Presentation intended for Undergraduate Seminar. Department of General Surgery, Viswabharathi Medical College, Kurnool.

1. HYPOTHYROIDISM
- D. VIGHNESH, 4th Year MBBS,
Dept. of General Surgery, VMCKNL

2. INTRODUCTION
Hypothyroidism results from low levels of thyroid hormone with varied etiology
and manifestations. Untreated hypothyroidism increases morbidity and mortality.
The patient presentation can vary from asymptomatic disease to myxedema
coma. Today, the diagnosis of hypothyroidism is easily made with simple blood
tests and can be treated with exogenous thyroid hormone.

3. CLASSIFICATION

5. CRETINISM
Cretinism is defined as thyroid hormone deficiency present at fetal / neonatal development
It must be diagnosed promptly because delay in treatment can lead to irreversible
neurological deficits.
Before the newborn screening program, it was one of the most common preventable causes
of intellectual disability. Newborn screening (NBS) programs have led to earlier diagnosis
and treatment, resulting in improved neurodevelopmental outcomes.

7. MANAGEMENT
Treatment with levothyroxine (L-T4) must be started immediately after the diagnosis of
congenital hypothyroidism (CH).
NBS programs and early L-T4 treatment initiation (prior to 2 weeks of life) can prevent
intellectual deficits and optimize neurodevelopmental outcomes. L-T4 alone is the treatment
of choice.
The initial dose depends upon the severity of CH. A higher initial L-T4 dose of 10 to 15
micrograms (ug)/kg/day (50 ug/day for full-term infants with severe CH) is recommended,
especially for neonates with a very low pretreatment T4 level. A high initial L-T4 dose can
normalize serum T4 in 3 days and TSH by two weeks of therapy.

8. ADULT HYPOTHYROIDISM

9. INVESTIGATIONS

10. TREATMENT

11. MYXOEDEMA
Myxedema is a serious disorder with
high mortality. Most patients die from
GI bleeding, sepsis, or respiratory
failure despite optimal treatment. Poor
prognostic factors include advanced age,
persistent hypothermia, and altered
mental status.
Treatment:
Bolus of 0,5 mcg T4 or 10 mcg T3,
preferably IV over every 4 to 6 hours.
Additionally, IV Broad spectrum
Antibiotics and Hydrocortisone are
recommended
DYSHORMONOGENESIS
Thyroid dyshormonogenesis continues to
be a significant cause of congenital
hypothyroidism because of genetic
deficiencies in enzymes overlooking
hormone synthesis.
Common family history.
Most commonly affects Thyroid
Peroxidase (TPO) and Thyroglobulin
activity. Pendred syndrome is a classical
example of the condition.

12. BENIGN TUMORS OF THE
THYROID

13. CLASSIFICATION OF THYROID
TUMORS

14. FOLLICULAR ADENOMA OF THYROID

15. INTRODUCTION
Follicular adenomas are one subset of benign neoplasms that can occur in the thyroid gland
or ectopic thyroid tissue. They typically present as a solitary thyroid nodule or in
association with nodular hyperplasia or thyroiditis. Thyroid nodules are palpable in 4 to 7
% of individuals, but the prevalence of nodules detected incidentally by ultrasound shows a
higher prevalence of 19 to 67 percent. The majority of thyroid nodules are asymptomatic..
Most of these are benign, although 5% exhibit malignant features. Although the
distinguishing line between the adenoma itself and its malignant counterpart is tricky, this
is for all practical purposes a benign neoplasm.

17. ETIOLOGY
Although follicular adenomas are mostly sporadic, multiple other etiological factors have been identified Other causes
implicated in the development of a follicular adenoma include:
● Iodine deficiency: This is a known risk factor seen in individuals consuming non-iodized sea salt regularly.
● Genetic alterations: PTEN hamartoma tumor syndrome (PHTS) includes several syndromes like Cowden
syndrome and BRRS. Multiple follicular adenomas may occur along with other clinical manifestations. PTHS is
due to mutations causing inactivation of the PTEN tumor suppressor gene. Other genetic mutations in BRAF,
NRAS, RET, and KRAS can also cause unexplained follicular adenomas. Follicular adenomas are also part of
various syndromes like Familial adenomatous polyposis(FAP), Carney Complex syndrome. Genetic
rearrangement of the PAX8-PPAR gene causes loss of follicular growth inhibition, thus facilitating the
development of follicular neoplasms.
● Prior I-131 radiation exposure also increases the risk of malignant lesions of the thyroid.

