Hypothyroidism | |
---|---|
Labrador Retriever with hypothyroidism | |
Specialty | Endocrinology |
Symptoms | Lethargy, endocrine alopecia, Obesity |
Complications | Infections, Bradycardia |
Usual onset | Usually older dogs for most forms, at birth for congenital hypothyroidism |
Duration | Lifelong if not treated |
Types | Congenital, Primary, Secondary, Tertiary |
Causes | Inadequate levels of thyroid-hormone |
Risk factors | Certain breeds |
Diagnostic method | Testing for thyroid hormone levels, Imaging of thyroid |
Differential diagnosis | Hypersomatotropism |
Treatment | Levothyroxine |
Prognosis | Depends on condition and state of thyroid gland; very poor for congenital and myxoedema coma. |
Frequency | 0.23% [1] |
Hypothyroidism is an endocrine disorder in which the thyroid gland fails to produce sufficient thyroid hormones. Hypothyroidism is one of the most common endocrinopathies in dogs. It is either acquired or congenital. [2]
Hypothyroidism is classified as either primary, secondary, or tertiary. Primary hypothyroidism is for when the cause is due to an abnormality of the thyroid gland, secondary hypothyroidism is when the cause is decreased thyroid-stimulating hormone levels, and tertiary hypothyroidism is when the cause is an inadequate amount of thyrotropin-releasing hormone being released. [2]
The causes of primary hypothyroidism include: [2]
Lymphocytic thyroiditis and idiopathic atrophy are the most common causes of primary hypothyroidism. [2]
The causes of secondary hypothyroidism include: [2]
The causes of tertiary hypothyroidism include: [2]
Lymphocytic thyroiditis is caused by an immune-mediated response to the thyroid gland. The exact mechanism is not known and the understanding of it is poor; however, it is believed that antibodies binding to the follicular cells, colloid, or thyroglobulin antigens activates the process that causes follicular destruction. Breed is an important factor given the increased incidence in certain breeds, such as the Beagle. [2]
After a tumour—either one originating in the thyroid gland or invading it—has destroyed 80% or more of the thyroid gland, symptoms of hypothyroidism may occur. Only approximately 10% of thyroid tumours cause hypothyroidism, this in part due to most thyroid tumours not affecting the whole thyroid gland. [2]
Idiopathic atrophy is the gradual reduction in the size of thyroid follicles and replacement of these follicles with adipose tissue. It may be the end stage of lymphocytic thyroiditis or a primary degenerative disorder. [2]
Iodine deficiency is a rare cause of hypothyroidism for dogs: commercial dog foods typically contain sufficient levels of iodine for dogs. In recent years there has been an interest in homemade diets for pets, these diets are not always providing sufficient levels of iodine. Working dogs fed all meat diets have been reported to suffer from hypothyroidism due to iodine deficiency. In addition to iodine deficiency, excessive amounts of iodine can cause thyroid impairment and lead to hypothyroidism. [2]
Goitrogens and anti-thyroid medication is a potential cause of primary hypothyroidism, but is rare in practice. [2]
Thyroidectomy may cause hypothyroidism: in one study more than 50% of dogs that underwent a bilateral thyroidectomy required long term thyroid hormone treatment. [3] [2]
Radioactive iodine used to treat thyroid neoplasia can also result in hypothyroidism. [2]
Secondary hypothyroidism occurs when pituitary thyrotrophs fail to develop, resulting in impaired thyroid-stimulating hormone secretion. Inadequate levels of thyroid-stimulating hormone causes a decrease in thyroid hormone synthesis and secretion and cause hypoplasia of the thyroid gland. [2]
Secondary hypothyroidism caused by naturally acquired defects of thyrotrophs, like those resulting from a neoplasia, are uncommon. Secondary hypothyroidism caused by thyrotroph suppression from a comorbidity, malnutrition, hormones or drugs is a very common cause of secondary hypothyroidism. [2]
The destruction of thyrotrophs by a pituitary neoplasia may cause secondary hypothyroidism, although pituitary neoplasias do not commonly cause secondary hypothyroidism. [2]
Tertiary hypothyroidism is caused by an inadequate amount of thyrotropin-releasing hormone being secreted by the hypothalamus. Thyrotropin-releasing hormone stimulates release of thyroid-stimulating hormones, thus a lack of thyrotropin-releasing hormone causes a decrease in thyroid-stimulating hormone which causes follicular atrophy. [2]
Congenital hypothyroidism is a rare and is often underdiagnosed due to dogs with the condition often dying as young puppies. Congenital hypothyroidism is caused by a defect in the hypothalamic–pituitary–thyroid axis or the thyroid hormone receptor. It is not uncommon for puppies with the condition to die early due to retarded growth and dwarfism. Signs of congenital hypothyroidism typically shown within the first 3 months. [2]
