Thyroids all explained: Causes and Treatments.

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Information About Thyroid

Information about thyroids, find extended information bout thyroids. main causes and treatments for thyroids, read on weather you have a problem with them or are a student and want some extended information on thyroids causes i.e Normal thyroid function, Physiology: Synthesis , Control of the hypothalamic-pituitary-thyroid axis. Physiological effects of thyroid hormones: Causes of hypothyroidism? Diagnoses, Causes of primary hypothyroidism, Atrophic (autoimmune) hypothyroidism, Hashimoto's thyroiditis, Postpartum thyroiditis,Causes of hypothyroidism

Goitre. thyroid
Goitre. thyroid

Symptoms: That your thyroid levels are not normal.

Note that severity of the symptom varies from person to person.

If you show any of these symptoms it is worth checking your thyroid hormone levels symptoms such as Nervousness and anxiety, hyperactivity where a person can’t stay still and is full of nervous energy, losing weight without an apparent reason when you are not on diet or you are eating as normal. And an obvious one is if you get a swelling and noticeable lump on the throat known as goitre. In these cases it is advisable to seek your doctor’s help and check your thyroid levels.

Physiology: Synthesis

Physiology: Synthesis

The thyroid synthesizes two hormones, L-thyroxine (T4) and triiodothyronine (T3), of which T3 acts at the cellular level and T4 is the prohormone. Inorganic iodide is trapped by the gland by an enzyme dependent system, oxidized and incorporated into the glycoprotein thyroglobulin to form mono- and diiodotyrosine and then T4 and T3.


More T4 than T3 is produced, but T4 is converted in some peripheral tissues (liver, kidney and muscle) to the more active T3 by 5'-monodeiodination; an alternative 3'-monodeiodination yields the inactive reverse T3 (rT3). The latter step occurs particularly in severe non-thyroidal illness.


In plasma, more than 99% of all T4 and T3 is bound to hormone-binding proteins (thyroxine-binding globulin, TBG; thyroid-binding prealbumin, TBPA; and albumin). Only free hormone is available for tissue action, where T3 binds to specific nuclear receptors within the cell. Many drugs and other factors affect TBG; all may result in confusing total T4 levels in blood, and most laboratories therefore now measure free T4 levels.

Normal thyroid function?

What is the normal thyroid function?

Normal thyroid function the thyroid gland consists of two lateral lobes connected by an isthmus. It is closely attached to the thyroid cartilage and to the upper end of the trachea, and thus moves on swallowing. It is often palpable in normal women. The thyroid gland consists of follicles lined by cuboidal epithelioid cells. Inside is the colloid (the iodinated glycoprotein thyroglobulin) which is synthesized by the follicular cells. Each follicle is surrounded by basement membrane, between which are parafollicular cells containing calcitonin-secreting C cells

Control of the hypothalamic-pituitary-thyroid axis.

Control of the hypothalamic-pituitary-thyroid axis.  

Thyrotrophin-releasing hormone (TRH), a peptide produced in the hypothalamus, stimulates TSH from the pituitary. TSH stimulates growth and activity of the thyroid follicular cells via the G-protein coupled TSH membrane receptor (Table 18.3). Circulating T4 is peripherally de-iodinated to T3 which binds to the thyroid hormone nuclear receptor (TR) on target organ cells to cause modified gene transcription. Two TR receptors exist (TRα and TRβ) and the tissue-specific effects of T3 are dependent upon the local expression of these TR receptors. TRα knockout mice show poor growth, bradycardia and hypothermia, whilst TRβ knockout mice show thyroid hyperplasia and high T4 levels in the presence of inappropriately normal circulating TSH, suggesting a role for the latter receptors in thyroid hormone resistance.

Physiological effects of thyroid hormones:

Physiological effects of thyroid hormones:

•Cardiovascular system - increased heart rate and cardiac output.

•Skeletal - increased bone turnover and resorption.

