Screening and diagnostic indications
A standard laboratory panel is used to assess thyroid function. Baseline screening includes measuring thyroid-stimulating hormone (TSH) and free thyroxine (fT4) levels. Additionally, autoantibodies are tested: anti-thyroperoxidase (anti-TPO) and anti-thyroglobulin (anti-Tg).
Regular screening (every 2 years) is indicated for patients after initial diagnosis of type 1 diabetes mellitus. More frequent testing is required in case of:
- appearance of clinical symptoms of hypothyroidism or hyperthyroidism;
- detection of autoantibodies;
- physical or instrumental confirmation of thyroid enlargement.
Hypothyroidism: classification and pathogenesis
Hypothyroidism occurs due to a deficiency in iodothyronine effects on target cells. The disease is classified according to the level of endocrine axis lesion:
- Primary (thyroidal) — the problem is localized in the gland itself. This can be an autoimmune process (Hashimoto's goiter) or iatrogenic damage (after surgery, radiation therapy, medications).
- Secondary (pituitary) — occurs due to TSH deficiency.
- Tertiary (hypothalamic) — associated with thyrotropin-releasing hormone deficiency. It develops against the background of encephalitis, tumor processes, or sarcoidosis.
There are also additional pathogenetic mechanisms: hormone inactivation in the blood (binding or destruction), decreased sensitivity of target cell receptors (hyporeactivity), and impaired conversion (when an excess of inactive reverse T3 is formed from T4).
The most frequent clinical form is chronic autoimmune thyroiditis (Hashimoto's disease). The pathology has a genetic predisposition (HLA-DR5, DR3, B8 loci). It is based on an inherited defect in T-suppressor function, which stimulates T-helper cells to produce autoantibodies against thyroglobulin, colloid, and the microsomal fraction. Antibodies damage the tissue, causing primary hypothyroidism, while compensatory TSH rise leads to goiter formation.
Hyperthyroidism (thyrotoxicosis): causes
Excess thyroid hormones lead to a state of hyperthyroidism. The main causes of primary hyperthyroidism:
- Diffuse toxic goiter (Graves' disease) — an autoimmune process accounting for up to 80% of all cases.
- Nodular toxic goiter (Plummer's disease) — predominantly occurs in elderly patients.
- Toxic adenoma — autonomous hyperproduction of hormones by a tumor node.
- Thyroiditis (viral, bacterial, parasitic, or immune etiology) — accompanied by the destruction of follicles and the release of hormones into the blood.
- Ectopic tumors — for example, ovarian teratomas or metastases of follicular carcinoma consisting of thyroid tissue.
- Induced thyrotoxicosis — occurs with uncontrolled intake of thyroid medications or excessive iodine intake (Jod-Basedow phenomenon).
Destructive thyroiditis
A group of diseases in which inflammation leads to the physical destruction of thyroid tissue. This group includes: acute (purulent), subacute, postpartum, painless ("silent"), traumatic, and drug-induced thyroiditis.
The main pathogenetic mechanism is tissue destruction, due to which previously synthesized hormones massively enter the bloodstream. The classical clinical manifestation is temporary thyrotoxicosis, which is usually milder than in endogenous hyperproduction.
The disease is characterized by a triphasic course:
- Thyrotoxic phase (hormone release).
- Hypothyroid phase (depletion of reserves and cell damage).
- Euthyroid phase (functional recovery).
Comparative characteristics of syndromes
Since hormones universally affect metabolism, the clinical picture of hypo- and hyperthyroidism is strictly opposite.
| Sign | Hypothyroidism | Hyperthyroidism (thyrotoxicosis) |
|---|---|---|
| Thyroid gland | From hypoplasia to goiter | Enlarged (goiter) |
| Development and weight | Growth retardation, weight gain | Normal/accelerated growth, weight loss |
| Nervous system | Sluggishness, lethargy, weakness | Agitation, nervousness |
| Skin | Dry, edematous | Warm to the touch |
| Eyes | Periorbital edema | Exophthalmos |
| Heart and GI tract | Bradycardia, constipation | Tachycardia, loose stools |
| Laboratory findings | Anemia, hypercholesterolemia | Usually unremarkable |
It is easy to remember the polarity of symptoms through associations: hypothyroidism is "winter" (the person feels cold, slows down, swells, gains weight, pulse is slow), while hyperthyroidism is "fire" (the person is burning, fussy, loses weight, pulse is fast, eyes are protruding).
Class and exam questions
Why does destructive thyroiditis cause thyrotoxicosis if the gland is being destroyed?
It is not newly synthesized hormones that enter the blood, but their reserves, which are released due to the physical destruction of thyroid follicles.
What is the difference between secondary and tertiary hypothyroidism?
Secondary hypothyroidism is caused by pituitary pathology and TSH deficiency, while tertiary is associated with hypothalamic damage and a lack of thyrotropin-releasing hormone.
How do cholesterol levels change in thyroid pathologies?
In hypothyroidism, due to general metabolic slowdown, hypercholesterolemia develops, whereas in thyrotoxicosis, specific changes in the lipid profile are usually not observed.
What else to study on this topic
- Pathogenesis and immunology of Graves' disease.
- Mechanisms of reverse T3 formation and peripheral hormone inactivation.
- The influence of HLA antigens on the development of Hashimoto's disease.
- The Jod-Basedow phenomenon: mechanisms of artificial thyrotoxicosis development.
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