Signs of hypothyroidism vary based on factors such as the type and breed. Due to the slow onset and progress of the disease clinical signs do not initially appear for example, clinical signs do not show until the 3rd stage of lymphocytic thyroiditis. It is not uncommon for owners to ignore certain signs of hypothyroidism due to the slow progression of metabolic symptoms. Often metabolic symptoms will go unnoticed until after a dog has received treatment for hypothyroidism. [2]
The most common signs of hypothyroidism are dermatological and changes relating to the decreased metabolism. [2] In one study the most common symptoms were dermatological conditions, obesity, and lethargy. Nearly 9/10 dogs had dermatological symptoms, lethargy and obesity were observed in almost half of all dogs. [4]
The lowered concentration of thyroid hormone has an affect on organs throughout the body. [5]
The decrease in thyroid hormone levels causes dermatological conditions, specifically alopecia, which is the most common dermatological symptom, as the hair sheds but cannot regrow fast enough due to the anagen stage of hair growth being stunted as thyroid hormone is important in that stage of hair growth. Other dermatological symptoms include: hyperkeratosis, hyperpigmentation, seborrhoea, pyoderma, otitis externa, and myxoedema. Breed variation in coats can impact the dermatological effect of hypothyroidism. Some dogs develop hypertrichosis and some develop either a wool-like or a coarse appearance. Immune dysregulation, caused by hypothyroidism, can lead to superficial bacterial infection. [2]
Myxoedema, also known as cutaneous mucinosis, occurs when hyaluronic acid builds up in the dermis, this build up may cause swelling and thickening of the skin. Myxoedema is a feature of severe cases of hypothyroidism and is sometimes used synonymously. The characteristic facial expression of hypothyroidism is in part caused by myxoedema. [2]
Hypothyroidism can affect the peripheral and central nervous system. Neurological symptoms vary widely and it is not currently known what is responsible for causing neurological symptoms, although multiple theories have been put forward. Some of the other proposed causes of neurological symptoms include: nerve entrapment, due to mucinous deposits; demyelination, due to disruptions to the metabolism of Schwann cells; vascular nerve damage, due to changes to the blood-nerve barrier; and disruption of the axonal cell transport. An immune-related cause has been put forward as well, due to the presence of immune-mediated thyroiditis in some dogs with hypothyroidism. [2]
There is a belief of an association between hypothyroidism and reproductive symptoms causing poor reproductive ability. Studies have not identified this association; however, there is no definitive evidence from studies that can rule out an association. It is recommended that when common causes of poor reproductive ability have been ruled out that hypothyroidism be considered as a possible cause. Hypothyroidism can result in excessive prolactin secretion due to increased thyrotropin-releasing hormone levels. Excessive prolaction secretion causes hyperprolactinaemia and may cause improper lactation in unspayed bitches. [2]
It is uncommon for cardiovascular symptoms to be diagnosed during a clinical exam. The cardiovascular symptoms that are most often diagnosed during examination are bradycardia and a deficit of the apical impulse. The exact mechanism behind the cause of cardiovascular and haemodynamic symptoms is unknown but may be due to the effects of hypothyroidism on the cardiac muscle. Most cardiac abnormalities in dogs with hypothyroidism are typically mild and thus is not a cause for concern aside outside of long surgical procedures. Heart failure may occur in cases of primary hypothyroidism; however, heart failure caused by hypothyroidism is rare, most cases of heart failure are a preexisting condition being exacerbated by the thyroid hormone deficiency. Thyroid hormone treatment usually results in a cessation of cardiac abnormalities, although it may take several months for this to occur. [2]
Myxoedema coma is a very rare but deadly form of severe hypothyroidism characterised by myxoedema, asthaenia, hypothermia, bradycardia and organ dysfunction, hypotension, hypoventilation and unresponsiveness. It may swiftly progress to stupor and coma. Dogs with the condition have similar test results as those with normal hypothyroidism but prognosis is very poor and most dogs will die from organ failure or an infection occurring alongside the condition. The condition often occurs after a bacterial infection or a bout of hypothermia. [2]
