The Principle Effects of The Thyroid Hormones
Primary Effects
- Aerobic energy metabolism
- Glucose metabolism
- Protein metabolism
- Lipid metabolism
- Iron transport
Secondary Effects
- Growth/Development
- Cardiac output
- Ventilation
- CNS activity
- Thermoregulation (Heat regulation)
- Muscle function
- GI activity
- Reproductive function
Hypothyroidism is a clinical syndrome caused by deficiency of thyroid hormones
The onset of symptoms is usually insidious, and the condition may go undetected for years
Epidemiology
Incidence
Predominant age in adult: middle-aged. Female > male 5–8:1
More common in woman with small body size at birth and during childhood
Prevalence
Prevalence varies from 0.1–2% in general population; 2% in women, but under 0.1% in men
Prevalence of subclinical hypothyroidism is higher, ranging from 4–10% of adults, with higher frequency in elderly woman
Common in elderly:
>65 years of age, (6–10% women, 2–3% men)
Mean serum TSH concentrations higher in white or Mexican-Americans than in African Americans
Up to 20% of patients with major depressive disorder
Prevalence of subclinical hypothyroidism is higher, ranging from 4–10% of adults, with higher frequency in elderly woman
Common in elderly:
>65 years of age, (6–10% women, 2–3% men)
Mean serum TSH concentrations higher in white or Mexican-Americans than in African Americans
Up to 20% of patients with major depressive disorder
Risk factors:
- Personal or family history of autoimmune diseases, including type 1 diabetes mellitus, Addison disease, Hashimoto thyroiditis
- Previous postpartum thyroiditis
- Previous head or neck irradiation
- History of Graves disease
- Treatment with lithium, immune modulators, such as IFN-α, or the iodine-containing amiodarone
- More common in persons of Japanese descent
Etiology
Hypothyroidism can be the consequence of three general processes
- Defective thyroid hormone synthesis , with compensatory goitrogenesis (goitrous hypothyroidism)
- Inadequate thyroid parenchyma function , usually due to thyroiditis, surgical resection of the gland or therapeutic administration of radioiodine
- Inadequate secretion of TSH by the pituitary or of thyroid-releasing hormone (TRH) by the hypothalamus
Pathogenesis
In primary hypothyroidism (>95%), loss of thyroid function leads to decreased production of TH and increased secretion of TSH and TRHCentral (secondary) hypothyroidism is caused by the pituitary’s failure to synthesize adequate amounts of TSH or a lack of TRH. Hypothalamic dysfunction results in low levels of TH, TSH, and TRH
Hypothyroid Conditions
Primary Hypothyroidism (Autoimmune Thyroiditis)
Goitrous Hypothyroidism
Congenital Hypothyroidism
Diagnosis
Clinical examFeatures of Hypometabolisme
- Hypothermia and sensitive to cold, weight gain/obesity, lethargy
- Cardiovascular: Bradycardia, decrease/absent of heart sounds, hypotension in later stage
- Digestive: Constipation
- Neuro-psychology
- Physical activity: Slow, asthenia, limited activity
- Psychic: Depression, memory disorder, metal retardation
- Behavioral disorders / dementia (elderly patients)
- Gynecology/Sexual: Decrease libido, secondary amenorrhea (by hyperprolactinemia)
Characteristic of edema
- Hard, non-pitting
- Face: Pale, round, puffy "moon face"
- Extremity: Pudgy hands and feet
- Tongue: macroglossia
- Vocal cords: Hoarse voice
- Eustachian tube: hypoacusia
- Nasal mucosa: snoring
Myxedema coma, is a life-threatening, end-stage expression of hypothyroidism
It is characterized by coma, hypothermia, cardiovascular collapse, hypoventilation, and severe metabolic disorders that include hyponatremia, hypoglycemia, and lactic acidosis
Cretinism refers to hypothyroidism developing in infancy or early childhood. This disorder formerly was fairly common in areas of the world where dietary iodine deficiency is endemic
Clinical features of cretinism include impaired development of the skeletal system and central nervous system, with severe mental retardation, short stature, coarse facial features, a protruding tongue, and umbilical hernia
Subclinical hypothyroidism is a common condition in which serum TSH is elevated but serum free T 4 or the free T 4 index is normal rather than decreased. Many affected patient’s progress to overt hypothyroidism. A greater degree of TSH elevation, the presence of symptoms that might be caused by hypothyroidism, and the presence of antithyroid antibodies are factors favoring a decision to treat
Investigation
- TSH level in blood stream
↑TSH: > 5mIU/L (0.5 to 4.5 mIU/L)
If TSH level normal (rarely decrease): Central thyrotropin insufficiency - Free T4 level
↑TSH + ↓fT4: Primary hypothyroidism
↑TSH + Normal fT4: Subclinical hypothyroidism
Evaluation
- CBC: Anemia (normo-, macrocytic)
- Blood chemistry: Hyponatremia (dilutional)
- Biology: Dyslipidemia (Hypercholesterolemia +/- ↑triglyceridemia)
- Prolactin (Amenorrhea): Secondary hyperprolactinemia due to TRH stimulation
- Polyglandular autoimmune syndrome (Type2): Glycemia (DM), cortisole-aldosterone (chronic adrenal insufficiency)
Etiologic diagnosis
- Medications, surgery (thyroidectomy)
- Anti-TPO anti body
- Anti-thyroglobulin anti body or anti-thyroid peroxidase
- MRI or Ultrasonography of pituitary region to look for pituitary-hypothalamic disease if free T4 low and TSH low or normal
Hypothyroidism conditions
PRIMARY HYPOTHYROIDISM (Autoimmune thyroiditis)
Primary hypothyroidism, like most thyroid disorders, is more common in women than in men. This include: Hashimoto disease, chronic lymphocytic thyroiditis
Epidemiology: ¾ of patients have circulating antibodies to thyroid antigens. The most common cause in US
Some cases of primary hypothyroidism are part of multiglandular autoimmune syndrome (MEN) which include others endocrine disease
