2. GENERAL ASPECTS OF
THYROID GLAND
• Anatomy : Weight ranges from 12
to 30 g
• Located in the neck, anterior to
the trachea
• Produces T4 and T3 (Active
hormones)
4. THYROID DISORDERS MAY BE
CLASSIFIED AS:-
Hyperthyroidism (Thyrotoxicosis)
•Overproduction of Thyroid hormones
Hypothyroidism
(Gland destruction)
•Underproduction of Thyroid
hormones
5. LABORATORY EVALUATION
Normal TSH levels practically excludes
abnormalities
If TSH is abnormal, next steps:-
Total and free T4 & T3 levels
TSI( Thyroid Stimulating Ig)
TPO(Thyroid Peroxidase Ab)
Anti mitochondrial Ab
Serum Tg (Thyroglobulin)
Radioactive uptake and Thyroid scanning
6. .
TSH high usually means Hypothyroidism
Rare causes
o TSH secreting pituitary tumor
o Thyroid hormone resistance
TSH low usually means Hyperthyroidism
Other causes
o First trimester of pregnancy
o After treatment of Hyperthyroidism
o Some medications (Esteroids-Dopamine)
8. GOITER
A goiter is a swelling of the neck or the
larynx resulting from the enlargement of the
thyroid gland ( Thyromegaly ).
Worldwide over 90 % cases of goiter are
caused by iodine deficiency.
It may be associated with both
Hypothyroidism and Hyperthyroidism.
9. .
SIGNS AND SYMPTOMS
For Hyperthyroidism:-
• Tachycardia
• Palpitations
• Nervousness
• Tremors
• Increased BP
• Heat intolerance
10. .
For Hypothyroidism
• Weight gain despite poor appetite
• Cold intoleration
• Constipation
• Lethargy
But, these symptoms are often non-
specific and makes diagnosis difficult.
13. .
CAUSES:
1. Iodine deficiency
2. Congenital hypothyroidism
3. Pituitary diseases
4. Thyroid cancer
5. Thyroid hormone insensitivity
TREATMENT:
It is treated according to the cause, if thyroid
gland is producing too much T4 and T3,
radioactive iodine is given to the patient to
shrink the gland.
If the cause is iodine deficiency, it is
supplemented as lugol’s solution or KI
14. GRAVE’S DISEASE
Also known as toxic diffuse goiter is an
autoimmune disease that affects the thyroid
gland.
It is the most common cause of
hyperthyroidism.
The exact cause of the disease is unclear.
However, it is believed to involve a
combination of genetic and environmental
factors.
15. SIGNS AND SYMPTOMS:
Almost all of the signs of the disease is
believed to be a result of hyperthyroidism.
These include insomnia, hand tremors,
hyperactivity, heat intolerance, excessive
sweating, weight loss despite increased
appetite, etc.
Exceptions are ophthalmopathy, goiter and
pretibial myxedema .
16. MECHANISM:
Thyroid stimulating immunoglobins
recognize and bind to Thyrotropin
receptor(TSH receptor) which further
stimulates the release of T3 & T4
Thyroxine receptors in the pituitary gets
activated by surplus hormone suppressing
further release of TSH in a negative
feedback loop.
The result is very high levels of circulating
thyroid hormone and a low TSH level.
18. TREATMENT
Treatment of graves’ disease include
antithyroid drugs which reduces the production
of thyroid hormones.
Radioiodine is also used as a measure.
Thyroidectomy(surgical excision of gland) is
also used in many cases.
Mild cases of ophthalmopathy could be treated
by lubricant eye drops or non-steroidal anti
inflammatory drops.
19. CRETINISM
Cretinism is a condition of severely stunted
physical and mental growth due to untreated
congenital deficiency of thyroid hormone,
usually due to maternal hypothyroidism.
PATHOPHYSIOLOGY
Cretinism can be endemic, genetic or sporadic.
Poor growth is apparent as early as the first year
of life. It causes mental deterioration, swelling of
skin and loss of hair. Bone maturation and
puberty is severely delayed.
Ovulation is impeded and infertility is common.
20. CAUSE AND TREATMENT
Most common cause is iodine deficiency.
Populations living in areas with low soil iodine
concentration are prone to this disease.
Sporadic and genetic cretinism results from abnormal
development or function of the fetal thyroid gland.
This type of cretinism has been almost completely
eliminated in developed countries by early diagnosis by
newborn screening schemes followed by lifelong treatment
with T4.
Frequent monitoring (every 2–3 weeks during the first
months of life) is recommended to ensure that infants with
congenital hypothyroidism remain within the high end of
normal range.
22. MYXEDEMA
Myxedema is a term used synonymously with severe
hypothyroidism
Myxedema develops in the patient with
almost total lack of thyroid hormone function
It is generally characterized by bagginess under the eyes
and swelling of the face.
In this condition, greatly increased
quantities of hyaluronic acid and chondroitin sulfate
bound with protein form excessive tissue gel in the
interstitial spaces, and this causes the total quantity of
interstitial fluid to increase.
23. .
Because of the gel nature of the excess fluid, it is
mainly immobile, and the edema is the nonpitting
type.
CAUSES
Myxedema can occur in:
Hyperthyroidism, associated with pretibial
myxedema and exophthalmos. Pretibial myxedema
can occur in 1–4% of patients with Graves' disease, a
cause of hyperthyroidism.
Hypothyroidism, including Hashimoto's thyroiditis
24. PATHOPHYSIOLOGY
Myxedema causes specific forms of dermal edema.
The connective fibres is separated by an increased amount
of mucosaccharides.
This protein-mucosaccharide complex binds water,
producing non-pitting boggy edema.
In particular around eyes, hands, and feet.
Myxedema is also responsible for thickening of tongue and
laryngeal and pharyngeal mucous membranes.
27. HASHIMOTO'S THYROIDITIS
It is an auto-immune disease in which the thyroid
gland is gradually destroyed.
Over time the thyroid may enlarge and form
painless goiter.
Some people eventually develop hypothyroidism.
After many years the thyroid shrinks in size.
It is thought to be caused due to a combination
of genetic and environmental factors.
28. SIGNS AND SYMPTOMS
Fatigue
Weight gain
Pale or puffy face
Feeling cold
Joint and muscle pain
Constipation
Dry and thinning hair
Irregular menstrual cycles
Depression etc
29. PATHOPHYSIOLOGY
Various auto-antibodies may be present
against thyroid peroxidase, thyroglobulin and
TSH receptors.
Gross morphological changes within the
thyroid are seen in the general enlargement
which is far more locally nodular and irregular
than more diffuse patterns