Due to the effect thyroid hormone has on the pituitary gland hypothyroidism can cause hypersecretion of growth hormone. [6]
Hypothyroidism symptoms are usually diagnosed in older dogs, this may be in part due to the slow onset of symptoms. [2]
Breed is a factor in the progression and likelihood of thyroiditis. Golden Retrievers and Doberman Pinschers are often reported as having a predilection for the condition. Breeds with a described mutation in the TPO gene include: Toy Fox Terriers, Rat Terriers, Tenterfield Terriers, and Spanish Water Dogs. Environmental factors have not been well described in the literature. [2]
In a study of more than 140,000 serum samples of suspected hypothyroidism, the five breeds with the highest prevalence of thyroglobulin autoantibodies were: English Setter (31%), Old English Sheepdog (23%), Boxer (19%), Giant Schnauzer (19%), and American Pit Bull Terrier (19%). [7]
No evidence exists of a predilection for any sex nor whether the animal is neutered or not. [2]
Congenital hypothyroidism has unique symptoms that distinguish it from other forms of hypothyroidism such as: dwarfism, growth retardation, kyphosis, retarded tooth eruption, shortened lower jaw, and an enlarged skull. The cause of the symptoms are due to the rule of thyroid hormone in bone and mental growth. [2]
Thyrotoxicosis is when an abnormally high amount of circulating thyroid-hormone is present, in this instance it does not refer to hyperthyroidism but instead excessive levels due to administration of thyroid-hormone treatment. Thyrotoxicosis is a rare side effect in dogs receiving levothyroxine treatment due to the half-life and poor absorption. Thyrotoxicosis occurs when a dog is either given too much levothyroxine or has issues with metabolising it. Symptoms include: polypynoea, anxiety, tachycardia, aggression, polyuria, polydipsia, polyphagia, and cachexia. [2]
Immune-mediated endocrine disorders such as diabetes mellitus and hypoadrenocoriticism often occur alongside lymphocytic thyroiditis. One study found 4% of dogs with hypoadrenocorticism also had hypothyroidism and one dog had hypoadrenocorticism, hypothyroidism, diabetes mellitus, and hyperparathyroidism. Orchitis occurring alongside thyroiditis has been documented in Beagles. The average time for a diagnosis of a second endocrinopathy is 4 months, with one dog having a period of 53 months between diagnosis. [2]
A pituitary tumour that causes pituitary destruction may cause hypothyroidism, alongside: hypocortisolism, diabetes insipidus, and sexual dysfunction. [2]
Lymphocytic thyroiditis is the infiltration of the thyroid gland by lymphocytes, plasma cells, and macrophages. The infiltration progressively causes destruction of follicles and secondary fibrosis. Clinical signs typically do not show before 80% of the thyroid gland has been destroyed. This destruction occurs over a long period of time, between 1–3 years. This destruction is classified into four stages: subclinical thyroiditis, when the infiltration of thyroid follicles occurs, test results will be positive for thyroglobulin and thyroid hormone autoantibodies; antibody positive subclinical hypothyroidism, when the loss of more than 60% of thyroid gland mass has occurred and in response there is an increase of thyroid-stimulating hormone, this stimulates the thyroid gland to maintain thyroxine levels; antibody positive overt hypothyroidism, when a majority of the functional thyroid tissue has been destroyed, test results will show a decrease in serum thyroid hormone concentration and an increase in thyroid-stimulating hormone concentration; and noninflammatory atrophic hypothyroidism, when the thyroid tissue has been replaced by fibrous and adipose tissue and a disappearance of inflammatory cells and circulating antibodies has occurred. [2]
Given the possible comorbidities and other causes of low serum concentrations of thyroxine it can be difficult to definitively diagnose hypothyroidism. Strong cause for a diagnosis exists when clinical signs are showing, test results are indicative, and no other illness is present. To exclude the possibility of a thyroid responsive disease after clinical symptoms vanish after thyroid supplementation treatment can be ceased, if symptoms re-occur after 6–8 weeks this excludes a thyroid responsive disease. [2]
Lymphocytic thyroiditis can be diagnosed as the cause of hypothyroidism via histological examination. Histological examination will reveal mononuclear cell infiltration, the absence of follicles containing colloid, and a change in the normal appearance and layout of the cells. Proteinuria may be identified in dogs with lymphocytic thyroiditis but otherwise urinalysis results should be normal. [2]
