The document provides an overview of the anatomy, physiology, and pathology of the thyroid gland. It discusses: - The anatomy of the thyroid gland including its location in the neck and blood supply. - Thyroid hormone synthesis which involves iodine uptake and incorporation into thyroglobulin to form T3 and T4. - Regulation of the thyroid axis by TSH from the pituitary gland and thyroid hormone feedback. - Types of thyroiditis including acute, subacute, silent, drug-induced, and chronic forms. Subacute thyroiditis is the most common type and can cause transient hypo- or hyperthyroidism. - Treatment for thyroiditis depends on the type but may

1. THYROIDITIS
DIMAS FUJIANSYAH

2. ANATOMY OF THYROID
1

3. Anatomy Overview
• The thyroid gland is divided into two lobes connected by
the isthmus
• Crosses the midline of the upper trachea at the second and
third tracheal rings
• Thyroid gland lies posterior to the sternothyroid and
sternohyoid muscles
• Wrapping around by the cricoid cartilage
• The thyroid attaches to the trachea via lateral suspensory
ligament or Berry’s ligament

4. LOOK THIS PICTURES

5. Blood Supply and Lymphatics
• The thyroid gland has an extremely rich blood supply
> six times as vascular as the kidney
> three to four times more vascular than the brain
• receives blood from the superior and inferior thyroid
arteries
> The superior thyroid artery branch of the external
carotid artery
> The inferior thyroid artery branches from the
thyrocervical trunk

6. Blood Supply and Lymphatics
• The thyroid gland is drained via the superior, middle, and
inferior thyroid veins
> The middle and superior thyroid veins drain into the
internal jugular vein
> The drainage of the inferior thyroid vein may enter either
the subclavian or brachiocephalic veins
• Lymphatic drainage of the thyroid gland involves
>cervical, prelaryngeal, pretracheal, and paratracheal
nodes

7. Nerves
• The autonomic nervous system primarily innervates the
thyroid gland
> vagus nerve provides the main parasympathetic
> inferior, middle, and superior ganglia of the sympathetic
trunk provides the sympathetic fibers
• These nerves do not play a role in the control of hormonal
production or secretio (but mostly influence vasculature)

8. Muscles
Platysma
• It sits in the anterior neck
• Extends from the superficial fascia of the deltoid, over the
clavicle

9. Muscles
Sternocleidomastoid
• The sternocleidomastoid is found anterolaterally relative to
the thyroid gland

10. Muscles
Digastric muscle
• This muscle extends from the mandibular tubercle, passes
deep and inferior to the hyoid

11. Muscles
• Infrahyoid muscles
• Omohyoid muscle
• Sternohyoid muscle
• Sternothyroid muscle
• Thyrohyoid muscle
• Inferior pharyngeal constrictor

12. PHYSIOLOGY
2

13. INTRODUCTION
• acts as a large iodine store
• The thyroid gland produces two related hormones, thyroxine (T4) and triiodothyronine
(T3) the active hormone
• Acting through thyroid hormone receptors α and β
• Hyperthyroidism is the excessive release of thyroid hormones (raised metabolism)
classically presents with the patient feeling hot and sweaty and complaining of
unexplained weight loss
• Hypothyroidism is the deficient release of thyroid hormone (low metabolism)
feeling lethargic and cold, with unexplained weight gain
• Main function:
• cell differentiation during development
• help maintain thermogenic > heat production
• metabolic homeostasis > increased rate of metabolism
• development of CNS and skeleton

14. Structures Of Thyroid Hormones
Thyroxine (T 4 ) contains four iodine atoms. Deiodination leads to
production of the potent hormone triiodothyronine (T 3 ), or the inactive
hormone reverse T 3 .

15. Histology of the thyroid gland

16. DEVELOPMENT
• The thyroid (Greek thyreos , shield, plus eidos , form)
• The thyroid gland develops from the floor of the primitive pharynx during the third
week of gestation
• developing gland migrates along the thyroglossal duct to reach its final location in
the neck
• thyroid medullary C cells that produce calcitonin (calcium-lowering hormone)
• The C cells are interspersed throughout the thyroid gland
• greatest in the juncture of the upper one-third and lower two-thirds of the gland

17. THYROID HORMONES
• stores large quantities of its secretory product
(approximately 100 days worth)
• deficiency can take a while to present clinically
• Three hormones are synthesized and secreted in the
gland:
• Thyroxine (T4)
• Tri-iodothyronine (T3)
• Calcitonin

18. SYNTHESIS
• T3 and T4 are derived from two molecules of the
amino acid and iodine
• T3 contains three iodine atoms and T4 contains four
• The synthesis of thyroid hormones occurs in the
follicle lumen

19. Thyroglobulin synthesis
• Tyrosine is converted into the glycoprotein
thyroglobulin

20. Iodine trapping
• Plasma iodide ions (I-) are actively transported from
the plasma into the follicular cells

21. Iodide oxidation
• Iodide is rapidly oxidized to iodine (I2) by hydrogen
peroxide
• reaction catalysed by a haem-containing enzyme,
thyroid peroxidase (TPO)

22. Iodination of thyroglobulin
• Reactive iodine rapidly attaches to the tyrosine
molecules
• The reaction is catalysed by TPO
• monoiodotyrosine (MIT or T1) and diiodotyrosine (DIT
or T2) are formed

23. Coupling
• Once tyrosine is iodinated, it is taken up into the
thyroglobulin colloid of the follicle and coupled
together
• Combinations of T1 and T2 can form thyroid hormones
• T3 (tri-iodothyronine) is made from T1þT2
• T4 (tetra-iodothyronine or thyroxine) is made from T2þT2.

