Synopsis and Background of the Case

“Claire”’ is a 47-year old accountant working regularly in a firm. She sought medical advice
from a physician after reporting her worsening fatigue as compared to the previous years. She
also complained of coldness even in warm temperatures, constipation, as well as having pale,
dry skin and thinning hair, which have gradually persisted and occurred over the course of her
adult life. Recently, she was also diagnosed with mild depression.

She attributed all of these to her corporate lifestyle coupled with the stresses of being a
mother to her school-aged children. Claire also reported that she was having overall muscle aches
and consistent stiffness at her neck which were not relieved by ibuprofen nor heat. Considering
her body weight, Claire had a hard time shedding pounds in spite of her busy work and family
schedule.

Moreover, after she turned 47, she recalled taking a month-long break from her work so
as to relieve her symptoms of chronic fatigue. Unfortunately, the tiredness persisted up to the
present. Taking a look at herself, she noticed a painless growing lump on her neck. The lump
persisted together with her symptoms for quite some time. Bothered by the status of her well-
being, she decided to seek medical advice and her case underwent a workup process to ascertain
her condition.

Below are the results of the different tests and examinations her physician requested:

Table 1: Physical Assessment Results

Test Result Reference Range /

Interpretation
Blood Pressure 125 mmHg / 70 mmHg Normal: systolic less than 120
mmHg; diastolic less than 80
mmHg

Elevated: systolic: 120-129

mmHg; diastolic: less than 80
mmHg

Hypertension: systolic: 130

mmHg or higher; diastolic: 80
mmHg or higher

(Davis, 2021)
 Neck Disability Index
43%
● 0-4 points (0-8%) no
disability,
● 5-14 points (10 – 28%)
mild disability,
● 15-24 points (30-48%)
moderate disability,
● 25-34 points (50- 64%)
severe disability,
● 35-50 points (70-
100%) complete
disability

(Macdermid, 2019)

Range of Motion Testing Cervical flexion limited to 10o

• Cervical Flexion 20-
45°
Cervical extension limited to
• Cervical Extension 70°
35o
• Cervical Rotation 90°
• Thoracic Spine Flexion
Cervical rotation limited to 26o 20-50°
• Bilateral Cervical Side
Thoracic spine flexion 10o Bending 35°
(Quinn, 2021)
Bilateral cervical side bending
15o

Phalen’s Test Positive (+) Suggestive of Carpal

Tunnel Syndrome

(Kuschner, 2017)

Tinel’s Sign Positive (+) Suggestive of Carpal

Tunnel Syndrome

(Kuschner, 2017)
2
Anthropometry BMI 38.5 kg/m
● Below 18.5 –
Underweight
● 18.5-24.9 - Normal
Weight
● 25.0-29.9 –
Overweight
● 30.0-34.9 - Obesity
Class I
● 35.0-39.9 - Obesity
Class II
 ● Above 40 - Obesity
Class III

(CDC, 2018)

Electrical Bioimpedance 46.9% body fat

(American Council on
Exercise, 2019)

Table 2: Comprehensive Metabolic Profile Results:

Test Result Reference Range / Interpretation

Chemical Examination (Bishop, 2018)

Fasting Glucose 101 mg/dL ● Normal 70-99 mg/dL

● Impaired 100-125 mg/dL
● Provisional diabetes diagnosis ≥ 126
mg/Dl

HbA1c 5.6% ● Pre-diabetes 5.7%-6.4%

● DM ≥ 6.5% on at least 2 occasions

● Desirable <150 mg/dL

TAG 153 mg/dL ● Borderline high 150-199 mg/dL
● High 200-499 mg/dL
● Very High >500 mg/dL
● Desirable <200 mg/dL
TChol 220 mg/dL ● Borderline high 200-239 mg/dL
● High >240 mg/dL
● Low <40 mg/dL
HDL 30 mg/dL ● High >60 mg/dL
 ● Optimal <100 mg/dL
LDL 151 mg/dL ● Near/above optimal 100-129 mg/dL
● Borderline high 130-159 mg/dL
● High 160-189 mg/dL
● Very High >190 mg/d

AST 21 U/L 5-35 U/L

ALT 33 U/L 30-90 U/L

BUN 27 mg/dL 10-50 mg/dL

Creatinine 0.8 mg/dL 0.6-1.1 mg/dL

Total Bilirubin 0.5 <1 mg/dL

Table 3: Electrolyte Panel Results:

Test Result Reference Range

Sodium 130 mmol/L 135-145 mmol/L

Potassium 3.2 mmol/L 3.5-5.1 mmol/L

Ionized Calcium (serum) 1.14 mmol/L 1.16-1.32 mmol/L

Magnesium 1.0 mmol/L 0.075-0.96 mmol/L

Chloride 110 mmol/L 98-107 mmol/L

Table 4: Thyroid Panel Results:

Test Result Reference Range

(Bishop, 2018)

TSH 9 μUI/mL 0.5-5 μUI/ml

TT3 68 ng/dL 71-180 ng/dL

TT4 4.9 ug/dL 5.5-12.5 μg/dL

FT3 1.75 pg/ml 1.81-4.4 pg/mL

 FT4 0.8 ng/dl 0.9-2.3 ng/dL

24 hour – RAIU 4% 8-35%

Table 5: Serology Results

Test Result Reference Range

Anti-Thyroglobulin 23 IU/mL <4.11 IU/mL

Anti-TPO 359.44 IU/mL <5.61 IU/mL

Table 6: Complete Blood Count Results

Test Result Reference Range

RBC count 3.78 x 10^12/L Male: 4.20-6.00 x 10^12/L

Female: 3.80-5.20x10^12/L

WBC count 4.0x10^9/L 3.6-10.6 x 10^9/L

Hct Male: 40-54%

35% Female: 35-49%

Hgb Male: 13.5-18.0 g/dL

12.5 g/dL Female: 12.0-15.0 g/dL

MCV 80 fL 80-100 fL

MCH 27 pg 26-34 pg

MCHC 33 fL 32-36 g/fL

Differential

Neutrophil 4.5x10^9/L 1.7-7.5x10^9/L

Eosinophil 0 x 10^9/L 0-0.3x10^9/L
Basophil 0.1x10^9L 0-0.2x10^9/L
Lymphocytes 2.0x10^9/L 1.0-3.2x10^9/L
Monocytes 1.2x10^9/L 0.1-1.3x10^9/L

Morphology Normal RBC morphology ---

 Table 7: Urinalysis Results

Test Result Reference Range/Normal

Values

Physical

Color Pale Yellow Pale Yellow to deep amber

Clarity Hazy Clear
Odor Aromatic Aromatic

Chemical

Leukocyte Esterase Neg Neg

Nitrite Neg Neg
pH 6.0 4.5-8.0
Protein Neg Neg
Blood Neg Neg
Specific Gravity 1.015 1.002-1.030
Ketones + Neg
Glucose + Neg
Bilirubin Neg Neg
Urobilinogen Neg Neg

Microscopic

Hyaline Casts 0-1/LPF 0-2/LPF

Mucus Threads Few/LPF ---
 Ultrasound Results

Figure 1. Transverse gray-scale

ultrasound (a) and color Doppler (b)
neck, of a 47-year-old female patient,
who presented with features of
hypothyroidism and had antithyroid
antibodies positive for the disease,
demonstrates diffuse enlargement of
thyroid gland with linear echogenic
fibrous bands (arrowheads) but normal
vascularity. Note a small hypoechoic
lymph node (arrow) in posterior aspect
of inferior pole of left lobe of the thyroid
gland.
FNAB Results