There are no tests for idiopathic atrophy and due to that it is made via diagnosis of exclusion. Negative results on tests for other forms and symptoms aligning with the condition are used to diagnose it. [2]
Secondary hypothyroidism can be histologically diagnosed by looking at the follicles of the thyroid gland, these follicles will by hypoplastic and lack in colloids in cases of secondary hypothyroidism. Testing will typically reveal decreased or absent levels of thyroid-stimulating hormone; however, this result does not confirm secondary hypothyroidism. [2]
In dogs with clinical hypothyroidism the symptoms are more pronounced. A goitre will be present if the hypothalamus-pituitary-thyroid axis is intact. Serum thyroid-stimulating hormone concentration varies based on aetiology. [2]
When tertiary hypothyroidism is suspected it can be confirmed via testing, if thyroid-stimulating hormone levels increase after thytropin-releasing hormones have been administered then a diagnosis of tertiary hypothyroidism has been confirmed. The sensitivity of the thyroid-stimulating hormone assays for dogs makes this is a difficult diagnosis. [2]
Dogs being treated for epilepsy may be incorrectly diagnosed as having hypothyroidism as anticonvulsant medication used to treat epilepsy can alter the results of tests that measure thyroid hormone levels. Dogs being treated with anticonvulsant medications that lower serum thyroxine levels such as phenobarbital do not appear to cause any symptoms of hypothyroidism. [2]
Euthyroid sick syndrome, also known as nonthyroidal illness syndrome, is a term to describe when a euthyroid patient has low levels of serum thyroid hormone due to nonthyroidal illness. Causes can be essentially any systemic illness, as well as trauma and insufficient calorie intake. Dermatological conditions are unlikely to affect thyroid function. Multiple mechanisms and conditions cause this condition. Different conditions do not appear to be more likely to cause more severe changes to serum thyroid hormone concentration but instead more severe illness causes more severe changes. Common causes of euthyroid sick syndrome include: neoplasia, renal disease, hepatic disease, neurological disease, cardiac failure, inflammatory disease, and diabetic ketoacidosis. [2]
In 40-50% of dogs with Cushing's syndrome thyroxine and triiodothyronine levels are decreased. Cushing's is a potential differential diagnosis for hypothyroidism when the patient presents with endocrine alopecia. Clinical history can be used to differentiate the two: polyuria, polydipsia, and polyphagia are symptoms of Cushing's but not hypothyroidism. If Cushing's is suspected a urinalysis of the cortisol/creatinine ratio can be used to diagnosis or exclude Cushing's. [2]
Common electrocardiographic findings in dogs showing symptoms of hypothyroidism include sinus bradycardia and atrioventricular blocks. [2]
Common echocardiographic findings in dogs showing symptoms of hypothyroidism include an increased systolic diameter of the left ventricle, a decreased thickness of the left posterior ventricular wall, and prolongation of the pre-ejection period when the heart muscle contracts; and changes to the left ventricular posterior wall, interventricular wall thickness, and diameter of the aorta. [2]
A form of anaemia that is normocytic, normochromic, and non-regenerative is diagnosed in approximately 30% of dogs with hypothyroidism. [2]
The most common finding in with a serum biochemistry panel is fasting hypercholesterolaemia, this finding appears in approximately 75% of dogs with hypothyroidism. Hypertriglyceridaemia is also a common finding. Neither of these are pathognomonic; however, they are supportive evidence of hypothyroidism. Increases in serum lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase activity. [2]
Radiography is not standard procedure for identifying acquired hypothyroidism. Cervical spine radiographs are only useful when neoplasia is suspected as the cause. [2]
Abnormalities can be detected via radiography in cases of congenital hypothyroidism and these include: retarded epiphyseal ossification; epiphyseal dysgenesis; brachycephalic skull, when untypical for the breed or shorter than expected; shortened vertebral body; reduced length of diaphyses of long bones; retarded ossification; and retarded maturation. [2]
An ultrasound is often used when a thyroid neoplasm is suspected. An ultrasound allows for a real time image of the thyroid gland to be evaluated. An ultrasound is a useful way to diagnose or exclude euthyroid sick syndrome. In cases of hypothyroidism the thyroid lobes appear round or oval in shape when viewed from the transverse plane, hypoechoic, and a smaller volume and area than clinically healthy patients. [2] A study in 2005 found an ability to diagnose hypothyroidism correctly 96% of the time when euthyroid sick syndrome was also suspected as a possible diagnosis. [8]
