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DISORDERS OF THE THYROID GLAND
By:- ABHISHEK.M
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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)
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THYROID GLAND REGULATION“NEGATIVE FEEDBACK AXIS”
HYPOTHALAMUS
(TRH) +ve effect
PITUITARY GLAND
(TSH) +ve effect
THYROID GLAND(T4 & T3)
-ve effect
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THYROID DISORDERS MAY BE CLASSIFIED AS:-
Hyperthyroidism (Thyrotoxicosis)•Overproduction of Thyroid hormones
Hypothyroidism (Gland destruction)
•Underproduction of Thyroid hormones
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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 AbSerum Tg (Thyroglobulin)
Radioactive uptake and Thyroid scanning
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TSH high usually means Hypothyroidism
Rare causeso TSH secreting pituitary tumor
o Thyroid hormone resistance
TSH low usually means Hyperthyroidism
Other causeso First trimester of pregnancy
o After treatment of Hyperthyroidismo Some medications (Esteroids-
Dopamine)
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Thyroid Gland Disorders
Goiter Graves Disease
Cretinism Myxedema
Hashimoto’s Disease
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GOITERA 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.
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SIGNS AND SYMPTOMS
For Hyperthyroidism:-
• Tachycardia• Palpitations• Nervousness
• Tremors• Increased BP
• Heat intolerance
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For Hypothyroidism
• Weight gain despite poor appetite
• Cold intoleration• Constipation
• Lethargy
But, these symptoms are often non-specific and makes
diagnosis difficult.
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CLASSIFICATION OF GOITERS
GROWTH PATTERN:-
• UNINODULAR • MULTINODULAR
• DIFFUSE
SIZE:-
• CLASS I• CLASS II• CLASS III
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CAUSES:1. Iodine deficiency
2. Congenital hypothyroidism3. Pituitary diseases
4. Thyroid cancer5. 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
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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.
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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 .
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MECHANISM:Thyroid stimulating immunoglobins recognize and bind to Thyrotropin receptor(TSH receptor) which further stimulates the release of T3 & T4Thyroxine 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.
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TREATMENTTreatment 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.
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CRETINISMCretinism is a condition of severely stunted physical and mental growth due to untreated congenital deficiency of thyroid hormone, usually due to maternal hypothyroidism.
PATHOPHYSIOLOGYCretinism 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.
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CAUSE AND TREATMENTMost 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.
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MYXEDEMAMyxedema is a term used synonymously with severe hypothyroidismMyxedema develops in the patient withalmost total lack of thyroid hormone function
It is generally characterized by bagginess under the eyes and swelling of the face.In this condition, greatly increasedquantities of hyaluronic acid and chondroitin sulfatebound with protein form excessive tissue gel in theinterstitial spaces, and this causes the total quantity of interstitial fluid to increase.
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Because of the gel nature of the excess fluid, it is mainly immobile, and the edema is the nonpitting type.
CAUSESMyxedema 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
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PATHOPHYSIOLOGYMyxedema 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.
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TREATMENT
1. Airway management
2. Thyroid hormone replacement
3. Gluco-corticoid therapy
4. Supportive measures
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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.
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SIGNS AND SYMPTOMSFatigueWeight gainPale or puffy faceFeeling coldJoint and muscle painConstipation Dry and thinning hairIrregular menstrual cycles Depression etc
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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
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TREATMENTManaging hormone levels:
Hypothyroidism caused by Hashimoto's thyroiditis is treated with thyroid hormone replacement agents. E.g.: Levothyroxine, triiodothyronine.
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