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Disorders of The Thyroid Gland

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Disorders of the

Thyroid Gland
Steps on Thyroid hormone synthesis

1. Taken up by NIS ( Na Iodine symporter)

2. Oxidized to I2 by Thyroid peroxidase

3. Organification – I2 add to tyrosine molecules sitting on thyroglobulin


to create MIT and DIT ( Mono-iodotyrosine and Di-iodothyroxine by
Thyroid peroxidase

4. Coupling by Thyroid Peroxidase to form T3 and T4


Hypothyroidism
Autoimmune Hypothyroidism
• The mean annual incidence rate of autoimmune
hypothyroidism is up to 4 per 1000 women and 1 per 1000
men
Laboratory Evaluation
Treatment
• 50–100 g levothyroxine (T4) daily. The dose is adjusted on the basis
of TSH levels, with the goal of treatment being a normal TSH, ideally
in the lower half of the reference range

• The clinical effects of levothyroxine replacement are slow to appear.


Patients may not experience full relief from symptoms until 3–6
months after normal TSH levels are restored.
Myxedema coma
• Clinical manifestations include reduced level of consciousness,
sometimes associated with seizures, Hypothermia can reach 23°C
(74°F
• usually precipitated by factors that impair respiration, such as drugs
(especially sedatives, anesthetics, antidepressants), pneumonia,
congestive heart failure, myocardial infarction, gastrointestinal
bleeding, or cerebrovascular accidents. Sepsis should also be
suspected. Exposure to cold may also be a risk factor.
• Levothyroxine can initially be administered as a single IV bolus of
500 g, continued at a dose of 50–100 g/d
• liothyronine (T3) intravenously or via nasogastric tube-10 to 25 g
every 8–12 h.
• levothyroxine (200 g) and liothyronine (25 g) as a single-
levothyroxine (50–100 g/d) and liothyronine (10 g every 8 h).
• External warming is indicated only if the temperature is <30°C
• Parenteral hydrocortisone (50 mg every 6 h) should be
administered, because there is impaired adrenal reserve in
profound hypothyroidism
• Any precipitating factors should be treated, including the early
use of broad-spectrum antibiotics, pending the exclusion of
infection.
• Ventilatory support with regular blood gas analysis is usually
needed during the first 48 hours
Thyrotoxicosis
• the state of thyroid hormone excess and is not synonymous
with hyperthyroidism, which is the result of excessive thyroid
function
• the major etiologies of thyrotoxicosis are hyperthyroidism
caused by Graves' disease, toxic MNG, and toxic adenomas
Graves' Disease
• accounts for 60–80% of thyrotoxicosis
• occurs in up to 2% of women but is one-tenth as frequent in
men
• typically occurs between 20 and 50 years of age; it also occurs
in the elderly
Clinical Manifestations
• features that are common to any cause of thyrotoxicosis &
those specific for Graves' disease

• In the elderly, features of thyrotoxicosis may be subtle or


masked, and patients may present mainly with fatigue and
weight loss, a condition known as apathetic thyrotoxicosis.
• The most common cardiovascular manifestation is sinus
tachycardia

• Atrial fibrillation is more common in patients >50 years of age

• Diffuse alopecia occurs in up to 40%


Graves' ophthalmopathy
• Many scoring systems have been used to gauge the extent and
activity of the orbital changes in Graves' disease. The "NO SPECS"
scheme is an acronym derived from the following eye changes:
• 0 = No signs or symptoms
• 1 = Only signs (lid retraction or lag), no symptoms
• 2 = Soft-tissue involvement (periorbital edema)
• 3 = Proptosis (>22 mm)
• 4 = Extraocular-muscle involvement (diplopia)
• 5 = Corneal involvement
• 6 = Sight loss
Treatment
• The hyperthyroidism of Graves' disease is treated by reducing
thyroid hormone synthesis, using antithyroid drugs, or
reducing the amount of thyroid tissue with radioiodine (131I)
treatment or by thyroidectomy
Thyrotoxic crisis, or thyroid
storm
• A life-threatening exacerbation of hyperthyroidism, accompanied by fever,
delirium, seizures, coma, vomiting, diarrhea, and jaundice.
• precipitated by acute illness (e.g., stroke, infection, trauma, diabetic
ketoacidosis), surgery (especially on the thyroid), or radioiodine treatment
of a patient with partially treated or untreated hyperthyroidism
• Management requires intensive monitoring and supportive care,
identification and treatment of the precipitating cause, and measures that
reduce thyroid hormone synthesis.
• Large doses of propylthiouracil (600 mg loading dose and 200–300 mg
every 6 h) should be given orally or by nasogastric tube or per rectum; the
drug's inhibitory action on T4 T3 conversion makes it the antithyroid drug
of choice. A saturated solution of potassium iodide (5 drops SSKI every 6
h) Propranolol , Additional therapeutic measures include glucocorticoids
(e.g., dexamethasone, 2 mg every 6 h), antibiotics if infection is present,
cooling, oxygen, and intravenous fluids.

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