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2. Thyrotoxicosis and Hyperthyroidism

3. Hyperthyroidism

4. Hyperthyroidism
• It is a term reserved for disorder
that result in overproduction of
hormone by the thyroid gland.
• In short in hyperthyroidism the
pathology is in the thyroid gland
itself.

5. Thyrotoxicosis

6. Thyrotoxicosis
• Biochemical and physiological
manifestation of Excessive thyroid
hormone.
• Thyrotoxicosis need not be due to
hyperthyroidism
• But hyperthyroidism mostly produce
thyrotoxicosis.

7. Hyperthyroidism Vs thyrotoxicosis

8. Hyperthyroidism Vs thyrotoxicosis
No Hyperthyroidism Toxicosis without
hyperthyroidism
1, Grave’s disease Subacute thyroiditis
2, Toxic nodular goitre Ectopic functioning thyroid
3, Toxic adenoma Silent thyroiditis
4, Jod – Basedow’s
disease
Struma ovarii
5, Metastatic follicular
carcinoma
6, Trophoblastic tumours
7, Postpartum thyroiditis

9. Thyroid Hormone Function

10. Thyroid Hormone Function
• Thyroid hormones affect almost every system
in the body .
• T3 increases oxygen consumption, basal
metabolic rate, and heat production by
stimulation of Na+/K+ ATPase in various
tissues

11. • The Jod-Basedow effect (also Jod-Basedow
syndrome and Jod-Basedow phenomenon) is
hyperthyroidism following administration of
iodine or iodide, either as a dietary supplement
or as iodinated contrast for medical imaging.

12. • Wolff-Chaikoff effect is an autoregulatory
phenomenon, whereby a large amount of
ingested iodine acutely inhibits thyroid
hormone synthesis within the follicular cells,
irrespective of the serum level of thyroid-
stimulating hormone

13. Diffuse toxic goitre
(Grave’s disease)

14. Diffuse toxic goitre
(Grave’s disease)
• This disorder is known as Graves' disease after
Robert Graves, an Irish physician who described
three patients in 1835.
• It is an autoimmune disease with a strong familial
predisposition, female preponderance (5:1).
• Peak incidence between the ages of 40 to 60 years.
• Graves' disease is characterized by thyrotoxicosis,
diffuse goiter, and extrathyroidal conditions
including ophthalmopathy, dermopathy (pretibial
myxedema), thyroid acropachy, gynecomastia, and
other manifestations.

15. Etiology, Pathogenesis, and
Pathology

16. Etiology, Pathogenesis, and
Pathology
• The exact etiology of the initiation of the
autoimmune process in Graves' disease is
not known.
• Postpartum state, iodine excess, lithium
therapy, and bacterial and viral infections
have been suggested as possible triggers.
• Genetic factors also play a role-HLA-B8
and HLA-DR3 and HLADQA1*0501.

17. Etiology, Pathogenesis, and
Pathology
• Some unknown factors Stimulate B lymphocytes,
which produce antibodies directed against the thyroid
hormone receptor.
• TSIs or antibodies that stimulate the TSH-R, as well
as TSH-binding inhibiting immunoglobulins or
antibodies have been described.
• The thyroid-stimulating antibodies stimulate the
thyrocytes to grow and synthesize excess thyroid
hormone, which is a hallmark of Graves' disease.
• Graves' disease also is associated with other
autoimmune conditions such as type I diabetes
mellitus, Addison's disease, pernicious anemia, and
myasthenia gravis.

18. Etiology, Pathogenesis, and
Pathology
• Macroscopically, the thyroid gland in patients
with Graves' disease is diffusely and smoothly
enlarged, with a concomitant increase in
vascularity.
• Microscopically, the gland is hyperplastic, and
the epithelium is columnar with minimal
colloid present.
• The nuclei exhibit mitosis, and papillary
projections of hyperplastic epithelium are
common.

19. Presentation

20. Presentation
• Variable.
• Increase in sympathetic nervous system
symptoms.
• Younger patients >sympathetic activation,
such as anxiety, hyperactivity, and tremor
• Older patients >more cardiovascular
symptoms, including dyspnea and atrial
fibrillation with unexplained weight loss

21. Clinical manifestation

22. Clinical manifestation
• Divided into those related to
hyperthyroidism and those specific to
Graves' disease.
• Hyperthyroid symptoms
-Heat intolerance
-Increased sweating and thirst
-Weight loss despite adequate
caloric intake

23. Epidemiology

24. Epidemiology
• incidence of hyperthyroidism is estimated
between 0.05% and 1.3%
• incidence increases with age.
• Graves disease predominantly affects those
aged 20-40 years
• A slight predominance of hyperthyroidism
exists among females.
• White and Hispanic populations in the United
States have a slightly higher prevalence

25. Clinical manifestation

26. Clinical manifestation
• Symptoms of increased adrenergic stimulation
-palpitations, nervousness, fatigue,
emotional lability, hyperkinesis,
heat intolerance and tremors.
• GI symptoms include increased frequency of
bowel movements and diarrhea.
• Female patients often develop amenorrhea,
decreased fertility, and an increased incidence of
miscarriages.
• Children experience rapid growth with early bone
maturation.
• Older patients may present with cardiovascular
complications such as atrial fibrillation and
congestive heart failure.