Figure 2. (A- Left) Fine needle aspiration in a Diff-Quik ® staining of a goiter in a background of
lymphocytic thyroiditis. There is a thin background of purple colloid in between grey staining red
blood cells amid follicular cells and dark blue staining nucleated lymphocytes recognized by crush
or stringing effects (Magnification 200×). (B-right) - Hurthle cells which are atrophic thyroid follicles
lined with epithelial cells with abundant eosinophilic, granular cytoplasm.
 Scintigraphy Results

Figure 3. Fluorescent thyroid scan in thyroiditis. The normal thyroid scan (left) allows
identification of a thyroid with normal stable (127I) stores throughout both lobes. A marked
reduction in 127I content is apparent throughout the entire gland involved with Hashimoto's
thyroiditis (right).
Molecular Testing Results

Molecular Detection and Genetic Mapping detected the presence of Hashimoto’s thyroiditis
susceptibility genes:
● MHC Region on chromosome 6p21
● CTLA-4 gene on chromosome 2q33
● PTPN22- on chromosome 1p13
● Thyroglobulin gene on chromosome 8q24
● Vitamin D receptor gene on chromosome 12q12
 Patient Family and Medical History

Family History

Figure 4: Pedigree depicting Hypothyroidism Cases in Claire’s Family

Claire’s family history reveals three clinically diagnosed cases of hypothyroidism coming
from her immediate family members. Comorbidities in the family include hypertension and type 2
diabetes mellitus which she does not apparently manifest. All members of the family are currently
alive (1st filial to 3rd filial generation). A detailed listing of the family’s medical profile are presented
below:

Table 1-2: Family History

Family Member Background Health History (with Age of

Onset)

Grandmother (Father’s Side) Age: 85 50: Diagnosed with

Sex: Female Hypertension and Type 2 DM
Height: 160 cm
Weight: 55 kg 63: Hospitalized for a
BMI: 21.5 (Normal) Hypertensive Crisis

Current Medications:
Amlodipine, Metformin
 Age 80: 35: Diagnosed with Salivary
Grandfather (Father’s Side) Sex: Male Gland Cancer
Height: 173 cm
Weight: 85 kg 36: Underwent Radiation
BMI: 28.4 (Overweight) Therapy

Current Medications: 36: Diagnosed with

Levothyroxine Radiation-Induced
Hypothyroidism

Age: 81 18: Diagnosed with

Grandmother (Mother’s Side) Sex: Female Tuberculosis
Height: 140 cm
Weight: 46 kg 34: Hospitalized after a Blunt
BMI: 23.5 (Normal) Trauma Accident

Current Medications:
--

Age: 83 43: Diagnosed with Type 2

Grandfather (Mother’s Side) Sex: Male DM
Height: 168 cm
Weight: 58 kg 74: Diagnosed with
BMI: 20.5 (Normal) Amebiasis

Current Medications:
Metformin, Metronidazole

Aunt 1 Age: 43 ---

Sex: Female
Height: 154 cm
Weight: 50 kg
BMI: 21.1 (Normal)

Current Medications:
---

Aunt 2 Age: 47 15: Diagnosed with

Sex: Female Tuberculosis
Height: 157 cm
Weight: 66 kg 40: Diagnosed with
BMI: 26.8 (Overweight) Hypertension

Current Medications:
Lisinopril
Aunt 3 Age: 52 34: Diagnosed With
Sex: Female Pernicious Anemia
Height: 151 cm
Weight: 80 kg 37: Diagnosed with
BMI: 35.1 (Obese Class II) Hashimoto’s Thyroiditis

Current Medications:
Levothyroxine, Vitamin B12
(until cobalamin levels
normalized)

Uncle 1 Age: 48 15: Suffered from Dengue

Sex: Male
Height: 172 cm 35: Diagnosed with
Weight: 98 kg Tuberculosis
BMI: 33.1 (Obese Class I)
48: Diagnosed with
Current Medications: Hypothyroidism (work-up is
Levothyroxine ongoing to ascertain cause
and type)

Uncle 2 Age: 45 ---

Sex: Male
Height: 176 cm
Weight: 55 kg
BMI: 17.8 (Underweight)

Current Medications:
---

Father Age: 68 23: Hospitalized after a car

Sex: Male accident
Height: 179 cm
Weight: 63 kg
BMI: 19.7 (Normal) 35: Diagnosed with Type 2
DM
Current Medications:
Metformin

Mother Age: 65 ---

Sex: Female
Height: 160 cm
Weight: 54 kg
BMI: 21.1 (Normal)

Current Medications:
---

Sister Age: 39 39: Recently Suffered from

Sex: Female Pseudomonas infection
 Height: 163 cm
Weight: 58 kg
BMI: 21.8 (Normal)

Current Medications:
Ceftazidime

Patient Medical History

Claire’s health during her childhood and adolescent years was noted as normal. She has
not been admitted at the hospital for a grave condition nor underwent a major surgery. Below
are the specifics of her medical profile:

Table 2-2: Claire’s Medical Profile

Details Remarks

Age: 47
Sex: Female
Height: 160 cm Class II Obesity
Weight: 98.5 kg
BMI: 38.5

Previous Vaccination(s):

Newborn
- Hepatitis B
- Diphtheria
- Tetanus
- Pertussis
- Polio
- Pneumococcal Vaccine
- Haemophilus influenzae type B No adverse reactions were noted after
administration of the said vaccines
Infant
- Diphtheria
- Tetanus
- Pertussis
- Poli
- Pneumococcal Vaccine
- H. influenzae type B
- Hepatitis B
- Flu Vaccination
Toddler
- Varicella
- MMR
- Influenza

Adolescent
- Influenza
- Hepatitis B

Adult
- Influenza
- Pneumococcal Vaccine
- HPV

Food Allergies:
Peanuts, Shellfish Albeit her restrictions in food, Claire had no
history of developing a serious condition due
Dietary Restrictions: to allergies
Same as Above
Claire lives a sedentary lifestyle brought
Other Pertinent Details: about by the nature of her work
Sedentary Lifestyle, with no regular exercise

Past Medical Condition(s) with Age of Onset:

Her cases of dengue and a previous dog bite
18 - Suffered from Dengue Fever were resolved following supportive therapy
and post exposure prophylaxis therapy,
respectively.
33 - Received Rabies PEP

47 - Clinically Diagnosed with Depression Sertraline was prescribed (50 mg/day)

Current Medical Condition(s) with Age of ---

Onset:

---
 Battery of Test

List of Tests

1. Physical examination - Physical findings are variable and depend on the extent of
hypothyroidism and other factors such as age. Physical examination enables the
experienced clinician to construct a narrow differential of its anatomical pathology.
Physical examination includes a range of motion testing, disability indices, and physical
signs among others.