24. Secretion
• This is controlled by thyroid-stimulating hormone (TSH
or thyrotrophin)
• Under the influence of TSH, iodinated thyroglobulin is taken
into the follicular cells by pinocytosis

26. REGULATION OF THE THYROID AXIS
• TSH
• secreted by the thyrotrope cells of the anterior pituitary, plays a role in
control of the thyroid axis and useful physiologic marker of thyroid
hormone action
• TSH is a 31-kDa hormone composed of α and β,
• subunits α subunit is common to the other glycoprotein hormones
[luteinizing hormone, follicle-stimulating hormone, human chorionic
gonadotropin (hCG)]
TSH β
• subunit is unique to TSH

27. REGULATION OF THE THYROID AXIS

28. REGULATION OF THE THYROID AXIS
• Hypothalamic TRH stimulates pituitary production of TSH, which stimulates thyroid
hormone synthesis and secretion
• Thyroid hormones, acting predominantly through thyroid hormone recetor β2
(TRβ2), feed back to inhibit TRH and TSH production
• Dopamine, glucocorticoids, and somatostatin suppress TSH
• TSH can be used for the diagnosis of hyperthyroidism (low TSH) as well as
hypothyroidism (high TSH)

29. REGULATION OF THE THYROID AXIS
• Hypothalamic TRH stimulates pituitary production of TSH, which stimulates thyroid
hormone synthesis and secretion
• Thyroid hormones, acting predominantly through thyroid hormone recetor β2
(TRβ2), feed back to inhibit TRH and TSH production
• Dopamine, glucocorticoids, and somatostatin suppress TSH
• TSH can be used for the diagnosis of hyperthyroidism (low TSH) as well as
hypothyroidism (high TSH)

30. THYROIDITIS
3

31. A clinically useful classification of thyroiditis is based
on the onset and duration of disease

32. CAUSES OF THYROIDITIS

33. SO WHAT IS IT?
• Thyroiditis is inflammation of the thyroid gland
• classified based on the onset of symptoms,
underlying etiology, and clinical symptoms
• The most common cause of thyroiditis is an
autoimmune disease
• Thyroiditis can cause transient or permanent
hypo and hyperthyroidism

34. ACUTE THYROIDITIS
• Acute thyroiditis is rare, In children and young adults, the most
common cause is the presence of a piriform sinus (branchial pouch
that connects the oropharynx with the thyroid)
• A long-standing goiter and degeneration in a thyroid malignancy
are risk factors in the elderly
• Fever, dysphagia, and erythema over the thyroid are common, as
are systemic symptoms of a febrile illness and lymphadenopathy

35. DIFFERENTIAL DIAGNOSIS OF THYROID PAIN
• subacute or, rarely, chronic thyroiditis
• hemorrhage into a cyst
• malignancy including lymphoma
• rarely, amiodarone-induced thyroiditis or amyloidosis
abrupt presentation and clinical features of acute thyroiditis rarely
cause confusion

36. HOW TO DIAGNOSIS?
• The erythrocyte sedimentation rate (ESR) and white cell count are
usually increased
• thyroid function is normal
• FNA biopsy shows infiltration by polymorphonuclear leukocytes
• culture of the sample can identify the organism
• Caution is needed in imunocompromised patients as fungal,
mycobacterial, or Pneumocystis thyroiditis can occur in this setting

37. HOW TO TREAT?
• Antibiotic treatment is guided initially by Gram stain and,
subsequently, by cultures of the FNA biopsy
• Surgery may be needed to drain an abscess (Can be localized by CT
scan or ultrasound)
• Tracheal obstruction, septicemia, retropharyngeal abscess may
complicate acute thyroiditis but are uncommon with prompt use
of antibiotics

38. SUBACUTE THYROIDITIS
• This is also termed de quervain’s thyroiditis, granulomatous
thyroiditis, or viral thyroiditis
• Many viruses have been implicated, including mumps, coxsackie,
influenza, adenoviruses, and echoviruses (do not influence
management)
• The diagnosis of subacute thyroiditis is often overlooked because
the symptoms can mimic pharyngitis
• Occurs at 30–50 years, and women are affected three times more
than men