19. HISTOPATHOLOGY
Follicular adenoma is grossly described as a solitary, encapsulated nodule; the size can be extremely variable,
ranging from a few millimeters to 10-15 cm. The color vary from tan to light brown with solid and fleshy
appearance. It can resemble multinodular goiter due to secondary changes in hemorrhage and cystic
degeneration
The two key characteristics that make the follicular lesion malignant is the evidence of capsular invasion and
angioinvasion.
Histological examination of the nodule reveals a follicular architecture present in the entire or nearly entire
lesion. The nodule can be described as either microfollicular or macrofollicular growth pattern, and the
thyrocytes have a normal cytological appearance.

21. CLINICAL PRESENTATION
● Most patients with a follicular adenoma present with solitary thyroid nodule in an
otherwise normal thyroid gland, however, it may occur in association with
thyroiditis or nodular hyperplasia. while taking history and performing a physical of
a patient with neck swelling, it is imperative to keep in mind the features of
hyperthyroidism or hypothyroidism that could accompany the presentation.
● Family history of Hashimoto disease, Grave disease thyroid carcinoma or familial
syndromes like Gardners all are valid points to consider. Commonly patients
present with and visually describe a slowly growing mass in the neck, pressure
sensation over the neck.

22. CLINICAL PRESENTATION
● Pain seldom accompanies a thyroid nodule unless spontaneous hemorrhage or
cystic degeneration has occurred within the nodule. Pressure symptoms could
cause dyspnea due to tracheal compression, increased coughing, voice hoarseness,
and choking spells due to recurrent laryngeal nerve irritation and dysphagia
secondary to esophagus compression
● Patients with a follicular adenoma present with a thyroid nodule that's palpable on
examination or identified on an imaging study. Nodules less than 1 cm are usually
challenging to palpate unless located anteriorly on the gland. There may be more
than one nodule that is palpated. However, even after neck palpation, nearly half of
these nodules go undetected and can only be picked up on ultrasonography

23. INVESTIGATIONS
● The four main parameters to assess in a thyroid nodule evaluation are detailed patient
history, physical examination, baseline serum TSH assay followed by an ultrasound.
● 5% of microfollicular adenomas, when subjected to histopathological examination, are
reported as follicular cancers
● CT scan and MRI have a limited role in the initial evaluation f solitary thyroid nodule.
Indications for these imaging techniques include suspected tracheal involvement,
either by invasion or compression, extension into the mediastinum, or recurrent
disease.
● FNA is performed to provide a cytological examination of the nodule, and it remains
the mainstay for assessing these lesions, although it may not provide a diagnosis in all
cases. The success rate of FNA is improved when the procedure is done under
ultrasound guidance.

24. MANAGEMENT
Medical Management
● If the patient is not clinically euthyroid, medical therapy done to achieve a
clinically euthyroid state.
● In such lesions, additional, free T3, T4 assay must be done. As mentioned
above, an iodine-123 thyroid scan may help determine the functionality of the
nodule. These patients must be appropriately treated with medication.
● The patient may undergo observation or levothyroxine suppression therapy as
an initial treatment modality. Levothyroxine is administered for six months to
determine if the nodule decreases in size.

25. MANAGEMENT
Surgical Management
● In the case of follicular neoplasms determined by FNA, the risk of malignancy is less than 1% in a
hyperfunctioning nodule, with a higher 20% risk if the nodule is hypo functioning.
● If the FNA result shows a follicular neoplasm, surgical management in the form of a thyroid
lobectomy with isthmusectomy is the norm. If the ultrasound shows suspicious features, the
surgeon should keep in mind the likelihood of malignancy.
● After due consideration of additional risk factors like family history, the presence of other
comorbidities, previous history of neck/head radiation, a decision of performing a total
thyroidectomy may be taken.
● Patients having a solitary toxic nodule, after determination of the functionality of the same, could
undergo therapeutic iodine-131 therapy. Surgically, a unilateral thyroid lobectomy is adequate.
● If the histopathological examination (HPE) examination confirms the Follciular neoplasm as an
adenoma, no further intervention is required.

26. Main Advantages of Surgical Therapy
● Relief from pressure-compressive symptoms like dyspnea,
dysphagia, hoarseness, etc
● Removal of the lesion helps alleviate the patient's anxiety
● Resolves the issues of thyrotoxicosis in a toxic follicular
adenoma
● Avoids unnecessary radiation exposure to the healthy part of
the thyroid

27. PROGNOSIS
● Follicular adenomas are benign neoplasms. They are slow-growing and can progress
to a size that may cause compressive symptoms. The patient should ideally be
reassured that these do not signify a malignant process but rather that the mass is
causing compression on another structure
● 20% of nonfunctioning follicular adenomas have oncogene mutations that may
progress to develop into a follicular carcinoma.
● Thyroxine supplementation is not recommended to suppress the gland unless
hypothyroidism occurs after gland lobectomy.

28. THANK YOU