm = micrograms
y pg/d = picograms per day
y uIU/ml = micro international unit per milliliter
Significance of iodine
In areas of the world where iodine is lacking in the dietthe 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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VI. PATHOPHYSIOLOGY
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.
Simple nontoxic goiter, the most common type of thyroid enlargement, is frequently noted at puberty, during
pregnancy, and at menopause. The cause at these times is usually unclear. Known causes include intrinsic thyroid
hormone production defects and, in iodine-deficient countries, ingestion of foods that contain substances that inhibit
thyroid hormone synthesis (goitrogens, eg, cassava, broccoli, cauliflower, cabbage). Other causes include the use of
drugs that can decrease the synthesis of thyroid hormone (eg, amiodarone or other iodine-containing
compounds, lithium ).
Iodine deficiency is rare in North America but remains the most common cause of goiter worldwide (termed endemic
goiter). Compensatory small thyroid stimulating hormone (TSH) elevations occur, preventing hypothyroidism, but the
TSH stimulation results in goiter formation. Recurrent cycles of stimulation and involution may result in nontoxic
nodular goiters. However, the true etiology of most nontoxic goiters in iodine-sufficient areas is unknown.
Symptoms and Signs
The patient may have a history of low iodine intake or overingestion of food goitrogens, but these phenomena are
rare in North America. In the early stages, the goiter is typically soft, symmetric, and smooth. Later, multiple nodules
and cysts may develop.
Diagnosis
y Thyroidal radioactive iodine uptake
y Thyroid scan
y Thyroxine (T4), triiodothyronine (T3), and TSH
In the early stages, thyroidal radioactive iodine uptake may be normal or high with normal thyroid scans. Thyroid
function tests are usually normal. Thyroid antibodies are measured to rule out Hashimoto's thyroiditis.
In endemic goiter, serum TSH may be slightly elevated, and serum T4 may be low-normal or slightly low, but serum
T3 is usually normal or slightly elevated.
Treatment
y Depends on cause
In iodine-deficient areas, iodine supplementation of salt; oral or IM administration of iodized oil yearly; and iodination
of water, crops, or animal fodder eliminates iodine-deficiency goiter. Goitrogens being ingested should be stopped.
In other instances, suppression of the hypothalamic-pituitary axis with thyroid hormone blocks TSH production (and
hence stimulation of the thyroid). Full TSH-suppressive doses of L-thyroxine (100 to 150 g/day po depending on the
serum TSH) are useful in younger patients. L-Thyroxine is contraindicated in older patients with nontoxic nodular
goiter, because these goiters rarely shrink and may harbor areas of autonomy so that L-thyroxine therapy can result
in hyperthyroidism. Large goiters occasionally require surgery or 131
I to shrink the gland enough to prevent
interference with respiration or swallowing or to correct cosmetic problems.
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MULTINODULAR GOITERS
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] :
y A bnormal iodine metabolism, probably of genetic origin
y Ingestion of large amounts of goitrogens from food sources, such as cabbage, soybeans, peanuts, peaches,
peas, strawberries, radishes, rutabagas, and spinach
y Ingestion of pharmaceutical goitrogens, such as glucocorticoids, dopamine, lithium, rifampin, adrenergic
antagonists, methimazole, and thiocarbanides
If goiters are diagnosed, this is an excellent opportunity for patient education regarding iodine
consumption. A dults generally require a minimum of 150 mcg of iodine daily, but pregnant and
breastfeeding women require an additional 100 mcg daily. Iodized salt contains 1 part iodine to 100,000
parts of salt. The average A merican ingests 6.2 grams of salt a day; this equates to 474 mcg of iodine if
the salt is iodized [11] .
NARRATIVE:
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 hormoneslevothyroxine 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 leadsto 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.
SCHE M ATIC DIAGRA M
Age (over 40 y/o), gender (female), and
goitrogens(like cabbage).
Iodine deficiency
Decreased production of thyroid
hormones: thyroxine (T4)
and triiodothyronine (T3)
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
oiter
Compression of the
trachea and esophagusSubtotal
thyroidectomy
Difficulty
swallowing
Difficulty
breathing
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NUR SING C ARE PL AN (A CTUA
Assessment Explanation of theProblem
Objectives Nursing Inte
S> ³Kumikirot angsugat ko.´ Pricking pain on theoperative site, rated as4/10 wherein 1 as thelowest and 10 as thehighest. Describedpain as continuouspricking and burningpain aggravated bysudden movements of
the neck, whilesitting,walking andstanding.
O>grimacing
>weak in appearance
>with limitedmovement >needs assistance in
performing ADL >with protective andguarding behavior onthe operative sitenoted
Unpleasant sensoryand emotionalexperience arisingfrom actual or potentialdamage or slow onsetof any intensity frommild to severe with ananticipated or predictable end.
STO: >Within 4 hours of nursing interventions,the patient¶s report of pain is reduce or relieve.
LTO:
>Within 8 hours of nursing interventions,the patient will be ableto demonstrate use of relaxation techniquesand divertionalactivities appropriateto situation.
Dx: >Assess paicharacter anunsing pain scale
>Assess vitanoting tachyincreased inpressure
>Monitor for hemorrhage checking beneck and shbleeding fromincision
Tx:
>Provide commeasures
>Add pillows
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Nursing Diagnosis: Acute pain related to
disruption of skin,tissue and muscleintegrity
support head
>Allow time
Edx: >Encourage relaxation tesuch as deebreathing ex
>Recommenpostoperativexercises to
instituted aftheals such aextension, roand lateral m
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NUR SING C ARE PL AN (A CTUA L
A SSESSM ENTEXPL ANATION OFTHE PROBLE M
OBJECTIVES NUR SI
INTERVEN
Subjective:
y ³Ilang araw naakong hindi
nakakatae, may
apat na araw
na siguro´
Objective:
y Hypoactivebowel sounds
noted at the
four quadrants
of the
abdomen.
y Straining withdefecation.
y Abdominaltenderness
without
palpable
abdominal
resistance.
y Frequentflatulence.
