Causes (Etiology)
Four main groups of factors leading to decreased glandular function are distinguished:
- Primary involvement: autoimmune thyroiditis (Hashimoto's thyroiditis) and idiopathic atrophy of the glandular tissue.
- Iatrogenic interventions: consequences of radical treatment for thyrotoxicosis (subtotal resection or radioactive iodine therapy).
- Drug-induced effects: long-term use of amiodarone, lithium, or high-dose iodine preparations.
- Central disorders: pathology at the level of the hypothalamic-pituitary system (secondary hypothyroidism).
Pathogenesis and specific edema
The key pathogenetic link is thyroid hormone deficiency, which inhibits oxidative reactions and disrupts all types of metabolism. Mucopolysaccharides accumulate massively in tissues, forming a specific mucous edema.
Externally, this manifests as skin thickening, puffiness of the face and lower legs. The edema spreads to mucous membranes, causing characteristic symptoms:
- Vocal cords: the voice becomes rough and hoarse.
- Eustachian tube: hearing is impaired.
- Tongue: macroglossia develops (enlargement of the tongue with distinct teeth indentations on its lateral surfaces).
Organ system involvement
The disease is systemic in nature and affects most bodily functions.
- Appearance and skin: Patients are lethargic, drowsy, and apathetic. Pronounced feeling of cold (hypothermia) is characteristic. The skin is cold, pale, dry, prone to peeling, and hair loss is observed.
- Cardiovascular system: Persistent bradycardia dominates, cardiac output and blood pressure are reduced. Cardiac borders are expanded due to myocardial dystrophy, interstitial edema, and fluid accumulation in the pericardium (effusion is best visualized on echocardiography). Heart sounds are muffled. ECG shows low voltage and pathological changes in the ST segment and T wave.
- Nervous system: Memory impairment and lethargy progress; in the elderly, severe depression and psychiatric disorders occur. Paresthesia and decreased tendon reflexes are objectively detected.
- Gastrointestinal and blood systems: Intestinal motility decreases (flatulence, persistent constipation). Malabsorption leads to hypochromic anemia, which may be combined with pernicious anemia.
- Reproductive system: Menorrhagia (heavy periods) in women, decreased libido in men.
Laboratory diagnostics and treatment
A constant metabolic marker of hypothyroidism is hypercholesterolemia. For precise topical diagnosis, the hormonal profile is evaluated:
- Primary hypothyroidism: decrease in free and total thyroxine (T4) against the background of a compensatory rise in TSH via a feedback mechanism.
- Secondary hypothyroidism: decreased T4 is accompanied by a drop in TSH levels (pathology in the pituitary gland or hypothalamus must be investigated).
- Borderline states: with normal T4 and borderline TSH, a thyrotropin-releasing hormone (TRH) stimulation test is performed (in primary disease, the TSH response will be excessive).
The basis of treatment is hormone replacement therapy with thyroid hormone preparations. Treatment success is confirmed by subjective improvement in well-being, increased heart rate (regression of bradycardia), normalization of appearance and laboratory parameters.
Briefly: answers to topical questions
What clinical and biochemical blood test parameters (other than thyroid hormones) change in hypothyroidism?
In hypothyroidism, clinical and biochemical blood tests reveal changes reflecting the development of anemia and metabolic disorders.
- Complete blood count — hypochromic anemia is observed (arising due to decreased intestinal absorption), and its combination with pernicious anemia is also possible.
- Biochemical blood test — persistent hypercholesterolemia is characteristic, serving as a constant sign of this disease.
- Blood electrolytes — hyponatremia may develop.
How exactly do tendon reflexes change in hypothyroidism, and which reflex is the most indicative?
In hypothyroidism, sources describe a decrease, weakening, or depression of tendon reflexes.
Sensory-motor polyneuropathy with symmetrical numbness, leg weakness, and depressed tendon reflexes is also described in connection with hypothyroidism. General descriptions of polyneuropathies indicate that tendon reflexes may weaken or be lost, especially the Achilles reflex. However, the Achilles reflex is not singled out in the cited sources as 'most specific' or 'most indicative' specifically for hypothyroidism.
Myxedema triad: E-N-B — Edema (mucinous), Neuropsychiatric lethargy, Bradycardia.
Class and exam questions
Why does hypothyroidism cause voice coarsening and hearing loss?
This occurs due to specific myxedematous edema—the accumulation of mucopolysaccharides in the tissues of the vocal cords and the mucous membrane of the Eustachian tube.
How to distinguish primary hypothyroidism from secondary hypothyroidism using blood tests?
In primary hypothyroidism, TSH levels will be compensatorily elevated via the feedback principle, whereas in secondary (central) disease, TSH levels are decreased.
Why do the dimensions of the heart increase in this disease?
Cardiomegaly is caused by myocardial interstitial edema, muscle fiber dystrophy, and pericardial effusion formation.
What ECG changes are typical for myxedema?
A general decrease in wave voltage is observed, along with pathological changes in the terminal part of the ventricular complex (ST segment and T wave).
What else to study on this topic
- Features of the clinical course of Hashimoto's autoimmune thyroiditis
- Methodology and interpretation of the thyrotropin-releasing hormone (TRH) stimulation test
- Mechanisms of anemia development in thyroid pathology
- Differential diagnosis of pericardial effusion
- Mental disorders and depression in elderly patients with uncompensated hypothyroidism
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