2. Comprehensive Metabolic Profile - These tests will provide a better insight on the status
of the health of liver, kidneys, metabolism, acid/base balance, electrolytes, and blood
proteins in relation to thyroid function (Ulta Lab Tests, 2020)

3. Thyroid Panel - The thyroid panel is used to see how well the thyroid gland is functioning.
Abnormal thyroid function, such as underactive thyroid (hypothyroidism) or overactive
thyroid (hyperthyroidism), can lead to a wide range of symptoms. A thyroid panel can also
be used to monitor the treatment of hyperthyroidism and assess patients receiving
levothyroxine therapy (Lab Tests Online, 2021).
● Thyroxine Measurement: T4 is measured after it is separated from its transport protein. It
is used in conjunction with TSH to differentiate thyroid diseases (hypothyroidism &
hyperthyroidism). Total T4 can be measured by electron capture gas chromatography,
high-performance liquid chromatography (HPLC), and isotope dilution liquid
chromatography-tandem mass spectrometry, which is considered the best method for
determining T4 reference values (Pagana, et al., 2018).
● FT4: Free T4 or free thyroxine is a method of measuring T4 that eliminates the effect of
proteins that naturally bind T4 and may prevent accurate measurement.
● Thyroid-stimulating hormone (TSH) is produced in the pituitary gland and regulates the
balance of thyroid hormones including T4 and T3 in the bloodstream. The TSH
concentration aids in differentiating primary from secondary hypothyroidism. Pituitary TSH
secretion is stimulated by hypothalamic thyroid-releasing hormone (TRH). Low levels of
triiodothyronine and thyroxine (T3 and T4) are the underlying stimuli for TRH and TSH.
Therefore, a compensatory elevation of TRH and TSH occurs in patients with primary
hypothyroid states. The TSH test is used as well to monitor exogenous thyroid
replacement. The goal of thyroid replacement therapy is to provide an adequate amount
of thyroid medication so that TSH secretion is in the low normal range, indicating a
euthyroid state (Pagana, et al., 2018).
● T3: triiodothyronine tests help diagnose hyperthyroidism or to show the severity of
hyperthyroidism. Low T3 levels can be observed in hypothyroidism, but more often this
test is useful in the diagnosis and management of hyperthyroidism, where T3 levels are
elevated (Cleveland Clinic, 2020).
4. Thyroid Autoantibodies - To detect the presence and measure the quantity of specific
thyroid antibodies in the blood. Thyroid antibody testing may look for several types of
thyroid antibodies:
● Antithyroglobulin antibody (Thyroid autoantibody, Thyroid antithyroglobulin antibody,
Thyroglobulin antibody): This test is used as a marker for autoimmune thyroiditis and
related diseases. Thyroglobulin autoantibodies bind thyroglobulin (Tg), which is a major
thyroid-specific protein that plays a crucial role in thyroid hormone synthesis, storage, and
release. Tg remains in the thyroid follicles until hormone production is required. Tg is not
secreted into the systemic circulation under normal circumstances (Pagana, et al., 2018).
● Antithyroid peroxidase antibody (Anti-TPO, TPO-Ab, Antithyroid microsomal antibody,
Thyroid autoantibody): This test is primarily used in the differential diagnosis of thyroid
diseases. Thyroid microsomal antibodies are commonly found in patients with various
thyroid diseases. Microsomal antibodies are produced in response to microsomes
escaping from the thyroid epithelial cells surrounding the thyroid follicle (Pagana, et al.,
2018).

5. Complete Blood Count - A complete blood count with platelets and differential is a routine
part of blood work, as it measures the level of white blood cells, hemoglobin, hemoglobin,
and red blood cells in the blood. When the thyroid is malfunctioning, there’s an effect on
blood cells, which can create other effects. By evaluating the results, a medical
professional can evaluate the effect that the thyroid malfunctioning is having on blood cells
(Ulta Lab Tests, 2020).

6. Urinalysis - Urinalysis serves as a valuable tool for detecting those patients suffering from
thyroid dysfunction, who might be undetected through standard blood tests. This test is
used as an adjunct to other indicators such as body temperature, symptomology and
standard blood thyroid tests (Genova Diagnostics, 2020).
7. Ultrasound - This imaging modality is useful for assessing thyroid size, echotexture, and
most importantly whether thyroid nodules are present. Features of Hashimoto thyroiditis
are usually identifiable on an ultrasonogram.

8. Fine Needle Aspiration Biopsy - Performing a fine-needle aspiration of any dominant or

suspicious thyroid nodules to exclude malignancy or the presence of a thyroid lymphoma
in fast-growing goiters (Alwan, 2018).

9. Scintigraphy- This test can be used to describe a nodule on the basis of its relative uptake
of radioactivity after the I123 administration. Thyroid scintigraphy is the only technique that
allows the assessment of thyroid regional function and detection of areas of autonomously
functioning thyroid nodules (Dankle, 2018).

10. Molecular Testing - This can measure cellular constituents either quantitatively or
qualitatively. Genes that predispose a patient to certain autoimmune conditions can also
be detected by molecular testing. Markers can also be used to diagnose or are expressed
in benign or cancerous cells (Sawka, 2018).
 Differential Diagnosis

Differential Diagnosis Introduction

For us to properly diagnose the patient; signs and symptoms should be checked together
with the complaints commonly seen in hypothyroidism. It is important also for us to carefully
examine the neck to look for enlargement of the thyroid gland and take a detailed history of family
members and medications. The patient had been subjected to physical examination. Coarse facial
features were taken into consideration as well as thickened skin. Also, the physician requested
blood tests. In primary hypothyroidism, the TSH level is increased, but the total T3, total T4, free
T3, and free T4 levels are decreased. Presence of TPO antibody was also noted and according
to Bishop (2018), it is positive for the 80% to 99% population of patients with chronic lymphocytic
thyroiditis. Aside from this we also assessed the thyroid hormone status which reflects glandular
function.

In primary hypothyroidism, the thyroid hormone levels fall while the level of TSH becomes
high. The measurement of TSH confirms the diagnosis of hypothyroidism. The combination of the
patient’s clinical history, antibody screening and a thyroid scan can help us diagnose the precise
underlying thyroid problem.

Concise Diagnosis of Hashimoto’s Disease

Figure 5: Flow diagram representing the diagnosis of Hashimoto’s thyroiditis (Alwan, 2018;
Gram Project, 2020)
 Figure 5 shows a concise step by step diagnosis of Hashimoto’s thyroiditis involving
thyroid gland dysfunction. The diagram at the same time shows how it is differentiated from
secondary hypothyroidism involving pituitary and hypothalamic dysfunction. Primary
hypothyroidism exhibits increased TSH level, but the total T3, total T4, free T3, and free T4 levels
are all decreased.

Differential tests

Thyroxine Measurement:

A low T4 level together with an increased TSH level usually indicates hypothyroidism, and an
increased T4 level with a decreased TSH level indicates hyperthyroidism. The patient has low T4
with increased TSH.

Triiodothyronine Analysis:

Most individuals with hyperthyroidism have increased T4 and T3, with higher levels of the latter.
T3 and T4 of the patient decreased. T3 levels are usually not useful in determining hypothyroidism
because they are normal in 15 % to 30% of cases.

Antithyroglobulin antibody Testing (Thyroid autoantibody, Thyroid antithyroglobulin

antibody, Thyroglobulin antibody):

In Hashimoto’s thyroiditis, follicular destruction through inflammation (Hashimoto thyroiditis) can

result in leakage of Tg into the bloodstream leads to an increased level. This results in the
formation of autoantibodies to Tg in some individuals. The anti-Tg test is usually performed in
conjunction with the antithyroid peroxidase antibody test.