27. Other manifestation of Grave’s

28. Other manifestation of Grave’s
• Approximately 50% of patients with Graves'
disease also develop clinically evident
ophthalmopathy, and dermopathy occurs in 1 to 2%
of patients.
• Eye signs - lid lag (von Graefe's sign), spasm of the
upper eyelid revealing the sclera above the
corneoscleral limbus (Dalrymple's sign), and a
prominent stare, due to catecholamine excess.
• True infiltrative eye disease results in periorbital
edema, conjunctival swelling and congestion
(chemosis), proptosis, limitation of upward and
lateral gaze (from involvement of the inferior and
medial rectus muscles, respectively), keratitis, and
even blindness due to optic nerve involvement.

29. Von Graefe's sign is the lagging of the upper
eyelid on downward rotation of the eye,

30. • Rare bony involvement leads to subperiosteal
bone formation and swelling in the
metacarpals (thyroid acropachy).
• Onycholysis, or separation of fingernails from
their beds, is a more commonly observed
finding.

31. Clinical signs

32. Clinical signs
• Weight loss and facial flushing may be evident.
• The skin is warm and moist and African American
patients often note darkening of their skin.
• Tachycardia or atrial fibrillation is present with
cutaneous vasodilation leading to a widening of the pulse
pressure and a rapid falloff in the transmitted pulse wave
(collapsing pulse).
• A fine tremor, muscle wasting, and proximal muscle
group weakness with hyperactive tendon reflexes often
are present.
• The thyroid usually is diffusely and symmetrically
enlarged, as evidenced by an enlarged pyramidal lobe.
• Overlying bruit or thrill and loud venous hum in the
supraclavicular space

36. Tests of Thyroid Function

37. Tests of Thyroid Function
Serum Thyroid-Stimulating Hormone (Normal
0.5–5 U/mL): Serum TSH levels reflect the ability of
the anterior pituitary to detect free T4 levels. Small
changes in free T4 lead to a large shift in TSH levels
(Inverse relation).
Total T4 (Reference Range 55–150 nmol/L) and T3
(Reference Range 1.5–3.5 nmol/L).
Free T4 (Reference Range 12–28 pmol/L) and Free
T3 (3–9 pmol/L).
Thyroid Antibodies : Thyroid antibodies include
anti-Tg, antimicrosomal, or anti-TPO and thyroid-
stimulating immunoglobulin (TSI).

38. Diagnostic Tests

39. Diagnostic Tests
• Suppressed TSH with or without an elevated free T4 or
T3 level.
• If eye signs are present, other tests are generally not
needed.
• In the absence of eye findings, an 123I uptake and scan
should be performed.
• An elevated uptake, with a diffusely enlarged gland,
confirms the diagnosis of Graves' disease
• It helps to differentiate it from other causes of
hyperthyroidism.
• Anti-Tg and anti-TPO antibodies are elevated in up to
75% of patients.
• Elevated TSH-R or thyroid-stimulating antibodies
(TSAb) are diagnostic of Graves' disease and are
increased in about 90% of patients

41. Management

42. Management
• Guidelines for the management of
hyperthyroidism and other causes of
thyrotoxicosis have been developed by the
American Thyroid Association (ATA) and
the American Association of Clinical
Endocrinologists.
• These guidelines include 100 evidence-
based recommendations concerning the care
of these patients.

43. Management
• Graves' disease may be treated by any of
three treatment modalities—
- Antithyroid drugs
- Thyroid ablation with radioactive 131I
- Thyroidectomy

44. Anti Thyroid Drugs

45. Anti Thyroid Drugs
• Antithyroid medications generally are administered
in preparation for RAI ablation or surgery.
• The drugs commonly used are propylthiouracil
(PTU, 100 to 300 mg three times daily) and
methimazole (10 to 30 mg three times daily, then
once daily).
• Both drugs reduce thyroid hormone production by
inhibiting the organic binding of iodine and the
coupling of iodotyrosines (mediated by TPO).
• PTU also inhibits the peripheral conversion of T4 to
T3, making it useful for the treatment of thyroid
storm.
• PTU has a lower risk of transplacental transfer.

46. Anti Thyroid Drugs
• Side effects of treatment include reversible
granulocytopenia, skin rashes, fever,
peripheral neuritis, polyarteritis, vasculitis,
and, rarely, agranulocytosis and aplastic
anemia.
• The catecholamine response of thyrotoxicosis
can be alleviated by administering beta-
blocking agents.
• Propranolol is the most commonly prescribed
medication in doses of about 20 to 40 mg four
times daily.

