Thyroid gland

Acquired hypothyroidism (primary hypothyroidism)

Causes of acquired hypothyroism:

• thyroidectomy (surgical removal);
• ablation of the gland with radiation for treatment of hyperthyroidism;
• lithium carbonate, and the antithyroid drugs propylthiouracil and methimazole in continuous dosage can block hormone synthesis and produce goiter with hypothyroidism
• Iodine deficiency (rare)
• Autoimmune disorder (Hashimoto thyroiditis) (most common). Predominant disease in women

Manifestastion of disorder are related largely to two factors:

1. hypometabolic state (due to thyroid hormone deficiency)
2. myxedematous involvement of body tissus

Hypometabolic state associated with:

• gradual onset of weakness and fatigue;
• tendency to gain weight despite a loss of appetite;
• cold intolerance.

In more progressed conditions:

• dry and rough skin;
• hair becomes coarse and brittle;
• face becomes puffy with edematous eyelids;
• thinning of the outer third of the eyebrows;
• Gastrointestinal motility is decreased, producing constipation^[1], flatulence^[2], and abdominal distention^[3].

[1] constipation - condition when people unable to completely empty bowel

[2] flatulence is passing gas from the digestive system out of the back passage. It's more commonly known as "passing wind", or "farting".

Myxedematous state 

• Myxedematous fluid is usually most obvious in the face;
• enlargement of tongue;
• the voice becomes hoarse and husky;

Thyroidectomy (surgical removal) or ablation of the gland with radiation for treatment of hyperthyroidism → Destruction or dysfunction of the thyroid gland (primary hypothyroidism) → Thyroid hormone deficiency due to autoimmune disorder (Hashimoto thyroiditis) → hypometabolic state → symptoms:

• gradual onset of weakness and fatigue;
• tendency to gain weight despite a loss of appetite;
• cold intolerance;
• dry and rough skin;
• coarse, dry, brittle hair;
• periorbital edema (edematous eyelids), and puffy face;
• gastric atrophy: constipation, flatulence, abdominal distention;
• CNS involement: mental dullness, lethargy, impaired memory; 
• Tongue enlargement;
• Deep, coarse voice

Mucopolysacharide deposits in the heart → generalized cardiac dilation, bradycardia, and other signs of altered cardiac output 

Hyperthyroidism (overactive thyroid) occurs when thyroid gland produces too much of the hormone thyroxine.

• The most common cause of hyperthyroidism is Graves disease. 
• Other causes are: multinodular goiter; adenoma of the thyroid; thyroiditis.
• Ioding-containin agents can induce hyperthyroidism

Many of the manifestations of hyperthyroidism are related to the increase in
oxygen consumption and use of metabolic fuels associated with the hypermetabolic state, as well as increase in symphathetic nervous system activity. 

Hypermetabolic state → complaints of nervousness, irritability, and fatigability, weight loss despite a large appetite. Other manifestations include:

• tachycardia;
• palpitations;
• shortness of breath;
• excessive sweating;
• muscle cramps;
• heat intolerance;
• fine muscle tremor;
• exophthalmos (bulging eyes) and infrequent blinking (staring);

Graves disease is an autoimmune disorder characterized by abnormal stimulation of the thyroid gland by thyroid-stimulating antibodies (TSH receptor antibodies) that act through the normal TSH receptors.

*TSH receptor - thyrotropin receptor is a receptor (and associated protein) that responds to thyroid-stimulating hormone

Sensitivity of T lymphocytes to antigens along thyroid follicular cells^[1] and orbital fibroblast secretion of cytokines → ophthalmopathy → cause severe eye problems: 

• tethering of the extraocular muscles resulting in diplopia (double vision or seeing double) 
• involvement of the optic nerve, with some visual loss;
• corneal ulceration because the lids do not close over the protruding
  eyeball (because of the exophthalmos).

[1] thyroid follicular cells - the major cell type in the thyroid gland, and are responsible for the production and secretion of the thyroid hormones thyroxine (T₄) and triiodothyronine (T₃).

Thyroid hormone regulation occurs as negative feedback loop. When levels of T3 and T4 decrease below normal, the hypothalamus releases thyrotropin-releasing hormone (TRH), stimulating the anterior pituitary gland to produce thyroid stimulating hormone (TSH). TSH binds to receptors on epithelial cells in the thyroid gland, stimulating synthesis and secretion of thyroid hormones. Once blood concentrations of thyroid hormones increase above a certain threshold, TRH-secreting neurons in the hypothalamus are inhibited and stop secreting TRH, which in turn inhibits the pituitary gland release of TSH.

https://www.nursingcenter.com/ncblog/july-2021/understanding-the-thyroid-negative-feedback-loop

The thyroid gland is a shield-shaped structure located immediately below the larynx in the anterior middle portion of the neck. It is composed of a large number of tiny, saclike structures called follicles.These are the functional units of the thyroid. Each follicle is formed by a single layer of epithelial (follicular) cells and is filled with a secretory substance called colloid, which consists largely of a glycoprotein–iodine complex called thyroglobulin.

1. The free T3 and T4  tests measure the fractions that are not bound to plasma proteins, which are therefore free to enter cells to produce effects.
2. TSH levels are used to differentiate between primary thyroid disorders (which originate at the thyroid gland) and secondary thyroid disorders (which originate at the pituitary gland). T3 and T4 levels (bound and free) are low in primary
   hypothyroidism; however, the TSH level is elevated.
3. The radioiodine (¹²³I) uptake test measures the ability of the thyroid gland
   to concentrate and retain iodine from the blood.
4. Thyroid scans (¹²³I, ^99mTcpertechnetate) can be used to detect thyroid nodules and determine the functional activity of the thyroid gland.