Blood testing can be used to measure the baseline serum thyroid hormone concentrations, which is in turn used to determine whether an animal has thyroid dysfunction. Measuring thyroid dysfunction via stimulation of the thyroid with thyroid-stimulating hormone is considered the most accurate method of diagnosing hypothyroidism; however, due to the cost of this method it is rarely performed. Other methods involve testing for the levels of thyroxine, triiodothyronine, and thyroid-stimulating hormone. Thyroxine makes up most of the thyroid hormone produced by the thyroid gland. Thyroxine is resilient to common forms of degradation and can survive over a week at room temperature. Certain breeds, including the Greyhound, Whippet, Sloughi, Saluki, Basenji, Irish Wolfhound, and some Alaskan sled dogs, have levels of thyroid hormone that differ from the norm.
Thyroid hormone levels can fluctuate due to a number of causes such as another illness, especially euthyroid sick syndrome. Levels of thyroxine and triiodothyronine in blood serum are increased in bitches during dioestrus, possibly due to progesterone improving the binding. [2]
A biopsy of the thyroid can be used to confirm a diagnosis of primary hypothyroidism in a patient with symptoms and test results that point towards hypothyroidism, especially with severe cases of lymphocytic thyroiditis and thyroid atrophy. A biopsy will not necessarily be able to inform about the health of the thyroid gland and its function. When symptoms and test results are less conclusive a biopsy is more likely to be unable to give a definitive answer. A large portion of the thyroid needs to be destroyed for thyroid failure is noted, this combined with the factors around surgery itself make it a rare procedure for a diagnosis of hypothyroidism. [2]
The main form of treatment for all forms of hypothyroidism is levothyroxine sodium. This method allows for normal levels of thyroid hormone in tissue and elsewhere whilst keeping the risk of iatrogenic hyperthyroidism low. The treatment dose for dogs is 10 times that of humans due to a shorter half-life of serum thyroxine and poorer gastrointestinal absorption. Many factors such as whether treatment is once daily or twice daily, route of administration, and physiology of the animal all have an effect and patients need to be monitored closely whilst undergoing treatment. It is not recommended to change the formulation for a patient. Serum concentrations of thyroxine and thyroid-stimulating hormone should be measured every 6–8 weeks or earlier if the animal does not respond well to treatment or thyrotoxicosis occurs. Measurements should be taken 4–6 hours after levothyroxrine treatment in dogs receiving treatment twice per day and 4–6 hours before and after in dogs treated once per day. In severe cases, such as myxoedema coma, when hypometabolism is occurring the treatment should be administered intravenously. [2]
Evaluation of treatment should not occur until at least 6–8 weeks have passed. Symptoms of hypothyroidism should resolve if treatment is effective. Lethargy and torpidity is usually resolved within the first month and obesity by around two months; however, other factors can impact obesity. While symptoms should have resolved after this 6–8 weeks full regrowth of the coat following endocrine alopecia may not occur until several months after starting treatment. Myocardial improvement can occur as early as a month but in some patients it will not occur until around a year has passed. [2]
Liothyronine treatment causes serum triiodothyronine levels to return to normal but thyroxine levels remain low. Liothyronine whilst not the initial choice of treatment may be used when levothyroxine treatment fails and there is reason to believe the cause of failure is gastrointestinal malabsorption. [2]
Historically, dogs with normal serum thyroxine levels but low serum levels of triiodothyronine would be treated with liothyronine sodium. A defect in the enzymes responsible for converting thyroxine to triiodothyronine was believed to be responsible; however, no evidence of such a defect occurring has been identified, furthermore if such a defect were to exist it would theoretically be present at birth and result in early death or cretinism. [2]
Myxoedema coma is often fatal but when identified and treated early prognosis is improved. Contrary to typical treatment where treatment is not started before serum thyroid concentration is measured — given the severity of the condition treatment should be started before waiting for results. Treatment involves treating the underlying hypothyroidism as well as the symptoms such as hypothermia, hypovolaemia, and hypoventilation. Improvement is typically seen within 24 hours, although death is still common.