47. Radioactive Iodine Therapy
(131I)

48. Radioactive Iodine Therapy
(131I)
• RAI forms the mainstay of Graves' disease treatment in
North America.
• The major advantages of this treatment are the
avoidance of a surgical procedure and its concomitant
risks.
• The 131I dose is calculated after a preliminary scan, and
usually consists of 8 to 12 mCi administered orally.
• After standard treatment with RAI, most patients
become euthyroid within 2 months.
• However, only about 50% of patients treated with RAI
are euthyroid 6 months after treatment, and the
remaining are still hyperthyroid or already hypothyroid

49. Radioactive Iodine Therapy
(131I)
• RAI therapy is therefore most often used in older
patients with small or moderate-sized goiters, those
who have relapsed after medical or surgical therapy.
• Contraindication :
Absolute : Women who are pregnant or
breastfeeding.
Relative : Young patients (i.e., especially children
and adolescents), those with thyroid
nodules, and those with
ophthalmopathy.

50. Surgical Treatment
• Surgery is recommended when RAI is
contraindicated
(a) Have confirmed cancer or suspicious
thyroid nodules.
(b) Young.
(c) Pregnant or desire to conceive soon
after treatment.
(d) Severe reactions to antithyroid medications
(e) Large goiters causing compressive
symptoms.
(f) Reluctant to undergo RAI therapy.

51. Surgical Treatment

52. Surgical Treatment
• What surgical Procedure ?
1) Near total thyroidectomy
2) Subtotal thyroidectomy
3) Total thyroidectomy
4) Hartley- Dunhill procedure
- Solely based on discretion of surgeon and
their experience.

53. Management of Ophthalmopathy
•

54. Management of Ophthalmopathy
• Tight-fitting sunglasses.
• Saline eye drops
Exposure keratitis
 Saline gel or drops
 Taping eyelids closed with paper tape
before sleep.
 Goggles at night to keep the eyes moist

55. Management of Ophthalmopathy
• A medical emergency -Optic nerve
compression with early loss of color vision
and orbital pain>permanent vision loss.
• High-dose glucocorticoids
• Orbital decompression surgery
• Ocular radiation therapy.

56. Toxic MNG

57. Toxic MNG
• Toxic multinodular goiters usually occur in older
individuals, who often have a prior history of a
nontoxic multinodular goiter.
• Over several years, enough thyroid nodules become
autonomous to cause hyperthyroidism.
• Hyperthyroidism also can be precipitated by
iodide-containing drugs such as contrast media and
the antiarrhythmic agent amiodarone (Jodbasedow
hyperthyroidism).
• Symptoms and signs of hyperthyroidism are similar
to Graves' disease, but extrathyroidal
manifestations are absent.

58. Toxic MNG
• Blood tests are similar to Graves' disease with
a suppressed TSH level and elevated free T4 or
T3 levels.
• USG shows nodules.
• RAI uptake also is increased, showing multiple
nodules with increased uptake and suppression
of the remaining gland.
• Treatment – After adequately controlling
hyperthyroid state total thyroidectomy is
treatment of choice.

59. Toxic Adenoma (Plummer's Disease)

60. Toxic Adenoma (Plummer's Disease)
• Hyperthyroidism from a single hyperfunctioning nodule
typically occurs in younger patients who note recent
growth of a long-standing nodule along with the
symptoms of hyperthyroidism.
• Most hyperfunctioning or autonomous thyroid nodules
have attained a size of at least 3 cm before
hyperthyroidism occurs.
• Physical examination usually reveals a solitary thyroid
nodule without palpable thyroid tissue on the
contralateral side.
• RAI scanning shows a "hot" nodule with suppression
the rest of the thyroid gland. These nodules are rarely
malignant.
• Surgery (lobectomy and isthmusectomy) is preferred to
treat young patients and those with larger nodules.

61. Thyroid Storm

62. Thyroid Storm
• Thyroid storm is a condition of hyperthyroidism
accompanied by fever, central nervous system agitation or
depression, cardiovascular dysfunction that may be
precipitated by infection, surgery, or trauma.
• Beta blockers are given to reduce peripheral T4 to T3
conversion and decrease the hyperthyroid symptoms.
• Oxygen supplementation and hemodynamic support
should be instituted.
• Non-aspirin compounds can be used to treat pyrexia and
Lugol's iodine or sodium ipodate (intravenously) should
be administered to decrease iodine uptake and thyroid
hormone secretion.
• PTU therapy blocks the formation of new thyroid
hormone and reduces peripheral conversion of T4 to T3.
• Corticosteroids often are helpful to prevent adrenal
exhaustion and block hepatic thyroid hormone conversion.

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