39. Pathophysiology
• The thyroid shows a characteristic patchy inflammatory infiltrate
with disruption of the thyroid follicles and multinucleated giant
cells within some follicles
• The follicular changes progress to granulomas accompanied by
fibrosis
• Finally, the thyroid returns to normal, usually several months after
onset

40. Phase
• INITIAL PHASE
follicular destruction, there is release of Tg and thyroid hormones, leading to
increased circulating T4 and T3 and suppression of TSH
• DESTRUCTIVE PHASE
iodine uptake is low or undetectable
• After several weeks, the thyroid is depleted of stored thyroid hormone and a
phase of hypothyroidism typically occurs > Low unbound T4 (and sometimes T3)
and moderately increased TSH levels
• iodine uptake returns to normal or is even increased as a result of the rise in
TSH RECOVERY

41. Clinical manifestations
• The patient usually presents with a
painful and enlarged thyroid,
sometimes accompanied by fever
• There may be features of
thyrotoxicosis or hypothyroidism,
depending on the phase of the
illness

42. Clinical manifestations
• Malaise and symptoms of an upper respiratory tract infection may precede
• The patient typically complains of a sore throat, and examination reveals a small
goiter that is exquisitely tender
• Pain is often referred to the jaw or ear

43. Laboratory evaluation
Thyroid function tests characteristically evolve through three distinct phases over
about 6 months
• THYROTOXIC PHASE
• T4 and T3 levels are increased, reflecting their discharge from the damaged thyroid
cells, and TSH is suppressed
• T4/T3 ratio is greater than in Graves’ disease, confirmed by a high ESR and low
radioiodine uptake
• The white blood cell count may be increased, and thyroid antibodies are
negative
• HYPOTHYROID PHASE
• RECOVERY PHASE
If the diagnosis is in doubt, FNA biopsy may be useful, particularly to
distinguish unilateral involvement from bleeding into a cyst or neoplasm

44. ● Relatively large doses of aspirin (e.g., 600 mg every 4–6 h) or NSAIDs
● If this treatment is inadequate, glucocorticoids should be given
> starting dose is 40–60 mg prednisone, depending on severity
> The dose is gradually tapered over 6–8 weeks
● Thyroid function should be monitored every 2–4 weeks using TSH and
unbound T4 levels
> antithyroid drugs play no role in treatment of the thyrotoxic phase
● Levothyroxine replacement may be needed if the hypothyroid phase is
prolonged
> doses should be low enough (50 to 100 μg daily) to allow TSH-mediated
recovery
TREATMENT

45. ● Painless thyroiditis, or “silent” thyroiditis
● underlying autoimmune thyroid disease
● It has a clinical course similar to that of subacute
thyroiditis
> except that there is little or no thyroid tenderness
● presence of TPO antibodies antepartum, and it is three
times more common in women with type 1 diabetes
mellitus
SILENT THYROIDITIS

46. ● Glucocorticoid treatment is not indicated for silent
thyroiditis
● Severe thyrotoxic symptoms can be managed with a brief
course of propranolol (20–40 mg three or four times
daily)
● Thyroxine replacement may be needed for the
hypothyroid (withdrawn after 6–9 months)
● Annual follow-up thereafter is recommended
TREATMENT

47. ● Patients receiving cytokines such as IFN-α or IL-2 may
develop painless thyroiditis
● used to treat chronic hepatitis B or C and hematologic and
skin malignancies
DRUG-INDUCED THYROIDITIS

48. ● presence of TPO antibodies, more common in otherwise
healthy women than men
● The most common chronic thyroiditis is Hashimoto’s
thyroiditis
> presents as a firm or hard goiter of variable size
● Riedel’s thyroiditis is a rare disorder that typically occurs
in middle-aged women
> insidious, painless goiter with local symptoms due to
compression of the esophagus, trachea, neck veins
CHRONIC THYROIDITIS

49. ● Treatment is directed to surgical relief of compressive
symptoms
TREATMENT

50. EDUCATION
4

51. Consult with your doctor
to discuss the right
treatment
Must me doing !

52. ● Avoid smoking or drinking alcohol
> if they smoke or drink alcohol, should put a stop to these
immediately
> it blocks the iodide ration and synthesis of hormones
● Say no to macronutrients
> low-carb diet can adversely affect the thyroid
● Stay away from sugar and caffeine
> Caffeine tends to stress the body and so does sugar
> caffeine can alter the TSH levels produced by the pituitary glands
● No self-medication
The Don’ts

53. THANK YOU
WORK HARD PLAY HARD

54. DAFTAR PUSTAKA
• Leung AKC, Leung AAC. Evaluation and management of the child with hypothyroidism. World J Pediatr. 2019 Apr;15(2):124-134.
[PubMed]
• Harrison's principles of internal medicine. (1998). New York :McGraw-Hill, Health Professions Division,
• Volpé R, Row VV, Ezrin C. Circulating viral and thyroid antibodies in subacute thyroiditis. J Clin Endocrinol Metab. 1967
Sep;27(9):1275-84. [PubMed]