Antithyroid peroxidase antibody (Anti-TPO, TPO-Ab, Antithyroid microsomal antibody,

Thyroid autoantibody):

They are present in 70% to 90% of patients with Hashimoto thyroiditis. Microsomal antibodies are
produced in response to microsomes escaping from the thyroid epithelial cells surrounding the
thyroid follicle. These escaped microsomes then act as antigens and stimulate the production of
antibodies. These immune complexes initiate inflammatory and cytotoxic effects on the thyroid
follicle causing an increased level.

Complete blood count:

Up to 30-40% of patients with hypothyroidism have anemia, usually from decreased

erythropoiesis. In 15% of patients, the anemia is of the iron deficiency type, with microcytosis and
hypochromia. Although this can be a normocytic normochromic anemia, the most common
morphologic abnormality is a macrocytic anemia that may be partially due to insufficient vitamin
B-12 and folate intake.
 Total and fractionated lipid profile:

Total cholesterol, LDL, and triglyceride levels may be elevated in hypothyroidism and may be
responsive to levothyroxine replacement.

FNAB:

A fine needle aspiration biopsy sample of the thyroid gland coming from Hashimoto patient during
the phase would reveal inflammatory cells attacking the thyroid gland. It usually reveals
lymphocytes, macrophages, scant colloid and epithelial cells which may show Hurthle cell
features.

Ultrasound:

This is to differentiate a normal gland from an enlarged gland as well as if there are symptoms of
esophageal compression, this procedure is performed to see if the gland is compressing either
esophagus or trachea.

Thyroid scanning (Thyroid scintiscan):

● Morphology
➢ The thyroid is often diffusely enlarged
➢ The capsule is intact
➢ The gland is well demarcated from adjacent structures
➢ The cut surface is pale, yellow-tan, firm and somewhat nodular.

Figure 6. Gross image. Symmetric enlargement with tan yellow cut surface and an intact
capsule (Matania, 2018).

On pathologic examination, there is a diffuse, symmetric enlargement of the thyroid

(Fig.6). The capsule is often intact with a prominent pyramidal lobe. When cut, the surface is
similar to that of lymph nodes, with a pale brown to yellow color. Interlobular fibrosis may or may
not be present.

Figure 7. Histologic Examination: Difference of normal thyroid (left) and chronic lymphocytic
thyroiditis (right) (Matania, 2018)

In figure 7, histological examination often reveals lymphoplasmacytic infiltration, lymphoid

follicles with germinal center formation, and epithelial cell. Thyroiditis destruction, the presence of
large follicular cells with abundant granular eosinophilic cytoplasm, known as oxyphilic, Hurthle
or Askanazy cells, and various degrees of fibrosis.
 Table 1-3. DIFFERENTIAL DIAGNOSIS FOR THYROID RELATED CONDITIONS

CONDITION CHARACTERISTIC/SI LABORATORY CONTRADICTORY SIGNS

GNS AND SYMPTOMS RESULTS AND SYMPTOMS/ LAB
RESULTS

Grave’s - Gland is - Elevations - Patient is usually

Disease diffusely and in serum euthyroid in early
(Autoimmune homogeneously free T3 and Hashimoto thyroiditis
hyperthyroidi enlarged. T4 and - The most common
sm) - With bulging of decreased immunoglobulin in
the eyes serum TSH Grave’s is Thyroid
(exophthalmos) Stimulating
Immunoglobulin (TSI)
while in Hashimoto’s
the most common
antibody is Thyroid
peroxidase antibody or
anti-TPO.
- The TSH is increased
and Free T4 is
decreased in the case
of Hashimoto’s
Thyroiditis while the
case is inverse with
Grave’s.

Secondary - Marked - Thyroid - T4 is decreased in

thyrotoxicosis enlargement of Panel Hashimoto’s while
Or T3 the thyroid gland shows Normal in Plummer’s
Thyrotoxicosi (goiter). increased disease.
s (Plummer's - Firm thyroid T3 with
disease) nodules, and Normal T4
overproduction and
of thyroid Decreased - TSH is increased in
hormone TSH. Hashimoto’s
(hyperthyroidism Thyroiditis and
). decreased in
Plummer’s Disease.
 - Plummer’s Disease
peaks in the sixth or
seventh decade of life.

- Presence of Hurthle
cells coupled with a
heterogeneous
population of
lymphocytes is more
suggestive of
Hashimoto’s Disease.

Subacute - Painful - A fine-needle - Hashimoto thyroiditis

Granulomato Thyroiditis aspiration has irregular and
us Thyroiditis - Happens post- (FNA) sample rubbery type of goiter
viral in subacute while Subacute
- Transient thyroiditis granulomatous
inflammation of contains a thyroiditis has hard
the thyroid mononuclear nodule.
- Clinical course is infiltrate
Variable composed - Hashimoto’s has a
- Solitary, hard mostly of painless goiter while
nodule lymphocytes Subacute
and Granulomatous
multinucleated Thyroiditis is a painful
giant cells. type.

Radel’s - The thyroid is - Elevation of - Hürthle cell metaplasia

Thyroiditis woody or Stony serum IgG4 and an enhanced
hard mass can be Doppler flow on
- Chronic found. ultrasound suggests
inflammation fibrosing Hashimoto,
and fibrosis of while extrathyroidal
the thyroid gland engagement (usually
adjacent strap muscle)
is present in RT.
 Subacute - Demonstrates - Initially, - Subacute lymphocytic
lymphocytic lymphocytic serum T4 thyroiditis condition
thyroiditis infiltration, and T3 are tends to have a phase
occasionally to elevated of hyperthyroidism
the point of and TSH is followed by a return to
lymphoid follicle suppressed. a euthyroid state, and
formation. In the then a phase of
- Usually an hypothyroid hypothyroidism,
absence of phase, followed again by a
thyroidal pain or these return to the euthyroid
tenderness. findings are state (Not a
- Examination may reversed. characteristic of
show normal to Hashimoto’s)
moderately enlarged
and firm thyroid gland. - Goiter in Hashimoto is
- With a painless and tender.
hyperthyroid
phase of several
weeks, often
followed by
transient
hypothyroidism
due to depleted
thyroid hormone
stores and
eventual
recovery to the
euthyroid state.

Iodine - Low Iodine - In iodine - Increase in Anti-TPO

Deficiency levels leads to patch test levels are noted in
hypothyroidism, the patch Hashimoto’s
since iodine is fades no Thyroiditis.
essential for sooner than
making thyroid 24 hours in
hormones. non-iodine
deficient
patient. But
a deficiency
will likely
cause the
 iodine to be
absorbed
into the skin
more
quickly.

Thyroid - Removal of the N/A - The patient has no

Surgery thyroid gland. history of thyroid
induced removal.
Hypothyroidis
m

Radioactive - RIA treats N/A - No history of

Iodine hyperthyroidism Radioactive Iodine
Treatment by damaging or treatment for the
destroying patient.
thyroid cells
through
radiation. This
may eventually
lead to
hypothyroidism.