Thyroid supplementation results in an increased demand for oxygen from the myocardium, an increased heart rate, and potentially a reduction in the ventricular filling time. Due to this, when a dog is known to have a cardiomyopathy the starting dose should 25%-50% lower. [2]
In cases of a patient with hypoadrenocorticism and hypothyroidism, treatment of the hypoadrenocorticism should occur before thyroid supplementation due to the potential for levothyroxine sodium treatment to worsen electrolyte imbalance. [2]
Hypothyroidism may cause insulin resistance; treatment for hypothyroidism in a diabetic patient may cause hypoglycaemia, thus diabetic patients need to have their blood glucose monitored. [2]
A dog with treated primary hypothyroidism should have a life expectancy equivalent to clinically healthy dogs. Prognosis is worse for myxoedema coma and congenital hypothyroidism. Death is still likely following early treatment for myxoedema coma. Prognosis is poor even for treated dogs with congenital hypothyroidism, many of the effects like cretinism and retarded growth result in lifelong complications such as osteoarthritis. Prognosis for secondary hypothyroidism is poor due to the tumour and pituitary gland destruction. [2]
The most common type is acquired primary hypothyroidism which makes up approximately 95% of hypothyroidism cases in dogs. Secondary hypothyroidism is rare and tertiary hypothyroidism is even rarer. [2]
The most common thyroid disorder for cats is hyperthyroidism. Hypothyroidism is a rare condition for cats, the most common causes of low serum concentration of thyroxine in cats is an underlying condition (non-thyroidal illness) or iatrogenic. Other causes are caused by birth defect. Adult-onset primary/secondary hypothyroidism is very rare. [2]
The most common cause of hypothyroidism in cats is iatrogenic, with most cases occurring following treatment for hyperthyroidism. Multiple treatments for hyperthyroidism can cause hypothyroidism, including: thyroidectomy, radiotherapy and thionamides. [2]
After 2–3 months most cats with iatrogenic hypothyroidism have regained normal thyroid function; however, some cats will need levothyroxine sodium treatment after this. [2]
Adult-onset primary hypothyroidism is very rare; in 2014 only 2 cases have been described in detail: one case involved lymphocytic thyroiditis and in the other case the thyroid gland was not identified during necropsy. A cat that suffered head trauma was reported to have developed secondary hypothyroidism. MRI showed the cat to have a small pituitary gland with the sella turcica being near empty. [2]
Common symptoms are lethargy, anorexia, obesity, and dermatological conditions such as alopecia. In addition the torpidity of the cat will cause a decrease in grooming which may lead to matting and poor coat condition. [2]
The most common non-iatrogenic cause of hypothyroidism; congenital hypothyroidism causes dwarfism in cats. Common causes include a resistance to thyroid-stimulating hormone, thyroid dyshormonogenesis, and thyroid dysmorphogenesis. Other causes have been reported in specific pedigrees or colonies including iodine organification and thyroid peroxidase deficiency. [2]
Prognosis is guarded and the issues relating to retarded growth are typically lifelong. [2]
Hyperthyroidism is the condition that occurs due to excessive production of thyroid hormones by the thyroid gland. Thyrotoxicosis is the condition that occurs due to excessive thyroid hormone of any cause and therefore includes hyperthyroidism. Some, however, use the terms interchangeably. Signs and symptoms vary between people and may include irritability, muscle weakness, sleeping problems, a fast heartbeat, heat intolerance, diarrhea, enlargement of the thyroid, hand tremor, and weight loss. Symptoms are typically less severe in the elderly and during pregnancy. An uncommon but life-threatening complication is thyroid storm in which an event such as an infection results in worsening symptoms such as confusion and a high temperature; this often results in death. The opposite is hypothyroidism, when the thyroid gland does not make enough thyroid hormone.
