Case Study Caballes

8/8/2019 Case Study Caballes

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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.



17

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.



18

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)



19

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



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



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



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



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



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



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.



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



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



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



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



35

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.



36

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.



37

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



38

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.



39

XI. APPENDICES

Case Study Caballes

Documents

Transcript of Case Study Caballes