د فائزة

1. Thyroid gland
April . 12. 2015

2. Thyroid gland
• Anatomy
• Histology
• Physiology
• Pathology
• Hyperthyroidism
• Hypothyroidism
• Tumors

3. 15-25
grams

4. In adults
•Two lateral lobes
•Isthmus;
level of 2nd – 3rd
tracheal rings.
•The highest rate
of blood flow

5. Thyroid blood supply

7. High mag of thyroid follicles – note Parafollicular or C-Cells (arrows)

8. Many vegetables are goiterogens, fruits are NOT
Goitrogens; chemical agents
inhibit function of the thyroid
gland.
Suppress T3 and T4 synthesis,
so the level of TSH increases,
&t hyperplastic enlargement of
the gland (goiter) follows.

9. Thyrotoxicosis
• A hypermetabolic state caused by elevated
circulating levels of free T3 and T4.
• hyperthyroidism

10. Disorders Associated with Thyrotoxicosis
Associated with Hyperthyroidism
Primary
• Diffuse hyperplasia (Graves disease)
• Hyperfunctioning (“toxic”) multinodular goiter
• Hyperfunctioning (“toxic”) adenoma
• Iodine-induced hyperthyroidism
• Neonatal thyrotoxicosis associated with maternal Graves disease
Secondary
TSH-secreting pituitary adenoma (rare)
Not Associated with Hyperthyroidism
Granulomatous (de Quervain) thyroiditis (painful)
Subacute lymphocytic thyroiditis (painless)
Struma ovarii (ovarian teratoma with ectopic thyroid)
Factitious thyrotoxicosis (exogenous thyroxine intake)

11. Thyrotoxicosis
• The 3 most common causes of thyrotoxicosis:
• Diffuse hyperplasia of the thyroid associated
with Graves disease (85% of cases)
• Hyperfunctional multinodular goiter
• Hyperfunctional thyroid adenoma

12. Hyperthyroidism
Clinical Course.
 Hypermetabolic state.
 Overactivity of the SNS
(increase in the β-adrenergic “tone”).

13. Hyperthyroidism
 Increase BMR
• The skin; soft, warm, and flushed because of
increased Bl. flow and peripheral vasodilation,
adaptations that serve to increase heat loss.
• Sweating is increased because of higher levels of
calorigenesis.
• Weight loss despite increased appetite.

14. Hyperthyroidism
• Cardiac manifestations
• Elevated cardiac contractility and cardiac output, in
response to increased peripheral O2 requirements.
• Tachycardia, palpitations.
• Arrhythmias, particularly Atrial fibrillation.
• Congestive HF.
• Cardiomegaly

15. Hyperthyroidism
Over activity of Sympathetic Nervous System;
• Tremor, hyperactivity, emotional labile, anxiety,
inability to concentrate, insomnia.
• Thyroid myopathy; Muscle weakness and decreased
muscle mass.
• GIT, hypermotility, diarrhea, & malabsorption

16. Hyperthyroidism
• Ocular changes;
• Staring gaze
• lid lag
• Proptosis (only in Graves
Dis)

18. Hyperthyroidism
• The skeletal system.
• Increased bone resorption & risk of
Osteoporosis & fractures
• Atrophy of skeletal M.
• Minimal liver enlargement due to fatty
changes in the hepatocytes;
• generalized lymphoid hyperplasia &
lymphadenopathy in Graves disease.

19. Thyroid storm
• The abrupt onset of Severe hyperthyroidism.
• Occurs in Graves disease, from an acute elevation in
catecholamine levels, (during infection, surgery,
cessation of antithyroid medication, or any form of
stress).
• Patients are often febrile and present with tachycardia
out of proportion to the fever.
• Thyroid storm is a medical emergency.
• Untreated patients die of cardiac arrhythmias.

20. Apathetic hyperthyroidism
• Thyrotoxicosis occurring in older adults, in whom
advanced age and co-morbidities may blunt the typical
features of hyperthyroidism.
• The diagnosis made during investigations for
unexplained weight loss or worsening CV disease.

21. Diagnosis of hyperthyroidism
• Both Clinical and laboratory findings.
• A low TSH value
• High free T4.
• Serum TSH is the most useful single screening test for
hyperthyroidism, because its levels are decreased even
at the earliest stages, when the disease may still be
subclinical.
• RAI uptake by the thyroid gland.

23. “T3 toxicosis”
• Occasionally, hyperthyroidism results from
increased circulating T3 (“T3 toxicosis”)
• In these cases, free T4 may decreased,
• And measurement of serum T3 may be useful

24. Graves disease
• The most common cause of endogenous hyperthyroidism.
• Characterized by a triad of clinical findings:
• • Hyperthyroidism associated with diffuse enlargement of the
gland
• • Infiltrative ophthalmopathy with resultant exophthalmos
• • Localized, infiltrative dermopathy, (pretibial myxedema,
which is present in a minority of patients

25. Graves disease
• peak incidence between 20 and 40 years of age.
• Women are affected 10 times more than men.
• affect 1.5% to 2% of women in USA

26. Pathogenesis of Graves disease
• Autoimmune disorder
• Autoantibodies against multiple thyroid proteins,
most importantly the TSH receptor.
• A variety of Abs that can either stimulate or block
TSH receptor
• Thyroid stimulating immunoglobulin (TSI) Abs, in
90% of patients
• TSI binds to the TSH receptor and mimics its actions,
stimulating adenyl cyclase and increasing the release
of thyroid hormones.