NursingDiagnosis:
y Constipation
Because of
decreased demand
of the body for
nutrients that
results from
decreased
physical
activity, the
digestive system
compensates
thereby
decreasing itsabsorption that
results to
decrease in its
motility as
manifested by
hypoactive bowel
sounds.
Decreased
peristaltic
movement of the
intestines wouldlead to
constipation.
Short Term Objective:
After 30 minutes
of proper
nursing
interventions
the patient will
be able to
verbalize
understanding of
etiology
constipation asevidenced by
enumerating the
factor that
could contribute
to constipation.
Long Term Objective:
y Within 24
Diagnostic
y Auscultabdomen
presenc
locatio
charact
s of bo
sounds.
y Palpateabdomen
y Investicomplai
pain wi
defecat
Therapeuti
y Providebath af
stool.
y Provideprivacy
routine
schedul
for
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related to
decreased
physical
activity.
hours of
proper nursing
interventions
the patient
will be able
to demonstratebehaviors of
lifestyle
changes to
prevent
recurrence of
problem as
evidenced by
ambulation and
increasing her
oral fluid
intake.
defecat
y Offer mfluids.
y Let patactivit
within
of indi
ability
Educative
y Encouradiet of
balance
and bul
includihigh-fi
fruit j
suggest
drinkin
stimula
fluids
coffee
tea.
NUR SING C ARE PL AN (POTENT
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A SSESSM ENTEXPL ANATION OFTHE PROBLE M
OBJECTIVES NUR SI
INTERVEN
Subjective:
y ³Kakaopera kolang kahapon
sa lalamunanko´
Objective:
y With intactdressing on
the wound.
y Wound ischaracterized
as not
swollen, not
erythematous,no signs of
bleeding and
dry.
y Withtemperature of
36.8oC.
Nursing
Diagnosis:y Risk forinfection
related to
inadequate
primary
The primary
defense of the
body against
infection is theskin. So, any
break in the
continuity of
this organ will
increase the
risk of
infection.
Like in the case
of our patient,
she had
undergone a
surgical
procedure. The
surgical
incision is
considered to be
discontinuity on
the skin and it
serving as the
portal of entry
for
microorganism.
Short Term Objective:
y After 30
minutes ofproper nursing
interventions
the patient
will be able
to verbalize
understanding
of individual
risk factors
as evidenced
by justifying
if heractivities
will prevent
infection.
Long Term Objective:
y Within 24hours of
proper nursing
interventions
the patient
Diagnostic
y Monitorsigns.
y Assess charact
s of wo
Therapeuti
y Maintai
steriletechniq
all
procedu
y Adminisprophyl
antibio
ordered
Educative
y Instrucproper
especia
hand wa
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defense. will be able
to demonstrate
lifestyle
changes to
prevent or
reduce therisk of
infection as
evidenced by
practicing
proper
hygiene.
y Encourainclude
protein
Vitamin
food indiet.
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VIII. DRUG STUDY
DRUG NAME CLASSIFICATION ACTION INDICAT
GENERIC NAME:
CELECOXIB
BRAND NAME:
CELEBREX
400mg OD
Nonsteroidal
Anti-
inflammatory
drugs
Thought to
inhibit
prostaglandin
synthesis,
impeding
cyclooxygenase-2
(COX-2), to
produce anti-
inflammatory,
analgesic, and
anti pyretic
effects.
- To rel
signs
sympto
osteoa
- To rel
signs
sympto
rheuma
arthri
- Acute
primardysmen
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GENERIC NAME:
AMLODIPINE
BRAND NAME:
NORVASC
10mg per tab. 1
tab OD
Anti-anginals
drug
Inhibits calcium
ion influx
across cardiac
and smooth-
muscle cells,thus decreasing
myocardial
contractility
and oxygen
demand; also
dilates coronary
artery
- Chroni
angina
vasosp
angina
- Hypert
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GENERIC NAME:RABEPRAZONE
BRAND NAME:
ACIPHEX
20mg 1 tab OD
Anti-ulcer drugs Blocks protonpump activity
and gastric acid
secretion by
inhibiting
gastric
hydrogen-
potassium
adenosine
triphosphatase
at secretory
surface of
gastric parietal
cells.
- Healinerosiv
ulcera
gastro
al ref
diseas
- Healin
duoden
ulcers
- Sympto
GERD,
includdaytim
nightt
heartb
- H. pyl
eradic
to red
risk o
duoden
recurr
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GENERIC NAME:
MECOBALAMINE
BRAND NAME:
METHYCOBAL
500mg 1 tab TID
Vitamin B-
complex
A coenzyme that
stimulates
metabolic
function and is
needed for cellreplication ,
hematopoiesis,
and
nucleoprotein
and myelin
synthesis
Megaloblast
anemia
GENERIC NAME:
ROXITHROMYCIN
BRAND NAME:
RULID
300mg 1 cap OD
Macrolide URTI, LRTI,
and soft ti
infections
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IX. CONCLUSION
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.
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X. RECO MM ENDATION
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.
To The Hospital
y 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.
y 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.
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To The Nursing Student
y 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.
y 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.
y 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.
To The University
y 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
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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.
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XI. APPENDICES