Transient - Temporary N/A - No history of recent

hypothyroidis deficiency of infection for the patient
m thyroid hormone nor recent birth.
after birth or
after having an
infection.
Table 2-3. DIFFERENTIAL DIAGNOSIS FOR HEREDITARY CONDITIONS MENTIONED IN
PATIENT’S HISTORY

CONDITION CHARACTERISTIC/SIGNS LABORATORY CONTRADICTORY

AND SYMPTOMS RESULTS SIGNS AND
SYMPTOMS/ LAB
RESULTS

Hypertension - Family pass traits - Normal - The patient

from one generation Blood has elevated
to another through pressure is blood
genes. These usually pressure
genes may also 120/80 but however,
play a role in this may Hypertension
passing down vary alone cannot
hypertensive traits depending cause an
from one generation on the age of increase in
to another. the patient. TSH.

Diabetes Mellitus - Characterized by - Glucose - Polyuria was

Type 2 Polyuria, polydipsia, level for not
polyphagia, and Provisional manifested by
weight loss. diabetes the patient
diagnosis is although
≥ 126 mg/dL fasting
glucose of the
patient was at
101 mg/dL
indicating
impaired
fasting
glucose.
- Goiter
however
cannot be
caused by
DM Type 2
alone as well
as elevation
in TSH.
Table 3-3. OTHER CONDITIONS THAT COULD BE ASSOCIATED WITH PATIENT’S SIGNS
AND SYMPTOMS AS WELL AS RESULTS

CONDITION CHARACTERISTIC/SIGNS LABORATORY CONTRADICTORY

AND SYMPTOMS RESULTS SIGNS AND
SYMPTOMS/ LAB
RESULTS

- Fatigue
Anemia - Weakness - Decreased
- Pale or yellowish Hgb, Hct, - Chest pain
skin RBC count in was not
- Irregular heartbeats CBC reported
- Shortness of breath - As well as
- Dizziness or irregular
lightheadedness heartbeat and
- Chest pain shortness of
- Cold hands and breath.
feet

Liver Disease - Jaundice - Increased - AST is

- Abdominal Pain Liver normal
and Swelling Enzymes - No Jaundice
- Swelling in the legs (AST, ALT, observed
or ankles ALP, GGT) - No
- Itchy Skin - Increased observable
- Dark Urine Color Bilirubin signs and
- Pale Stool Color - Decreased symptoms
- Chronic Fatigue Total Protein that lead to a
- Nausea or Vomiting clinical
impression of
liver disease

- Muscle pain
Chronic Fatigue - Multi-joint without - Persistent - Patient does
Syndrome (CFS) redness or swelling chronic not
- Tender and swollen fatigue (at experience
lymph nodes in least 6 impairment of
your neck months) or memory or
- Fatigue intermittent, concentration
- Heat and cold that does not (psychiatric
sensitivity improve with disorder).
- Polyuria rest.
- Chest pain
 - Impaired memory
or mental
concentration
- Unrefreshing sleep
- Post- exertional
malaise (PEM)

- Fatigue
Kidney Disease - Have trouble - Increased - Urinalysis
sleeping Serum result of the
- Dry and Itchy Skin creatinine patient was
- Frequent Urination - Increased normal
- Blood in urine BUN - Polyuria was
- Puffiness around - Hematuria not observed
the eyes - Proteinuria - No blood in
- Muscle cramps - urine of the
patient

Comprehensive Pathophysiology

Patient’s Condition

Based on the signs and symptoms as well as the reported results, the condition of the
patient is Hashimoto’s Thyroiditis, which is an autoimmune condition and is the most common
cause of hypothyroidism in the developed world (Bishop, 2018). Also known as chronic
lymphocytic thyroiditis, the disease condition was discovered in Japan in 1912 by Dr. Hakaru
Hashimoto. It is now considered to be the most common autoimmune disease, affecting about 8
out of every 1,000 individuals. The disease is most often seen in middle-aged women; in addition,
women are 5 to 10 times more likely to develop the disease than men. Patients develop an
enlarged thyroid called a goiter, which is irregular, rubbery, and painless. Patients also produce
thyroid-specific autoantibodies and cytotoxic T cells. Immune destruction of the thyroid gland
occurs, which results in a state of decreased thyroid function called hypothyroidism (Stevens and
Miller, 2017).

Epidemiology

Hypothyroidism is defined as a low free T4 level with a normal or high TSH, occurring in
5% to 15% of women over the age of 65. Symptoms of hypothyroidism vary, depending on the
degree of hypothyroidism and the rapidity of its onset. When thyroid hormone is significantly
decreased, symptoms of cold intolerance, fatigue, dry skin, constipation, hoarseness, dyspnea
on exertion, cognitive dysfunction, hair loss, and weight gain will be reported. Some of these signs
were reported present to our patient.
 On physical examination, those with severe hypothyroidism may have low body
temperature, slowed movements, bradycardia, delay in the relaxation phase of deep tendon
reflexes, yellow discoloration of the skin (from hypercarotenemia), hair loss, diastolic
hypertension, pleural and pericardial effusions, menstrual irregularities, and periorbital edema
(Bishop, 2018). In the Philippines according to Jimeno (2012), prevalence of hypothyroidism is
0.41% or 4 per 1,000 and it is more common in older women and ten times more common in
women than in men. This makes our patient more susceptible because of her gender.

Kinds of Hypothyroidism

Hypothyroidism can be divided into primary, secondary, or tertiary disease, depending on

the location of the defect. The most common cause of hypothyroidism in developed countries is
chronic lymphocytic thyroiditis, or Hashimoto’s thyroiditis. This disorder is an autoimmune disease
targeting the thyroid gland, often associated with an enlarged gland, or goiter. TPO antibody
testing is positive in 80% to 99% of patients with chronic lymphocytic thyroiditis. Other common
causes of hypothyroidism include iodine deficiency, thyroid surgery, and radioactive iodine
treatment. Occasionally, individuals will experience transient hypothyroidism associated with
inflammation of the thyroid gland. Examples of transient hypothyroidism include recovery from
non-thyroidal illness and the hypothyroid phase of any of the forms of subacute thyroiditis (painful
thyroiditis, postpartum thyroiditis, and painless thyroiditis) (Bishop, 2018). Hashimoto’s Thyroiditis
is an example of a primary type of hypothyroidism because the condition shows low T3 and T4
with increased TSH.

Hashimoto’s at a Cellular Level

Hashimoto’s Thyroiditis is caused by a breakdown in self-tolerance to thyroid

autoantigens. As seen in the majority of Hashimoto patients, it is characterized by the presence
of circulating autoantibodies against thyroglobulin and thyroid peroxidase. Abnormalities may
involve; regulatory T cells (Tregs), or exposure of normally sequestered thyroid antigens. Similar
to other autoimmune diseases, Hashimoto thyroiditis has a strong genetic component. Increased
susceptibility to thyroiditis is associated with polymorphisms in immune regulation-associated
genes, including cytotoxic T lymphocyte-associated antigen-4 (CTLA4) and protein tyrosine
phosphatase-22 (PTPN22), both of which code for regulators of T-cell responses. Susceptibility
to other autoimmune diseases, such as type 1 diabetes, is also associated with polymorphisms
in both CTLA4 and PTPN22. Induction of thyroid autoimmunity is accompanied by a progressive
depletion of thyroid epithelial cells by apoptosis and replacement of the thyroid parenchyma by
mononuclear cell infiltration and fibrosis. Multiple immunologic mechanisms may contribute to
thyroid cell death, including: CD8+ cytotoxic T cell-mediated cell death since CD8+ cytotoxic T
cells has the capacity to destroy thyroid follicular cells. Cytokine-mediated cell death Activation of
CD4+ T cells leads to the production of inflammatory cytokines such as interferon-γ in the thyroid
gland, with resultant recruitment and activation of macrophages and damage to follicles. A less
likely mechanism involves binding of antithyroid antibodies such as antithyroglobulin, and
antithyroid peroxidase antibodies. It is followed by antibody-dependent cell mediated cytotoxicity
(Kumar et al, 2015).
Figure 8. Pathogenesis of Hashimoto at Cellular Level