Pathogenesis: inflammatory destruction of thyroid tissue by infiltration of lymphocytes and circulating thyroid autoantibodies (antithyroid peroxidase and antithyroglobulin antibodies)
Induction of apoptosis are involved in the tissue destruction seen in Hashimoto thyroiditis
Nongoitrous hypothyroidism may also result from antibodies that block TSH or TSH receptors without activating the thyroid
Epidemiology: ¾ of patients have circulating antibodies to thyroid antigens. The most common cause in US
Some cases of primary hypothyroidism are part of multiglandular autoimmune syndrome (MEN) which include others endocrine disease
Pathogenesis: inflammatory destruction of thyroid tissue by infiltration of lymphocytes and circulating thyroid autoantibodies (antithyroid peroxidase and antithyroglobulin antibodies)
Induction of apoptosis are involved in the tissue destruction seen in Hashimoto thyroiditis
Nongoitrous hypothyroidism may also result from antibodies that block TSH or TSH receptors without activating the thyroid
GOITROUS HYPOTHYROIDISM
Etiology: iodine deficiency, antithyroid agents (drugs or dietary goitrogens), long-term iodide intake and a number of hereditary defects in thyroid hormone synthesis
Endemic Goiter
Endemic goiter is goitrous hypothyroidism due to dietary iodine deficiency in locales with a high prevalence of the disease
More than 200 million persons worldwide still have the disease
The pathologic evolution of endemic goiter is similar to that of nontoxic goiter but rarely cause hyperthyroidism
Rx: Administration of iodine may reverse the early, diffuse stage of endemic goiter but has little effect on fully developed multinodular goiter
More than 200 million persons worldwide still have the disease
The pathologic evolution of endemic goiter is similar to that of nontoxic goiter but rarely cause hyperthyroidism
Rx: Administration of iodine may reverse the early, diffuse stage of endemic goiter but has little effect on fully developed multinodular goiter
Common goitrogenic drugs include lithium (which is used to manage bipolar disorders), phenylbutazone and p-aminosalicylic acid. Certain cruciferous vegetables (turnips, rutabaga, cassava) contain goitrogens, and their ingestion can potentiate an iodine-deficient diet to produce goitrous hypothyroidism. Consumption large amounts of iodide, either as a medicinal component (potassium iodide containing expectorants) or in foods particularly rich in this halide (e.g., seaweed in Japan)
CONGENITAL HYPOTHYROIDISM
Cretinism may be endemic, sporadic or familial and is twice as frequent in girls as boys
In non-endemic regions, 90% of cases result from developmental defects of the thyroid (thyroid dysgenesis). In 1 of every 4000 live births are affected
The remainder is principally caused by a variety of inherited metabolic defects, including mutations in the genes for TRH and its receptor, TSH and its receptor, sodium–iodide symporter, thyroglobulin and thyroid oxidase
Dx: Hypothyroidism at birth presents clinically with high birthweight, hypothermia, delay in passing meconium, and neo-natal jaundice
Without early screening, hypothyroidism may not be evident until after 4 months of age
Symptoms include difficulty eating, hoarse cry, and protruding tongue caused by myxedema of oral tissues and vocal cords; hypotonic muscles of the abdomen with constipation, abdominal protrusion, and umbilical hernia; subnormal temperature; lethargy; excessive sleeping; slow pulse rate; and cold. Mental retardation; skeletal growth is stunted because of impaired protein synthesis, poor absorption of nutrients, and lack of bone mineralization; the child will be dwarfed with short limbs, if not treated
Cord blood can be examined in the first days of life: serum T4 and T3 levels are low, and TSH levels are high (unless the problem relates to a lack of TSH secretion itself)
Prognosis: The probability of normal growth and intellectual function is high if treatment with levothyroxine is started before the child is 3 or 4 months old. The earlier thyroid hormone replacement is initiated, the better the child’s outcome
In non-endemic regions, 90% of cases result from developmental defects of the thyroid (thyroid dysgenesis). In 1 of every 4000 live births are affected
The remainder is principally caused by a variety of inherited metabolic defects, including mutations in the genes for TRH and its receptor, TSH and its receptor, sodium–iodide symporter, thyroglobulin and thyroid oxidase
Dx: Hypothyroidism at birth presents clinically with high birthweight, hypothermia, delay in passing meconium, and neo-natal jaundice
Without early screening, hypothyroidism may not be evident until after 4 months of age
Symptoms include difficulty eating, hoarse cry, and protruding tongue caused by myxedema of oral tissues and vocal cords; hypotonic muscles of the abdomen with constipation, abdominal protrusion, and umbilical hernia; subnormal temperature; lethargy; excessive sleeping; slow pulse rate; and cold. Mental retardation; skeletal growth is stunted because of impaired protein synthesis, poor absorption of nutrients, and lack of bone mineralization; the child will be dwarfed with short limbs, if not treated
Cord blood can be examined in the first days of life: serum T4 and T3 levels are low, and TSH levels are high (unless the problem relates to a lack of TSH secretion itself)
Prognosis: The probability of normal growth and intellectual function is high if treatment with levothyroxine is started before the child is 3 or 4 months old. The earlier thyroid hormone replacement is initiated, the better the child’s outcome
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