27. Graves ophthalmopathy
• Exopthalmos, protrusion of the eyeball is associated with;
increased Vo. Of retroorbital CT & extraocular M., for several
reasons;
• (1) infiltration of retroorbital space by mononuclear cells;
• (2) inflammation, edema and swelling of extraocular M;
• (3) accumulation of ECM, glycosaminoglycans such as
hyaluronic acid and chondroitin sulfate;
• (4) increased numbers of adipocytes (fatty infiltration).
• These changes displace the eyeball forward and can interfere
with the function of the extraocular muscles.

28. The thyroid gland is symmetrically enlarged due
to diffuse hypertrophy and hyperplasia of thyroid
follicular epithelial cells
Graves disease

29. Graves disease

30. Graves Disease
• ■ Graves disease, the most common cause of endogenous
hyperthyroidism,
• characterized by the triad of thyrotoxicosis, ophthalmopathy,
and dermopathy.
• ■ It is an autoimmune disorder caused by activation of thyroid
epithelial cells by autoantibodies to the TSH receptor that
mimic TSH action (thyroid-stimulating immunoglobulins).
• ■ The thyroid in Graves disease is characterized by diffuse
hypertrophy and hyperplasia of follicles and lymphoid
infiltrates;
• glycosaminoglycan deposition and lymphoid infiltrates are
responsible for the ophthalmopathy and dermopathy.
• ■ Laboratory features include elevations in serum free T3 and
T4 and decreased serum TSH.

33. G
O
I
T
E
R

34. Hyperfunctional thyroid adenoma

35. • The antithyroid agent
propylthiouracil;
• inhibits the oxidation of iodide and
thus blocks the production of thyroid
hormones;
• & inhibits the peripheral deiodination
of circulating T4 into T3, thus
ameliorating symptoms of thyroid
hormone excess

36. • Iodide, when given in large doses to
individuals with thyroid hyperfunction,
also blocks the release of thyroid
hormones by inhibiting the proteolysis
of thyroglobulin.
• Thus, thyroid hormone is synthesized
and incorporated into colloid, but it is
not released into the blood.

37. Hypothyroidism
• Primary and Secondary
• caused by a structural or functional derangement
that interferes with the production of thyroid
hormone
• common disorder
• increases with age,
• 10 fold more in women than men.
• Myxedema (coma)
– Sluggishness
– Cool skin

38. Causes of Hypothyroidism
Primary
Iodine deficiency*
Autoimmune hypothyroidism
Hashimoto thyroiditis*
Postablative
Surgery, radioiodine therapy, or external irradiation
Genetic defects in thyroid development (PAX8, FOXE1, TSH receptor
mutations) (rare)
Thyroid hormone resistance syndrome (THRB mutations) (rare)
Drugs (lithium, iodides, p-aminosalicylic acid)*
Congenital biosynthetic defect (dyshormonogenetic goiter) (rare) *
Secondary (Central)
Pituitary failure (rare)
Hypothalamic failure (rare)

39. Hypothyroidism
• Primary hypothyroidism
• form majority of cases,
• +/- (goiter).
• Primary hypothyroidism can be
• congenital,
• autoimmune,
• iatrogenic.

40. Congenital hypothyroidism
• Most often due to Endemic iodine deficiency in the
diet.
• Rarely due to Inborn Errors of Metabolism,
(dyshormonogenetic goiter), defect in synthesis of
thyroid hormones.
• Complete absence of thyroid (rare)

41. Autoimmune hypothyroidism
• The most common cause of hypothyroidism in
iodine-sufficient areas of the world.
• The majority are due to Hashimoto thyroiditis.
• Circulating autoantibodies, are;
• antimicrosomal, antithyroid peroxidase, and
antithyroglobulin antibodies,
• Thyroid is enlarged (goitrous).
• can occur in isolation or in conjunction with
autoimmune polyendocrine syndrome.

42. Iatrogenic hypothyroidism
• Surgery
• Radiation-induced ablation.
• Drugs (e.g., methimazole, & propylthiouracil)
agents used to treat nonthyroid conditions
(lithium, p-aminosalicylic acid).

43. Secondary (central) hypothyroidism
• Deficiencies of TSH or, more uncommonly, TRH.
• Any of the causes of hypopituitarism or of
hypothalamic damage from tumors, trauma,
radiation therapy, or infiltrative diseases can cause
central hypothyroidism.

44. Cretinism
• Hypothyroidism in infancy
or early childhood.
• impaired development of
the skeletal system and CNS,
• severe mental retardation,
• short stature,
• coarse facial features,
• protruding tongue
• Umbilical hernia.
• The severity of the mental impairment related to the
time at which thyroid deficiency occurs in utero.

45. Cretinism

46. Cretinism

47. Cretinism

48. • Myxedema is applied to hypothyroidism
developing in the older child or adult.

51. Endocrine - Thyroid
•Embryology – Thyroglossal Duct Cyst (TGDC)

52. THYROGLOSSAL DUCT CYST