Normal Thyroid Function

In normal conditions, the thyroid gland functions by producing hormones that regulate the
body's metabolic rate; controlling heart, muscle and digestive function, brain development and
bone maintenance. Its correct functioning depends on a good supply of iodine from the diet. Cells
producing thyroid hormones are very specialized in extracting and absorbing iodine from the blood
and incorporate it into the thyroid hormones. The signal comes from a small gland located at the
bottom of our brain called the pituitary gland. The pituitary gland produces and sends out a
hormone called thyroid-stimulating hormone (TSH). TSH then tells the thyroid gland how much
hormones to produce and secrete (Your Hormones, 2018).

The pituitary gland responds either directly to the thyroid hormones in the blood, but it also
responds to signals from the hypothalamus, which sits above the pituitary gland as part of your
brain. The hypothalamus releases its own hormone thyrotropin-releasing hormone (TRH). TRH
in turn stimulates the release of TSH in the pituitary, which then signals to the thyroid gland. This
whole network is also referred to as the hypothalamic-pituitary-thyroid axis (HPT) and it adapts to
metabolic changes and your body’s needs (Your Hormones, 2018).

Signs and Symptoms

In the case of Hashimoto’s Thyroiditis, the disease progresses gradually but with harmful
effects. It may then progress to more advanced signs and symptoms over months to years. Some
of the early signs and symptoms according to Lee (2020), include: fatigue, constipation, dry skin
and weight gain. More advanced symptoms however include: cold intolerance, hair loss, slowed
movement and loss of energy, decreased sweating and mild nerve deafness. The patient
manifested some of these symptoms such as fatigue, cold intolerance, thinning hair and dry skin.
As for the paleness of the skin according to Safer (2017), the skin tends to be pale due to dermal
mucopolysaccharides and dermal water content. The symptom was due to the deposition of
connective tissue components such as glycosaminoglycans, hyaluronic acid and
mucopolysaccharides. Protein mucopolysaccharide complex binds water, resulting in non-pitting
edema thus the resulting paleness of skin due to mucopolysaccharide and dermal water content.
The build-up of mucopolysaccharide as well as the build-up of water, is medically termed as
myxedema. Excess deposition of glycosaminoglycans, hyaluronic acid and some
mucopolysaccharides in subcutaneous tissues causes dermal edema, in myxedema. The build-
up of mucopolysaccharide was also associated to one of the symptoms which is the paleness of
the skin.

Aside from its function in metabolism the thyroid hormones are also crucial for
development, growth, differentiation, metabolism and thermogenesis. Skeletal muscle (SM)
contractile function, myogenesis and bioenergetic metabolism are influenced by TH. Hashimoto
thyroiditis (HT) may lead to muscle weakness due to hypothyroid dysfunction (Bloise et al, 2018).
This explains the complaint of the patient regarding overall muscle aches.

Depression and Hashimoto’s

Clinical depression, or major depression, is a mental health disorder characterized by

persistently depressed mood or loss of interest in activities, causing significant impairment in daily
life. Depression affects more women than men, and the symptoms and severity of depression can
vary from person to person. In Hashimoto’s, there is a breakdown of the thyroid gland, which can
rush thyroid hormones into the bloodstream, resulting in transient hyperthyroidism. Symptoms of
agitation, anxiety, and even psychosis can occur to anyone who has experienced symptoms of
hyperthyroidism because of the fluctuations of thyroid hormone. Furthermore, although the
association between depression and Hashimoto’s is not well understood, Siegmann (2018), in
her study found out that “AIT have a higher chance to show symptoms of depression and anxiety
compared with healthy controls.” According to her approximately 16.8% of the patients with AIT
developed depression. Our patient was diagnosed with mild depression and correlating it to her
thyroid panel results strengthen Hashimoto diagnosis.

In addition to this, hyperthyroid phase in Hashimoto’s usually results from increased

synthesis and release of thyroid hormone. Hashitoxicosis is seen in about 5% of cases of
Hashimoto’s thyroiditis. Although it usually subsides over time, a small proportion of patients will
have waxing and waning of thyroid hormone levels.
 Clinical Course

The condition may take many years to develop and is thought to be triggered by damage
to the thyroid gland. This results in immune cells congregating in the thyroid gland, and eventually
losing their ability to differentiate the thyroid gland from a foreign invader. According to Wentz
2020, the 5 stages of Hashimoto’s Thyroiditis are;

Stage 1: Genetic Predisposition

A person may have genetic predisposition to Hashimoto but they will not have been exposed to
the necessary triggers, and thus will have normal TSH and T4/T3 hormones.

Stage 2: Attack Begins

A person may test positive for thyroid antibodies and may have changes consistent with
Hashimoto’s on an Ultrasound but will have normal TSH level.

Stage 3: Thyroid Falters

Thyroid gland loses its ability to make enough thyroid hormone for the body. There will be slight
increase in TSH but with normal T3 and T4. More symptoms are evident.

Stage 4: Thyroid Fails

The thyroid gland fully loses its ability to compensate, and a person will have elevated TSH and
lowered T3 and T4 levels. With overt hypothyroidism, Hashimoto’s and hypothyroidism are often
diagnosed. With obvious signs and symptoms.

Stage 5: Additional Autoimmune progression

There is progression to Autoimmune response and other types of Autoimmune condition may
develop.

As for the condition of the patient presented, the patient is at the 4th stage of Hashimoto’s
Thyroiditis progression. TSH of the patient is high coupled with a decrease in the T3 and T4.
Figure 9. The 5 Stages of Hashimoto’s Thyroiditis

Physical Assessment Result

In the results presented the patient has borderline hypertension given her result of 125
mmHg / 70 mmHg and comparing to the reference ranges according to Macdermid (2019). Apart
from the reason of her having a family history of hypertension the effect of hypothyroidism to her
metabolism can also be associated to her blood pressure result. 43% neck disability index, which
is interpreted according to Macdermid (2019), as moderate disability. This is due to the tender
palpable mass on the anterior aspect of her neck suggestive of goiter. As for the range of motion:
Cervical flexion of the patient was limited to 10o where the normal range was 20-45o, cervical
extension was limited to 35o the normal cervical extension range of motion is usually 70o, Cervical
rotation limited to 26o where the supposed normal range of motion is 90o, thoracic spine flexion
at 10o was also limited given the normal range of 20-50o ,lastly, bilateral cervical side bending is
limited at 15o where in 35o is the supposed normal range of motion according to Quinn (2021).
The limited motion of the neck can still be associated to the growing lump in the neck of the
patient.

