HPERTHYROIDISM

Definition:
•The most common form is Graves' disease, which increases thyroxine (T4) production, and
enlarges the thyroid gland (goiter) and causes multiple system changes
Causes:
 Thyrotoxicosis may result from both genetic and immunologic factors, including:
 •Increased incidence in monozygotic twins, pointing to an inherited factor, probably
autosomal recessive gene.
 •Occasional coexistence with other endocrine abnormalities, such as type 1 diabetes
mellitus, thyroiditis, and hyperparathyroidism
 Clinical thyrotoxicosis precipitated by excessive dietary intake of iodine or possibly
stress .
 Stress, such as surgery, infection, toxemia of pregnancy, or diabetic ketoacidosis, can
precipitate thyroid storm (inadequately treated thyrotoxicosis).

Pathophysiology:
 •The thyroid gland secretes the thyroid precursor, T 4, thyroid hormone or
triiodothyronine (T3), and calcitonin.
 •T4 and T3 stimulate protein, lipid, and carbohydrate metabolism primarily through
catabolic pathways.
 •Calcitonin removes calcium from the blood and incorporates it into bone
 Biosynthesis, storage, and release of thyroid hormones are controlled by the
hypothalamic-pituitary axis through a negative-feedback loop.
 •Thyrotropin-releasing hormone (TRH) from the hypothalamus stimulates the release
of TSH by the pituitary
 Circulating T 3 levels provide negative feedback through the hypothalamus to
decrease TRH levels, and through the pituitary to decrease TSH levels.
 •Although the exact mechanism isn't understood, hyperthyroidism has a hereditary
component, and it is frequently associated with other autoimmune endocrinopathies
 Graves' disease is an autoimmune disorder characterized by the production of
autoantibodies that attach to and then stimulate TSH receptors on the thyroid gland.
 • A goiter is an enlarged thyroid gland, either the result of increased stimulation or a
response to increased metabolic demand.The latter occurs in iodine-deficient areas of
the world, where the incidence of goiter increases during puberty (a time of increased
metabolic demand).
 These goiters often regress to normal size after puberty in males, but not in females.
Sporadic goiter in non–iodine-deficient areas is of unknown origin.
 •Endemic and sporadic goiters are nontoxic and may be diffuse or nodular. Toxic
goiters may be uninodular or multinodular and may secrete excess thyroid hormone
Signs and symptoms:
 Enlarged thyroid (goiter)
 Nervousness
 Heat intolerance and sweating
 Weight loss despite increased appetite
 Frequent bowel movements
 Tremor and palpitations
 Exophthalmos
 Difficulty concentrating
 Moist, smooth, warm, flushed skin.
 Fine, soft hair; premature patchy graying and increased hair loss in both sexes.
 Systolic hypertension, and tachycardia.
 Increased respiratory rate
 Weakness, fatigue, and muscle atrophy

Complications:
 Muscle wasting
 Visual loss or diplopia
 Cardiac failure
 Hypoparathyroidism after surgical removal of thyroid
 Hypothyroidism after radioiodine treatment

Diagnosis:
 The following tests confirm the disorder:
 Radioimmunoassay showing increased serum T4 and T3 levels
 Low TSH levels
 Thyroid scan showing increased uptake of radioactive iodine 131 ( 131I) in graves'
disease and, usually, in toxic multinodular goiter and toxic adenoma; low radioactive
uptake in thyroiditis and thyrotoxic factitia (test contraindicated in pregnancy)
 Ultrasonography confirming subclinical ophthalmopathy.

Treatment:
 The primary forms of therapy include:
 Antithyroid drugs
 Surgery (Thyroidectomy
 HYPOTHYRODISM
Definition:
 Hypothyroidism results from hypothalamic, pituitary, or thyroid insufficiency or
resistance to thyroid hormone.
 Hypothyroidism is more prevalent in women than men.
Causes:
 Inadequate production of thyroid hormone, usually after thyroidectomy or radiation
therapy, or due to inflammation, chronic autoimmune thyroiditis (Hashimoto's disease).
 Pituitary failure to produce TSH, hypothalamic failure to produce thyrotropinreleasing
hormone (TRH).
 Inborn errors of thyroid hormone synthesis
 Iodine deficiency (usually dietary), or use of such antithyroid medications.
Pathophysiology:
 Hypothyroidism may reflect a malfunction of the hypothalamus, pituitary, or thyroid
gland.
 Chronic autoimmune thyroiditis, also called chronic lymphocytic thyroiditis, occurs when
autoantibodies destroy thyroid gland tissue.
 Chronic autoimmune thyroiditis associated with goiter is called Hashimoto's thyroiditis.
The cause of this autoimmune process is unknown, although heredity has a role, and
specific human leukocyte antigen subtypes are associated with greater risk.
 Outside the thyroid, antibodies can reduce the effect of thyroid hormone in two ways.
 First, antibodies can block the thyroid-stimulating hormone (TSH) receptor and prevent
the production of TSH.
 Second, cytotoxic antithyroid antibodies may attack thyroid cells.
Signs and symptoms:
 •Weakness
 •Fatigue
 •Forgetfulness
 •Sensitivity to cold
 •Unexplained weight gain
 •Constipation
 •Decreasing mental stability
 •Puffy face, hands, and feet.
 •Somnolence
 •Increase sleeping hours
 •Increase risk of cardiovascular disease
 •Decrease body metabolism
Diagnosis:
 Diagnosis of hypothyroidism is based on:
 •Radioimmunoassay showing low triiodothyronine (T3) and thyroxine (T4) levels.
 •Increased TSH level with cause of thyroid disorder; decreased with hypothalamic or
pituitary disorder cause.
 •Elevated serum cholesterol, alkaline phosphatase, and triglyceride levels.
 Normocytic, normochromic anemia.
 •Low serum sodium levels, decreased pH, and increased partial pressure of carbon
dioxide, indicating respiratory acidosis (myxedema)
Complications:
 •Heart failure
 •Myxedema
 •Coma
 •Infection
 •Megacolon
 •Organic psychosis
 •Infertility.
Treatment:
 •Gradual thyroid hormone replacement with T4 and, occasionally, T3.
 •Surgical excision, chemotherapy, or radiation for tumors