•Respiratory - maintains normal hypoxic and hypercapnic drive in respiratory centre.

•Gastrointestinal - increases gut motility.

•Blood - increases red blood cell 2,3-BPG facilitating oxygen release to tissues.

•Neuromuscular - increases speed of muscle contraction and relaxation and muscle protein turnover.

•Metabolism of carbohydrates - increases hepatic gluconeogenesis/glycolysis and intestinal glucose absorption.

•Metabolism of lipids - increased lipolysis and cholesterol synthesis and degradation.

•Sympathetic nervous tissue - increases catecholamine sensitivity and β-adrenergic receptor numbers in heart, skeletal muscle, adipose cells and lymphocytes. Decreases cardiac α-adrenergic receptors.

Iodine

Globally, dietary iodine deficiency is a major cause of thyroid disease, as iodine is an essential requirement for thyroid hormone synthesis. The recommended daily intake of iodine should be at least 140 μg, and dietary supplementation of salt and bread has reduced the number of areas where 'endemic goitre' still occurs.

Thyroids information symptoms causes explained hypothyroidism (part 2)

part 2: on thyroids information symptoms causes explained

Thyroids explained part 2, in this pages you will find infromation Causes of hypothyroidism. Diagnoses, the Causes of primary hypothyroidism Autoimmune ?, Atrophic (autoimmune) hypothyroidism, information on Hashimoto's thyroiditis , Postpartum thyroiditis, PERIPHERAL RESISTANCE TO THYROID HORMONE, Defects of hormone synthesis Iodine deficiency, Dyshormonogenesis, and Investigation of primary hypothyroidism and treatment

Causes of hypothyroidism. Diagnoses

what is the Causes of hypothyroidism Diagnoses underactivity of the thyroid is usually primary, from disease of the thyroid, but may be secondary to hypothalamic-pituitary disease (reduced TSH drive) (Table 18.11). Primary hypothyroidism is one of the most common endocrine conditions with an overall UK prevalence of over 1% in women, but under 0.1% in men; lifetime prevalence for an individual is higher - perhaps as high as 9% for women and 1% for men with mean age at diagnosis around 60 years. The world-wide prevalence of subclinical hypothyroidism varies from 1 to 10%.

Atrophic (autoimmune) hypothyroidism

Causes of primary hypothyroidism Atrophic (autoimmune) hypothyroidism

This is the most common cause of hypothyroidism and is associated with antithyroid autoantibodies leading to lymphoid infiltration of the gland and eventual atrophy and fibrosis. It is six times more common in females and the incidence increases with age. The condition is associated with other autoimmune disease such as pernicious anaemia, vitiligo and other endocrine deficiencies. In some instances intermittent hypothyroidism occurs with recovery from disease; antibodies which block the TSH receptor may sometimes be involved in the aetiology.

Peripheral Resistance to Thyroid Hormone

what is peripheral resistance to thyroid hormone

The PERIPHERAL RESISTANCE TO THYROID HORMONE is usually a transient phenomenon observed following pregnancy. It may cause hyperthyroidism, hypothyroidism or the two sequentially. It is believed to result from the modifications to the immune system necessary in pregnancy, and histologically is a lymphocytic thyroiditis. The process is normally self-limiting, but when conventional antibodies are found there is a high chance of this proceeding to permanent hypothyroidism. Postpartum thyroiditis may be misdiagnosed as postnatal depression, emphasizing the need for thyroid function tests in this situation.


Causes of hypothyroidism

Causes of hypothyroidism, Primary DISEASE OF THYROID, SECONDARY (TO HYPOTHALAMIC-PITUITARY DISEASE)

Hashimoto's thyroiditis

Hashimoto's thyroiditis

The Hashimoto's thyroiditis This form of autoimmune thyroiditis, again more common in women and most common in late middle age, produces atrophic changes with regeneration, leading to goitre formation. The gland is usually firm and rubbery but may range from soft to hard. TPO antibodies are present, often in very high titres (> 1000 IU/L). Patients may be hypothyroid or euthyroid, though they may go through an initial toxic phase, 'Hashi-toxicity'. Levothyroxine therapy may shrink the goitre even when the patient is not hypothyroid.

