2. TSH
• Produced by Adenohypophysis Thyrotrophs
• Upregulated by TRH
• Downregulated by T4, T3
• Stimulates several processes
• Iodine uptake
• Colloid endocytosis
• Growth of thyroid gland
3. Thyroid Hormone
Majority of circulating hormone is T4
98.5% T4
1.5% T3
Total Hormone load is influenced by serum
binding proteins
Albumin 15%
Thyroid Binding Globulin 70%
Transthyretin 10%
Regulation is based on the free component of
thyroid hormone
5. Iodine deficiency
Iodine deficiency most common cause
of goiter & hypothyroidism worldwide
Effect of I deficiency aggravated by
goitrogens foods, with anti-thyroid
properties
(Africa, South America)
10. Goiter
Etiology
Diet: Iodine deficiency
Brassica (cabbage, turnips, cauliflower, broccoli)
Hashimoto’s thyroiditis
Early stages only, late stages show atrophic changes
May present with hypo, hyper, or euthyroid states
Graves’ disease
Due to chronic stimulation of TSH receptor
Chronic Iodine excess
Iodine excess leads to increased colloid formation and
can prevent hormone release
Medications
Immunosuppressants, antiretrovirals, heart drug
prevents release of hormone, causes goiter in 6% of
chronic users
11. Goiter Classification
Goiter: Chronic enlargement of the thyroid
gland not due to neoplasm
• Endemic goiter
• Areas where > 5% of children 6-12 years of age have
goiter
• Common in China and central Africa
• Sporadic goiter
• Areas where < 5% of children 6-12 years of age have
goiter
• Familial
12. Morphology Classification
Regarding morphology, goiters may be classified either as the
growth pattern or as the size of the growth:
•Growth pattern
•1. Uninodular (struma uninodosa) - can be either inactive or a
toxic nodule
•2. Multinodular (struma nodosa) - can likewise be inactive or
toxic, the latter called toxic multinodular goiter
•3. Diffuse (struma diffuse), with the whole thyroid appearing to
be enlarged.
•Size Class I - palpation struma - in normal posture of the head,
it cannot be seen; it is only found by palpation.
•Class II - the struma is palpative and can be easily seen.
•Class III - the struma is very large and is retrosternal; pressure
results in compression marks.
13. * Pathogenesis:
a. Parenchymatous goiter:
•Iodine deficiency → decreased thyroid hormone
synthesis → increases TSH secretion → thyroid glands
hyperplasia.
•The acini are increased in number and lined by tall
columnar cells and contain little colloid.
•If iodine deficiency is corrected after a short time, the
acini return to the normal state.
14. DIFFUSE NONTOXIC (SIMPLE) GOITER
GROSS
Diffuse symmetrical
enlargement of the
gland
SIZE: Rarely exceeds
100-150gm
C/S: Brown, glassy,
translucent
MICROSCOPY
Follicles lined by low
cuboidal or flattened
epithelial cells
Abundant colloid during
involution
16. Multinodular Goiter (MNG)
• MNG is an enlarged thyroid gland containing
multiple nodules
– The thyroid gland becomes more nodular with
increasing age
– In MNG, nodules typically vary in size
• MNG may be toxic or nontoxic
– Toxic MNG occurs when multiple sites of autonomous
nodule hyperfunction develop, resulting in
THYROTOXICOSIS
– Toxic MNG is more common in the elderly
24. Clinical Manifestations
• If thyroid function is preserved, most
goiters are asymptomatic
• If the thyroid is markedly enlarged, it can
cause tracheal or esophageal compression
25. •Swollen front of the neck
•Protruding (popping out) eyes
•A tight feeling in the throat
•Coughing
•Difficulty in swallowing & breathing
26. • Substernal goiter
– May obstruct the thoracic inlet
– Respiratory flow measurements and CT or MRI
should be used to evaluate substernal goiter in
patients with obstructive signs or symptoms
• Pemberton's sign
– Symptoms of faintness with evidence of facial
congestion and external jugular venous
obstruction when the arms are raised above the
head, a maneuver that draws the thyroid into the
thoracic inlet
27. Symptoms also include:
•Fatigue
•Frequent bowel movements
•Heat intolerance
•Increased appetite
•Increased sweating
•Menstrual irregularities (in women)
•Muscle cramps
•Nervousness
•Restlessness
•Weight loss
29. Enlargement
• 0 – the gland is not palpated
• I – some part of the gland can be palpated
• II- the gland can be seen although the neck is in a
normal shape
• III – shape of the neck is being changed
• IV – configuration of the neck is being changed
• V – an giant goiter with complications
31. Treatment Options
1. Symptom relief medications
2. Anti Thyroid Drugs – ATD
Methimazole, Carbimazole
Propylthiouracil (PTU)
1. Radio Active Iodine treatment – RAI
Rx.
2. Thyroidectomy – Subtotal or Total
3. NSAIDs and Corticosteroids – for
SAT
32. •The use of iodized table salt
•Avoid goiter promoting foods such as
cabbage, Brussels sprouts, & soy
•Thyroid Replacement Therapy
•Thyroidectomy- surgery to remove part or all
of the thyroid.
33.
34. Complications
• Heart complications:
• Atrial fibrillation
• Congestive heart failure
• Rapid heart rate
• Superior vena cava obstruction
• Other complications:
• Bone loss leading to Osteoporosis
Multinodular Goiter (MNG).
The thyroid gland becomes more nodular with age.1 MNG develops in an enlarged thyroid gland and is especially prevalent in populations in iodine-deficient areas.2 Thyroid enlargement may have progressed from a simple nontoxic goiter or have been associated with Hashimoto disease.3 MNG usually results from a low-grade, probably intermittent stimulus to the thyroid gland from iodine deficiency, goitrogens (foods that induce hypothyroidism and goiter in the diet such as cabbage, broccoli, cauliflower, and brussels sprouts),4 decreased thyroid hormone production, or an autoimmune disease, which causes multiplication and growth of small groups of thyroid cells.3 After Graves disease, toxic multinodular goiter (TMG) is the most common cause of hyperthyroidism5 and thyrotoxicosis in the elderly.6 TMG occurs most often in patients aged 50 or older and mainly in women, when the nodules in a nontoxic MNG become autonomous5 and function independent of TSH stimulation.7 It is very prevalent in geographic regions with iodine deficiency and rarely occurs in places where iodine intake is sufficient. Thyroid autonomy is most frequently found in TMGs.7 Patients are often asymptomatic or very mildly toxic, and have a goiter, and lab findings that indicate suppressed TSH with normal FT4 and T3 levels.5
References
1. Hurley DL, et al. Geriatrics. 1995;50:24-26,29-31.
2. Tonacchera M, et al. J Clin Endocrinol Metab. 2002;87:352-367.
3. Bayliss RIS, Tunbridge WMG. Thyroid Disease: the Facts. 3rd ed. Oxford, UK: Oxford University Press; 1998:121.
4. Stoewsand GS. Food Chem Toxicol. 1995;33:537-543.
5. Fisher JN. South Med J. 2002;95:493-505.
6. Vitti P, et al. J Endocrinol Invest. 2002;25(10 Suppl):16-18.
7. Krohn K, et al. J Clin Endocrinol Metab. 2001;86:3336-3345.