The thyroid, or thyroid gland, is an endocrine gland in vertebrates. In humans, it is in the neck and consists of two connected lobes. The lower two thirds of the lobes are connected by a thin band of tissue called the isthmus (pl.: isthmi). The thyroid gland is a butterfly-shaped gland located in the neck below the Adam's apple. Microscopically, the functional unit of the thyroid gland is the spherical thyroid follicle, lined with follicular cells (thyrocytes), and occasional parafollicular cells that surround a lumen containing colloid. The thyroid gland secretes three hormones: the two thyroid hormones – triiodothyronine (T3) and thyroxine (T4) – and a peptide hormone, calcitonin. The thyroid hormones influence the metabolic rate and protein synthesis and growth and development in children. Calcitonin plays a role in calcium homeostasis. Secretion of the two thyroid hormones is regulated by thyroid-stimulating hormone (TSH), which is secreted from the anterior pituitary gland. TSH is regulated by thyrotropin-releasing hormone (TRH), which is produced by the hypothalamus.
Hypothyroidism is a disorder of the endocrine system in which the thyroid gland does not produce enough thyroid hormones. It can cause a number of symptoms, such as poor ability to tolerate cold, extreme fatigue, muscle aches, constipation, slow heart rate, depression, and weight gain. Occasionally there may be swelling of the front part of the neck due to goitre. Untreated cases of hypothyroidism during pregnancy can lead to delays in growth and intellectual development in the baby or congenital iodine deficiency syndrome.
Congenital hypothyroidism (CH) is thyroid hormone deficiency present at birth. If untreated for several months after birth, severe congenital hypothyroidism can lead to growth failure and permanent intellectual disability. Infants born with congenital hypothyroidism may show no effects, or may display mild effects that often go unrecognized as a problem. Significant deficiency may cause excessive sleeping, reduced interest in nursing, poor muscle tone, low or hoarse cry, infrequent bowel movements, significant jaundice, and low body temperature.
Thyroid-stimulating hormone (also known as thyrotropin, thyrotropic hormone, or abbreviated TSH) is a pituitary hormone that stimulates the thyroid gland to produce thyroxine (T4), and then triiodothyronine (T3) which stimulates the metabolism of almost every tissue in the body. It is a glycoprotein hormone produced by thyrotrope cells in the anterior pituitary gland, which regulates the endocrine function of the thyroid.
Myxedema is a term used synonymously with severe hypothyroidism. However, the term is also used to describe a dermatological change that can occur in hypothyroidism and (rare) paradoxical cases of hyperthyroidism. In this latter sense, myxedema refers to deposition of mucopolysaccharides in the dermis, which results in swelling of the affected area. One manifestation of myxedema occurring in the lower limb is pretibial myxedema, a hallmark of Graves disease, an autoimmune form of hyperthyroidism. Myxedema can also occur in Hashimoto thyroiditis and other long-standing forms of hypothyroidism.
Hashimoto's thyroiditis, also known as chronic lymphocytic thyroiditis and Hashimoto's disease, is an autoimmune disease in which the thyroid gland is gradually destroyed. A slightly broader term is autoimmune thyroiditis, identical other than that it is also used to describe a similar condition without a goiter.
Thyroid disease is a medical condition that affects the function of the thyroid gland. The thyroid gland is located at the front of the neck and produces thyroid hormones that travel through the blood to help regulate many other organs, meaning that it is an endocrine organ. These hormones normally act in the body to regulate energy use, infant development, and childhood development.
Thyroiditis is the inflammation of the thyroid gland. The thyroid gland is located on the front of the neck below the laryngeal prominence, and makes hormones that control metabolism.
De Quervain's thyroiditis, also known as subacute granulomatous thyroiditis or giant cell thyroiditis, is a self-limiting inflammatory illness of the thyroid gland. De Quervain thyroiditis is characterized by fever, flu-like symptoms, a painful goiter, and neck pain. The disease has a natural history of four phases: thyroid pain, thyrotoxicosis, euthyroid phase, hypothyroid phase, and recovery euthyroid phase.
Thyroid function tests (TFTs) is a collective term for blood tests used to check the function of the thyroid. TFTs may be requested if a patient is thought to suffer from hyperthyroidism or hypothyroidism, or to monitor the effectiveness of either thyroid-suppression or hormone replacement therapy. It is also requested routinely in conditions linked to thyroid disease, such as atrial fibrillation and anxiety disorder.