Defects of hormone synthesis

Defects of hormone synthesis

Iodine deficiency

Dietary iodine deficiency still exists in some areas as 'endemic goitre' where goitre, occasionally massive, is common. The patients may be euthyroid or hypothyroid depending on the severity of iodine deficiency. The mechanism is thought to be borderline hypothyroidism leading to TSH stimulation and thyroid enlargement in the face of continuing iodine deficiency. Iodine deficiency is still a problem in the Netherlands, Western Pacific, SouthEast Asia (e.g. the mountainous areas of the Himalayas) and Africa. Some countries affected by iodine deficiency, e.g. China and Kazakhstan, are taking action by providing iodine in salt but others, e.g. Russia, have so far not done so. Of the 500 million with iodine deficiency in India, about 2 million have cretinism.

Primary Disease of Thyroid

PRIMARY DISEASE OF THYROID
PRIMARY DISEASE OF THYROID

Dyshormonogenesis

Dyshormonogenesis

This rare condition is due to genetic defects in the synthesis of thyroid hormones; patients develop hypothyroidism with goitre. One particular familial form is associated with sensorineural deafness due to a deletion mutation in chromosome 7, causing a defect of the transporter pendrin (Pendred's syndrome).

It can usually be diagnosed by simply measuring TSH. If thyroxine production is too low, then TSH is high and vice versa.

The hypothyroidism may be caused by an autoimmune disorder (such as Hashimoto’s thyroiditis where there are autoantibodies to thyroperoxidase for example), giving rise to the presence of autoantibodies in blood, but the underlying cause is not treatable, so a simple thyroxine replacement regime is used. The aim of treatment is to keep TSH within the normal range, so the level of thyroxine replacement is titrated to achieve this.


A low free T4 level confirms the hypothyroid state. Thyroid specific destructive antibodies may also be present.

Investigation of primary hypothyroidism

Investigation of primary hypothyroidism

Serum TSH is the investigation of choice; a high TSH level confirms primary hypothyroidism. A low free T4 level confirms the hypothyroid state (and is also essential to exclude TSH deficiency if clinical hypothyroidism is strongly suspected and TSH is normal or low).


Thyroid and other organ-specific antibodies may be present

Treatment

Treatment

thyroid treatment there is a large pool of thyroxine (T4) in the body; it has a low turnover and is found mainly in the circulation. There is a small pool of triiodothyronine (T3) in the body; it has a fast turnover and is found mainly intracellularly. T3 is the active form at the cellular level, being formed from T4 in target tissues. For „non-severe‟ hypothyroidism T4 is preferred as being more physiological, also its longer half-life makes it more convenient for patients to take. T3 is prescribed in severe hypothyroid states where a more rapid response is required.


T4 is an effective and relatively safe treatment. However unwanted effects may occur with overdose. In addition to the signs and symptoms of hyperthyroidism (high metabolic rate, increase in skin temperature and sweating and a marked sensitivity to heat, nervousness, tremor etc.) there is the more serious possibility of precipitating angina pectoris, cardiac dysrhythmias or cardiac failure.


Replacement therapy with levothyroxine (thyroxine, i.e. T4) is given for life. The starting dose will depend upon the severity of the deficiency and on the age and fitness of the patient, especially their cardiac performance: 100 μg daily for the young and fit, 50 μg (increasing to 100 μg after 2-4 weeks) for the small, old or frail. Patients with ischaemic heart disease require even lower initial doses, especially if the hypothyroidism is severe and long-standing. Most physicians would then begin with 25 μg daily and perform serial ECGs, increasing the dose at 3- to 4-week intervals if angina does not occur or worsen and the ECG does not deteriorate.

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