Edema syndrome: myxedema
A classic manifestation of thyroid hormone deficiency is endocrine mucinous edema, or myxedema. Unlike cardiac or renal edema, in myxedema fluid does not move freely in the interstitium, but is chemically bound to excess proteoglycans (glycosaminoglycans), forming a dense gel. Because of this, no pit remains when pressing on the skin.
Local complications of mucinous edema:
- Respiratory and phonetic system: edema of the vocal cords causes roughness and hoarseness of the voice, and slowed speech becomes a typical marker of the disease.
- ENT organs: swelling of the Eustachian tube mucosa leads to hearing loss.
- Digestive tract: macroglossia (enlarged tongue) is accompanied by the appearance of clear tooth impressions along the edges.
- Serous cavities: pathological fluid accumulation occurs with the development of hydropericardium and ascites.
Cardiovascular complications
Deficiency of T3 and T4 hormones sharply reduces the sensitivity of the myocardium to catecholamines, depriving the heart of adequate stimulation. Against the background of dystrophic changes in muscle fibers, a "myxedema heart" is formed.
Key cardiological manifestations:
- Bradycardia and hypotension. Caused by a drop in cardiac output, the absence of a positive chronotropic effect, and decreased arteriolar tone. The total circulating blood volume decreases.
- Diastolic hypertension. Occurs paradoxically due to the loss of elasticity of the vascular wall and an increase in total peripheral resistance.
- Hydropericardium. The most common endocrine cause of pericardial effusion. Tamponade is rare because the fluid accumulates slowly. ECG shows low QRS voltage and QT prolongation.
- CHD and heart failure. The risk of their development is critically elevated even in subclinical courses due to concomitant persistent hypercholesterolemia.
Nervous system and cretinism
The decrease in the intensity of oxidative processes directly affects the central and peripheral nervous system. In adult patients, pronounced adynamia, pathological drowsiness, depressed mood, impaired memory and tendon reflexes, as well as the development of neuropathies are observed. Intellect is not fatally impaired; mental activity simply slows down.
A critical complication occurs with thyroid hormone deficiency in early childhood — cretinism. It is characterized by severe mental and physical developmental delay, impaired ossification processes, and skeletal disproportions.
Involvement of other organs and systems
Generalized hypometabolism affects all tissues, causing a number of specific disorders:
- Skin and appendages: alopecia (hair loss) is observed. The skin itself becomes dry, rough, and thickened, acquiring a yellowish tint due to carotene accumulation (normally, thyroid hormones ensure its conversion into vitamin A).
- Gastrointestinal tract: characteristic slowing of peristalsis leading to stubborn constipation (diarrhea occurs as an exception), as well as the development of achlorhydria.
- Muscular and skeletal systems: isolated hypothyroid myopathy (muscle weakness, myalgia) without additional triggers is recorded in half of patients, often accompanied by arthralgia.
- Reproductive system: puberty is delayed in adolescents, and amenorrhea may occur in adult women.
Portrait of facial myxedema: a puffy mask with narrow eye slits (eyelid edema), yellowish tint (carotene), and a large tongue (macroglossia), speaking with a low hoarse voice (vocal cord edema).
Class and exam questions
Why does mucinous edema leave no pitting upon pressure?
Fluid does not move freely in the intercellular space, but is chemically bound as a dense gel due to an excess of glycosaminoglycans in the skin and subcutaneous tissue.
What causes the yellowish skin discoloration in hypothyroidism?
The color is due to the accumulation of carotene. Due to thyroid hormone deficiency, the enzymatic process of converting carotene into vitamin A is blocked.
How does the hormonal profile change in primary hypothyroidism?
A decrease in total and free T4 levels is observed against the background of elevated TSH. The pituitary gland, via negative feedback, attempts to stimulate the affected thyroid gland.
What else to study on this topic
- Pathogenesis of decreased myocardial sensitivity to catecholamines in T3 and T4 deficiency
- Mechanisms of secondary hypothyroidism formation at the hypothalamo-pituitary level
- Differential diagnosis of mucinous edema from oncotic and hemodynamic edema
- Thyrotropin-releasing hormone stimulation test in borderline TSH and normal T4 values
- Mechanism of development of paradoxical diastolic hypertension against the background of bradycardia
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