Subacute thyroiditis refers to a temporal classification of the different forms of thyroiditis based on onset of symptoms. The temporal classification of thyroiditis includes presentation of symptoms in an acute, subacute, or chronic manner. There are also other classification systems for thyroiditis based on factors such as clinical symptoms and underlying etiology.
Postpartum thyroiditis refers to thyroid dysfunction occurring in the first 12 months after pregnancy and may involve hyperthyroidism, hypothyroidism or the two sequentially. According to the National Institute of Health, postpartum thyroiditis affects about 8% of pregnancies. There are, however, different rates reported globally. This is likely due to the differing amounts of average postpartum follow times around the world, and due to humans' own innate differences. For example, in Bangkok, Thailand the rate is 1.1%, but in Brazil it is 13.3%. The first phase is typically hyperthyroidism. Then, the thyroid either returns to normal or a woman develops hypothyroidism. Of those women who experience hypothyroidism associated with postpartum thyroiditis, one in five will develop permanent hypothyroidism requiring lifelong treatment.
The hypothalamic–pituitary–thyroid axis is part of the neuroendocrine system responsible for the regulation of metabolism and also responds to stress.
Myxedema coma is an extreme or decompensated form of hypothyroidism and while uncommon, is potentially lethal. A person may have laboratory values identical to a "normal" hypothyroid state, but a stressful event precipitates the myxedema coma state, usually in the elderly. Primary symptoms of myxedema coma are altered mental status and low body temperature. Low blood sugar, low blood pressure, hyponatremia, hypercapnia, hypoxia, slowed heart rate, and hypoventilation may also occur. Myxedema, although included in the name, is not necessarily seen in myxedema coma. Coma is also not necessarily seen in myxedema coma, as patients may be obtunded without being comatose.
Prior to the availability of sensitive TSH assays, thyrotropin releasing hormone or TRH stimulation tests were relied upon for confirming and assessing the degree of suppression in suspected hyperthyroidism. Typically, this stimulation test involves determining basal TSH levels and levels 15 to 30 minutes after an intravenous bolus of TRH. Normally, TSH would rise into the concentration range measurable with less sensitive TSH assays. Third generation TSH assays do not have this limitation and thus TRH stimulation is generally not required when third generation TSH assays are used to assess degree of suppression.
Liotrix is a 4:1 mixture of thyroxine (T4) and triiodothyronine (T3) made synthetically. It is used to replenish thyroid hormones in thyroid deficiency and hypothyroidism. The only brand of liotrix available in the U.S. is Thyrolar, manufactured by Forest Laboratories.
Thyroid disease in pregnancy can affect the health of the mother as well as the child before and after delivery. Thyroid disorders are prevalent in women of child-bearing age and for this reason commonly present as a pre-existing disease in pregnancy, or after childbirth. Uncorrected thyroid dysfunction in pregnancy has adverse effects on fetal and maternal well-being. The deleterious effects of thyroid dysfunction can also extend beyond pregnancy and delivery to affect neurointellectual development in the early life of the child. Due to an increase in thyroxine binding globulin, an increase in placental type 3 deioidinase and the placental transfer of maternal thyroxine to the fetus, the demand for thyroid hormones is increased during pregnancy. The necessary increase in thyroid hormone production is facilitated by high human chorionic gonadotropin (hCG) concentrations, which bind the TSH receptor and stimulate the maternal thyroid to increase maternal thyroid hormone concentrations by roughly 50%. If the necessary increase in thyroid function cannot be met, this may cause a previously unnoticed (mild) thyroid disorder to worsen and become evident as gestational thyroid disease. Currently, there is not enough evidence to suggest that screening for thyroid dysfunction is beneficial, especially since treatment thyroid hormone supplementation may come with a risk of overtreatment. After women give birth, about 5% develop postpartum thyroiditis which can occur up to nine months afterwards. This is characterized by a short period of hyperthyroidism followed by a period of hypothyroidism; 20–40% remain permanently hypothyroid.
Thyroid's secretory capacity is the maximum stimulated amount of thyroxine that the thyroid can produce in a given time-unit.
Feline hyperthyroidism is an endocrine disorder in which the thyroid gland produces too much thyroid hormone. Hyperthyroidism is the most common endocrinopathy of cats. The complete pathogenesis is not fully understood.