Other tests performed on the patient were Phalen’s Test and Tinel’s Sign all of which were
positive. These tests are used to diagnose the patient with carpal tunnel syndrome.
Hypothyroidism is one of the most important causes of the CTS, which, if diagnosed early can be
effectively treated. In the narrow space of carpal tunnel, deposition of pseudo-mucinous
substances on the median nerve sheath leads to compression of the nerve and leads to CTS.
Bilateral CTS is more frequently associated with systemic disorder. Anatomically, Carpal Tunnel
is a narrow space formed between carpal bones and transverse carpal ligament. It is through this
space, median nerve passes to provide motor and sensory function to palm of hands and first
four digits of hand. CTS is nonfatal condition but if untreated can cause severe median nerve
damage leading to loss of hand function (Karne & Bhalerao, 2016).

The anthropometric result of the patient was 38.5 kg/m2 this falls in the Obesity class II
according to the set standards of CDC, (2018). This is consistent with the reported difficulty of the
patient in losing some weight. Thyroid hormones are responsible also for the stimulation of
metabolic activities of most tissues. One consequence of this activity is to increase body heat
production, which seems to result, at least in part, from increased oxygen consumption and rates
of ATP hydrolysis (Bowen, 2020). Since the thyroid hormones of the patient is low therefore the
metabolic activity of her body is also affected leading to a difficulty in losing weight. The electrical
bioimpedence of the patient was 46.9% body fat also, falling into the obese category basing on
the set standards by American Council on Exercise, (2019). All of these tests together with the
difficulty in losing weight of the patient reveals that the patient is obese. Furthermore, the patient
was also reported as having constipation. Constipation occurs either because too much water is
absorbed from your food or your colon isn't contracting frequently or strongly enough. In either
case, the stool moves too slowly as a result. Sluggish, slower, or weaker colon contractions,
known as reduced gut motility, are characteristic of hypothyroidism (Shomon, 2020). Thyroid
hormone as well as the thyroid gland itself plays a significant role in bowel motility. The thyroid
gland produces motilin, a hormone, which stimulates the nerve and muscle complex that moves
food through the GI tract. In cases where the thyroid gland has been damaged or destroyed due
to radiation, medication, removal, or immune attack, thyroidal production of motilin is reduced or
eliminated. The reduction or elimination of motilin often results in slowed motility or constipation,
pain, bloating, gas, and other common GI symptoms (Chester, 2021).

Comprehensive Metabolic Profile

Further tests done to the patient includes fasting glucose where her result was 101 mg/dL.
This result shows an impaired fasting glucose result according to Bishop, (2018). Given that the
patient’s HbA1C result is 5.6%, the patient is nearly to be considered as prediabetic. The most
probable reason why thyroid dysfunction could lead to T2DM can be attributed to perturbed
genetic expression of a constellation of genes along with physiological aberrations leading to
impaired glucose utilization and disposal in muscles, overproduction of hepatic glucose output,
and enhanced absorption of splanchnic glucose (Wang, 2013).
 The triglycerides of the patient at 153 mg/dL is considered Borderline high based on the
150-199 mg/dL normal range set in the book of Bishop (2018). Total cholesterol of the patient
was 220 mg/dL which is also considered Borderline high since it falls in the 200-239 mg/dL range
set in the book still of Bishop (2018). The HDL was only 30 mg/dL, which is interpreted as low
according to Bishop (2018) since it was below 40 mg/dL. The LDL of the patient was 151 mg/dL
which is interpreted as Borderline high according still to Bishop, (2018) since it falls between 130-
159 mg/dL

Furthermore, the body needs thyroid hormones to make cholesterol and to get rid of the
cholesterol it doesn’t need. When thyroid hormone levels are low in the state of hypothyroidism,
the body doesn’t break down and remove LDL cholesterol as efficiently as usual. LDL cholesterol
can then build up in the blood as seen in the case of the patient and since there is no thyroid
hormone that is needed to make the good cholesterol therefore it is depleted which was also seen
in the patient’s result (Weatherspoon, 2019).

Aminotransferase of the patient was 21 U/L which is normal since it is still within the
normal range of 5-35 U/L. Along with the ALT, BUN, Creatinine and total bilirubin which rules out
the possibility of a liver disease that can be confused with the condition.

There was also a slight disturbance in the electrolyte of the patient base on the results.
According to Ambedkar (2012); thyroid hormones are involved in controlling various metabolisms,
more importantly lipid metabolism and that of various electrolytes, the hypothyroid patient
generally suffers from a slow metabolism resulting in dyslipidemias and electrolyte disturbances.
In his study he indicated that in the case of Hashimoto thyroiditis patients, they will exhibit serum
electrolyte disturbances such as low sodium, low potassium, low calcium levels and high
magnesium and phosphorus levels all of which were consistent with the patient’s case.

Thyroid Panel

The thyroid panel of the patient revealed that the Thyroid stimulating hormone of the was
elevated above the reference range of 0.27-4.20 μUI/ml (Bishop, 2018), since the result of the
patient was 9 μUI/mL. On the other hand, the tropic hormones T3 or Triiodothyronine and T4 or
Thyroxine were depleted as well as the free T3 and T4 indicating therefore primary
hypothyroidism.

Serology Results

With all these tests mentioned according to Bishop (2018) TPO antibody (Thyroid
peroxidase antibody) assay is the best test for this condition. It is present in 10% to 15% of the
general population and 80% to 99% of patients with autoimmune hypothyroidism. The enzyme
thyroid peroxidase (TPO) plays an important role in the synthesis of hormones triiodothyronine
(T3) and its precursor, thyroxine (T4), by oxidizing iodine ions, allowing for their incorporation into
the tyrosine residues of thyroglobulin to produce the building blocks for the hormones (Stevens
and Miller, 2017). If there is an increase in anti-TPO, this will promote destruction of thyroid
peroxidase and will thus affect the production of thyroid hormones. The TPO antibody of the
patient is high at 359.44 IU/mL wherein the normal range is only < 5.61 IU/mL. Furthermore, the
diagnosis is supported by the result of Anti-Thyroglobulin and results. The anti-Thyroglobulin
result of the patient was 23 IU/mL wherein the normal test result should only be <4.11 IU/mL.
Destruction of the thyroid cells are supported by the results seen in Scintigraphy testing.

Complete Blood Count Results

On the other hand, the RBC count of the patient was low, while Hematocrit as well as Hemoglobin
results of the patient are at the border of the lower limit based on the reference range. Anemia
usually sets in when the patient is already in the stage 4 of the disease condition where most of
the signs and symptoms are already evident (Wentz, 2020). However, in the case of our patient
the values in her complete blood count are somehow still near the lower limit since she is still in
the state of early stage 4. Her CBC results are suggestive of a condition that may lead to anemia.

Urinalysis Results

The patient has normal Urinalysis results narrowing down the diagnosis and removing the
chances of confusion with kidney disease as the possible disease condition of the patient.

Ultrasound & FNAB Results

The ultrasound result of the patient also revealed an increase in the size of her thyroid
gland. The enlargement of the thyroid gland is clinically termed as goiter. Depending on the type
of swelling, location, how it affects gland function and how long it has been present, goiter has
various effects and is treated in a variety of different ways (Your Hormones, 2020). The thyroid
epithelial cells will undergo apoptosis and will be replaced by the infiltration and fibrosis of
mononuclear cells. The thyroid follicles are atrophic and are lined in many areas by epithelial cells
distinguished by the presence of abundant eosinophilic, granular cytoplasm, termed Hürthle cells.
This is a metaplastic response of the normally low cuboidal follicular epithelium to ongoing injury.

