An Increase In Peripheral Resistance To Blood Flow Is Thyroid Hypothyroidism – Clinical Manifestations

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Thyroid Hypothyroidism – Clinical Manifestations

The clinical consequences of thyroid endocrine insufficiency are summarized below. Hypothermia is characteristic and the patient may complain of cold intolerance. A low basal metabolic rate leads to weight gain despite reduced food intake.

Thyroid hormones are required for normal development of the nervous system. In hypothyroid infants, synapses develop abnormally, myelination is defective, and mental retardation occurs. Hypothyroid adults have many reversible neurologic abnormalities, including mental retardation, forgetfulness, hearing loss, and ataxia. Some patients have severe psychotic symptoms, including reversible dementia or overt psychosis (“myxedema madness”).

Cerebrospinal fluid protein levels are abnormally high. However, total cerebral blood flow and oxygen consumption are normal. Deep tendon reflexes are sluggish, with a slow (“hang-up”) resting state. Paresthesias are common, frequently triggered by compression neuropathy due to accumulation of myxedema (carpal tunnel syndrome and tarsal tunnel syndrome).

Hypothyroidism is associated with muscle weakness, cramps, and stiffness. Serum creatine kinase (CK) levels may be elevated. The pathophysiology of muscle disease in hypothyroidism is poorly understood. Studies of bioenergetic abnormalities in hypothyroid muscle suggest hormone-dependent, reversible mitochondrial impairment. Changes in energy metabolism are not observed in hyperthyroid muscle.

Patients who have been made acutely hypothyroid by total thyroidectomy show decreased cardiac output, decreased stroke volume, decreased resting diastolic volume, and increased peripheral resistance. However, pulmonary capillary wedge tension, right atrial pressure, heart rate, left ventricular ejection fraction, and left ventricular systolic pressure-volume relationship (a measure of contractility) were not significantly different from the euthyroid state.

Thus, in early hypothyroidism, changes in overall cardiac performance are likely primarily related to loading problems and changes in exercise-related cardiac output rather than to changes in myocardial contractility. In chronic hypothyroidism, echocardiography shows features suggestive of bradycardia and cardiomyopathy, including increased thickening of the intraventricular septum and ventricular wall, decreased regional wall motion, and decreased systolic and diastolic global left ventricular function.

These changes may be due to excessive accumulation of mucopolysaccharides in the interstitium between myocardial fibers, leading to fiber degeneration, reduced contractility, decreased cardiac output, cardiac dilatation, and heart failure. A pericardial effusion (with a high protein content) may lead to elevated electrocardiographic voltage and flat T wave findings, but cardiac tamponade is rare.

Hypothyroid patients show a reduced ventilatory response to hypercapnia and hypoxia. Untreated hypothyroidism has a high prevalence of sleep apnea; Such patients occasionally present with upper airway muscle myopathy. Weakness of the diaphragm also occurs frequently and, when severe, can lead to chronic alveolar hypoventilation (CO2 retention). Pleural effusion (with high protein content) may occur.

In hypothyroidism, plasma cholesterol and triglyceride levels increase, which reduces lipoprotein lipase activity and the production of LDL receptors in the liver. In hypothyroid children, bone development is slowed and skeletal maturation (closure of the epiphyses) is delayed. Pituitary secretion of endocrine growth may also be depressed because the thyroid gland is required for its synthesis. Hypothyroid animals have reduced width of the epiphyseal development plate and articular cartilage, and reduced epiphyseal and metaphyseal trabecular bone volume.

These changes are not due to pituitary growth hormone deficiency alone, as administration of exogenous growth endocrine does not restore normal cartilage morphology or bone remodeling, whereas administration of T4 does. If undiagnosed, chronic adolescent hypothyroidism results in permanent height loss.

Decreased erythropoiesis may lead to normochromic, normocytic anemia. Alternatively, moderate macrocytic anemia may occur due to decreased absorption of cyanocobalamin (vitamin B12) from the intestine and decreased fat-burning capacity of the bone marrow. Frank megaloblastic anemia suggests coexisting pernicious anemia.

Constipation is common and GI motility is reduced. Achlorhydria occurs when hypothyroidism is combined with pernicious anemia. Ascitic fluid with high protein content may accumulate.
Skin color is dry and cool in hypothyroidism. Normally, skin contains complex proteins including polysaccharides, chondroitin, sulfuric acid, and hyaluronic acid. In hypothyroidism, these complexes accumulate, promote sodium and water retention, and produce a characteristic exudative, nonpitting puffiness of the skin (myxedema).

The patient’s face appears puffy with rough features. Relative accumulation of mucopolysaccharides in the larynx may cause hoarseness. Hair is brittle and lacks luster, and body hair often falls out, especially over the scalp and side brows. If thyroid is administered intravenously, protein complexes aggregate, increase urine volume, and resolve myxedema.

Carotenemia (manifested as a yellow-orange discoloration of the skin) can occur in hypothyroidism because thyroid hormones are needed to convert carotene to vitamin A in the liver. In the absence of adequate hormones, carotene accumulates in the bloodstream and skin.

In women, hypothyroidism can cause menorrhagia due to anovulatory cycles. Alternatively, menses may decrease or disappear secondary to reduced gonadotropin secretion. Since the thyroid gland normally exerts an inhibitory effect on prolactin secretion, hypothyroid patients exhibit hyperprolactinemia with galactorrhea and amenorrhea. In men, hypothyroidism can cause infertility and gynecomastia due to increased secretion of prolactin.

Hyperprolactinemia occurs because TRH stimulates the release of prolactin. Decreased renal blood flow with reduced glomerular filtration rate. Vascular constriction may be due to low plasma ANP concentrations. As a result, hyponatremia can occur due to a decreased ability to excrete the drinking water load. However, serum creatinine levels are usually normal.

Prolonged untreated severe hypothyroidism can lead to a condition known as myxedema coma. Affected patients have a characteristic myxedematous face and skin color, bradycardia, hypothermia, alveolar hypoventilation, and severe obtundation or coma.

This condition is usually caused by an underlying disease, such as an infection or stroke, or by medication, such as a sedative-hypnotic. The mortality rate reaches 100% if myxedema coma is not recognized and treated promptly.

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