Thyroid gland maintains levels of metabolism in tissues.
Thyroid hormones stimulate oxygen consumption in most cells of the body.
Regulates lipid and CHO metabolism.
Necessary for normal growth and maturation.
Absence causes mental and physical slowing.
Excess causes body wasting nervousness tachycardia and tremors.
Controlled by Thyroid stimulating hormones(TSH)
Thyroid tissue is present in all vertebrates
Originates from evagination of the floor of the pharynx and thyroglossal duct marking the path of the thyroid from tongue to neck.
2 lobes connected by isthmus
Sometimes pyramidal lobe arising from the isthmus.
Well vascularised
Multiple follicles
Follicle surrounded by cells filled with colloids
When inactive, colloid is abundant and follicle large.
When active follicles are small.
The principal hormones secreted by thyroid gland are Thyroxine(T4) and triiodothyronine(T3)
T3 is also formed in the peripheral tissue by deiodination of T4
Both hormones are iodine-containing amino acids.
T3 is more active than T4
Calcitonin is also produced by thyroid in response to increased calcium levels .
Structure of thyroid hormones
T3 and T4 are synthesized in the colloid by iodination
The hormones are bound to thyroglobulin within the thyroid cells
Thyroglobulin is also synthesized in the thyroid cells
The hormones remain bound to thyroglobulin until secreted
When secreted, the colloids is ingested by thyroid cells, peptide bonds are hydrolyzed and free T3 and
T4 are discharged into the system
Iodine is the raw material for thyroid hormone synthesis.
Ingested iodine is converted to iodide and then absorbed
The principal organs that take up the iodide are the thyroid which uses it to make thyroid hormones and the kidneys which excrete it in the urine.
Thyroid concentrates iodide by actively transporting it from circulation to the colloid
The transport mechanism is called “iodide trapping” mechanism or the “iodide pump”
The pump is an example of a secondary active transport system
In the gland, iodide is oxidized and bound to tyrosine.
In the thyroid, iodide is oxidized to iodine and bound within secs to tyrosine attached to thyroglobulin
The enzyme responsible for the oxidation and binding of iodide is Thyroid peroxidase
Monoiodotyrosine (MIT) is next iodinated to
Diiodotyrosine(DIT)
2 DIT molecules undergo oxidative condensation to form Thyroxine(T4)
T3 is probably formed by condensation of MIT and
DIT.
Large amounts of T3 and T4 are bound to plasma proteins.
The unbound T3 and T4 are the physiologically active forms of the hormones.
Free T3 and T4 inhibit the secretion of TSH.
The plasma proteins that bind thyroid hormones are albumin,transthyretin and thyroxin-binding globulin(TBG)
Most of the circulating T4 is bound to TBG
T3 is bound to albumin
TBG levels are increased in estrogen-treated patients and pregnant women
TBG levels are reduced by glucocorticoids and androgens.
Majority of action of thyroid hormones are secondary to stimulation of oxygen consumption.
Regulates lipid metabolism
↑ absorption of CHO from the intestine
↑ mentation and concentration
↑ sensitivity of heart to chronotropic(heartbeat) and inotropic (muscle contractions) effects of catecholamine.
↓ circulating cholesterol levels.
Essential for normal growth and skeletal maturation.
Hypothyroidism —caused by
Hashimoto’s Thyroiditis
Ord’s thyroiditis
Post operative Hypothyroidism
Congenital hypothyroidism(cretinism)
Hyperthyroidism---caused by
Grave’s Disease
Anatomical –Goitre-Endemic
-Diffuse
-Multinodular
Signs and symptoms of hypo or hyper thyroidism are consequences of effect of thyroid hormones.
Hypothyroidism-
Syndrome of hypothyroidism is called myxedema.
Term also used to describe skin changes in hypothyroidism.
May be end result of secondary pituitary failure
(pituitary hypothyroidism)
May be due to hypothalamic failure( hypothalamic hypothyroidism)
May be due to thyroid disorder.
Children with hypothyroidism from birth are called cretins
They have reduced growth and mentally retarded.
Potbellies
Enlarged protruding tongue
Causes-
Maternal iodine deficiency
Fetal thyroid dysgenesis
Inborn errors of thyroid synthesis
Maternal antibodies that cross placenta
Fetal hypo pituitary hypothyroidism
Autoimmune disease where antibodies attack thyroid cells.
Females>males
Atrophic (degeneration) form is known as Ord’s thyroiditis
Causes :
Genetic
Chromosomal disorders associated:Turners,klinfelter’s and Down’s syndrome
Presentation: hypothyroidism and goiter
Nervousness
Wt loss
Hyperphagia
Heat intolerance
Increased pulse pressure
Fine tremors on outstretched fingers
Warm soft skin
Sweating
Increased BMR
Most common cause of hyperthyroidism
Also known as exophthalmic goiter
Thyroid is diffusely enlarged
Protrusion of the eyeballs
Autoimmune disorder
Circulating antibodies formed against TSH receptors which activate the receptors and make gland hyperactive.
4 types of antibodies-TSH stimulating,TSHblocking,Tg antibody,Tpo antibody
↑ T3 ,T4 levels
Inhibition of the TSH
Presentation:
Palpitation
Tachycardia
↑ BP
↑ sweating
Tremors
↑ appetite
Wt loss
Protruding eyeballs
When dietary intake drops,thyroid hormones synthesis is inadequate and secretion is reduced.
TSH is increased and thyroid hypertrophies producing an iodine deficiency Goiter.
Endemic goiter-mountainous areas..
Thyroid response to low intake of iodine.
In most cases if iodine is deficient in the diet but not absent, the individual will remain euthyroid (normal fxn thyroid) but will develop a goiter.
This is called Endemic goitre.
The enlarged gland may make maximum use of the iodine available and may be able to just maintain normality but at the expense of a large goitre, hence the description endemic goitre.
Prevention : supplementation of iodine, which can be added to a staple food such as flour or salt.
Iodine uptake is an index of thyroid function
Uptake can be measured by using tracer doses of radioactive isotopes of iodine that have no effect on thyroid gland.
Tracer is administered orally
Gamma ray counter placed over the neck
Large amount of radioactive iodine destroys the thyroid tissue.
Radioiodine therapy is useful in some cases of thyroid cancer although can cause radiation carcinogenesis.
Pathological Changes in Thyroid Hormone Secretion
T4 TSH
1. *Primary hypothyroidism
TRH
2. Pituitary hypothyroidism
(secondary
)
3. Hypothalamic hypothyroidism
(tertiary
)
4 Pituitary hyperthyroidism
(secondary)
)
5
. Grave’s disease (autoimmune