In a fine-needle aspiration biopsy sample of the patient showed presence of lymphocyte

infiltrates. Kumar et al (2015) stated that “In fine-needle aspiration biopsy samples, the presence
of Hürthle cells in conjunction with a heterogeneous population of lymphocytes is characteristic
of Hashimoto thyroiditis.” Furthermore, he added that, in “classic” Hashimoto thyroiditis, interstitial
connective tissue is increased and may be abundant. Unlike Reidel thyroiditis, the fibrosis does
not extend beyond the capsule of the gland (Kumar et al, 2015).

In addition, patients with Hashimoto thyroiditis are at increased risk for developing other
autoimmune diseases such as; endocrine diseases like type 1 diabetes and autoimmune
adrenalitis. It may also induce; nonendocrine associated diseases like systemic lupus
erythematosus, myasthenia gravis, and Sjögren syndrome. They are also at increased risk for the
development of extranodal marginal zone B-cell lymphomas within the thyroid gland. However,
its relationship with thyroid epithelial cancers remains controversial, with some morphologic and
molecular studies suggesting a predisposition to papillary carcinomas (Kumar et al, 2015).
 Scintigraphy Results

Scintigraphy is used for special type of nuclear medicine procedure that uses small amounts of
radioactive material to diagnose and assess the severity of a variety of bone diseases as well as
used for the diagnosis of thyroid diseases. In the test result of the patient it showed that there is
a marked reduction in 127I content, which is indicative of Hashimoto’s thyroiditis.

Molecular Testing

Lastly molecular testing of the patient also showed that CTLA-4 gene on chromosome 2q33 and
PTPN22- on chromosome 1p13. These genes are coding for regulators of T-cell responses and
are therefore crucial in promoting immune cascade. Notable presence of these genes are
therefore associated to autoimmunity most specifically thyroid autoimmunity.

Treatment Regimen

Treatment for Hashimoto's disease may include observation and the use of medications.
The treatment of choice for Hashimoto thyroiditis (or hypothyroidism from any cause) is thyroid
hormone replacement. The drug of choice is orally administered levothyroxine sodium, usually for
life (Lee, 2020; McPherson & Pincus, 2017). Synthetic levothyroxine (Synthroid, Levoxyl,
Unithroid, and levothroid) is used to treat an underactive thyroid gland (hypothyroidism). This oral
medication restores adequate hormone levels and reverses all the symptoms of hypothyroidism
(clinically and biochemically euthyroid state). An average replacement dose is 1.6 μg/kg body
weight/day for adults, up to 4.0 μg/kg body weight/day for children, and lower doses for older
individuals (1.0 μg/kg body weight/day). Patients younger than 50 years old who have no history
or evidence of cardiac disease can usually be started on full replacement. Excessive amounts of
thyroid hormone can accelerate bone loss, which may make osteoporosis worse or add to your
risk of this disease. Overtreatment with levothyroxine can also cause heart rhythm disorders
(arrhythmias).

According to McPherson & Pincus (2017), a serum TSH between 0.5 and 2.0 μU/mL is
the therapeutic goal level for L-T4 replacement in primary hypothyroidism. A serum FT4
concentration in the upper third of the reference interval is the therapeutic target in central
hypothyroidism. If the thyroglobulin level is undetectable and no evidence of recurrence is noted
5 to 10 years after thyroidectomy, the dose of L-T4 can be reduced to give low-normal TSH values
(<0.4 μU/mL). According to an article in WebMD (2020), hair loss may occur during the first few
months of treatment. This effect is usually temporary as the body adjusts to this medication. The
most common side effects are increased appetite, weight loss, heat sensitivity, excessive
sweating, irritability, mood swings, tiredness, changes in menstrual periods, vomiting, stomach
cramps, and diarrhea.

Also, Sertraline is used to treat depression, panic attacks, obsessive compulsive disorder,
post-traumatic stress disorder, social anxiety disorder (social phobia), and a severe form of
premenstrual syndrome (premenstrual dysphoric disorder).This medication may improve the
mood, sleep, appetite, and energy level and may help restore your interest in daily living. Taking
MAO inhibitors with this medication may cause a serious (possibly fatal) drug interaction. Avoid
taking MAO inhibitors (isocarboxazid, linezolid, methylene blue, moclobemide, phenelzine,
procarbazine, rasagiline, safinamide, selegiline, tranylcypromine) during treatment with this
medication. Most MAO inhibitors should also not be taken for two weeks before and after
treatment with this medication. Initial dose is 50 mg orally once a day. Dose adjustments may be
made at intervals of at least one week (Cunha, 2021).

On the other hand, carpal tunnel syndrome treatment options include wrist splinting,
medications (pain relief such as ibuprofen), more frequent-breaks to rest the hands. Moreover,
avoiding activities that make symptoms worse.Since the patient experiencing mild immobility,
physical therapy to improve strength and movement (Mayo Clinic, 2020).

Patient Response to Therapy

After Claire’s diagnosed with Hashimoto’s thyroiditis, she was advised to start her
treatment immediately. Levothyroxine is prescribed as medication with an average dose of less
than 1.0 μg/kg body weight/day. To determine the right dosage of levothyroxine initially, generally
check the level of TSH after six to eight weeks of treatment and again after any dose changes.
Once the dose that normalizes your thyroid tests is determined, she will be likely subjected to
check the TSH level about every 12 months as the dosage if necessary to change. Thus, thyroid
hormone treatment may cause regression of the nodes or nodules. If after full evaluation
uncertainty persists (if nodules remain present) surgical exploration is indicated (McPherson &
Pincus, 2017). Thus, Sertraline used by Claire for her depression will not affect the ability to
absorb levothyroxine. It may take a few weeks or longer before we see the effects (Cunha, 2021).

Recommendations for Prevention Wellness or Alleviation

Unfortunately, there is no known way to prevent Hashimoto's thyroiditis (or inflammation

of the thyroid gland. But on the bright side, this disorder is very treatable. Like any disease,
diagnosing Hashimoto's thyroiditis early is important because it gives an earlier access to
treatment. Since hashimoto's thyroiditis is an autoimmune disorder, it is caused by a malfunction
of the immune system. Due to the fact that this disease cannot be prevented, it is much more
important to recognize the symptoms, considered as the best chance of preventing progression
(Milas, 2017).
 According to Lee (2020), there is no special diet for Hashimoto’s disease but some foods,
medicines or supplements may affect the ability to absorb levothyroxine (thyroid medication).
These include iron-containing multivitamins and calcium carbonate supplements, the ulcer
medicine sucralfate, cholestyramine and aluminum hydroxide (found in some antacids) and other
antacids. Taking these four hours before or after the levothyroxine may solve this problem.
Medications that enhance the metabolism and clearance of levothyroxine may necessitate an
increase in the replacement dose. These medications include phenytoin, carbamazepine, and
rifampin.

Eating well and a healthy lifestyle such as exercising, sleeping well and controlling stress
or practicing self-care. These can help the immune system. And most importantly, keep taking
the medications prescribed by the physician if diagnosed with hypothyroidism. Research shows
that diet and lifestyle modifications may drastically improve symptoms, in addition to standard
medication. Every person with Hashimoto’s disease responds differently to treatment, which is
why an individualized approach for this condition is so important.