16. If it becomes enlarged (goiter), doctors can feel it easily, and a prominent bulge may appear below or to the sides of the Adam's apple.
17.
18. Thyroid hormones affect many vital body functions: the heart rate, the respiratory rate, the rate at which calories are burned, skin maintenance, growth, heat production, fertility, and digestion.
19. The two thyroid hormones are T4 (thyroxine) and T3 ( triiodothyronine).T4, the major hormone produced by the thyroid gland, has only a slight, if any, effect on speeding up the body's metabolic rate. Instead, T4 is converted into T3, the more active hormone
26. Thyroxine, or 3,5,3',5'-tetraiodothyronine (often abbreviated as T4), a form of thyroid hormons is the major hormone secreted by the follicular cells of the thyroid gland.
27. Thyroxine is synthesized via the iodination and covalent bonding of the phenyl portions of tyrosine residues found in an initial peptide, thyroglobulin, which is secreted into thyroid granules.
28. These iodinated diphenyl compounds are cleaved from their peptide backbone upon being stimulated by thyroid-stimulating hormone.
29. More in the T3 and T4 section of thyroid.THYROXINE StructuralFormulae
30.
31. T4 is involved in controlling the rate of metabolic processes in the body and influencing physical development.
32.
33. T4 is converted in the tissues by deiodinases, including thyroid hormone iodine peroxidase (TPO), to T3.
34. The "D" isomer is called "Dextrothyroxine"and is used as a lipid modifying agent.The half-life of thyroxine once released into the blood circulatory system is about 1 week.
35. The hormone was synthesised in 1927 by British chemists Charles Robert Harington and George Barger.GEORGE BARGER
36.
37. It affects almost every physiological process in the body, including growth and development, metabolism, body temperature, and heart rate.Production of T3 T3 is metabolically active hormone that is produced from T4. T4 is deiodinated by two deiodinase enzymes to produce the more-active triiodothyronine:1. Type I present within the liver and accounts for 80% of the deiodination of T42. Type II present within the pituitary gland. T4 is synthesised in the thyroid gland follicular cells as follows. 1. The Na+/I-symporter transports two sodium ions across the basement membrane of the follicular cells along with an iodine ion. This is a secondary active transporter that utilises the concentration gradient of Na+ to move I- against its concentration gradient.2. I- is moved across the apical membranae into the colloid of the follicle.
38. 3. Thyroperoxidaseoxidises two I- to form I2. Iodide is non-reactive, and only the more reactive iodine is required for the next step.4. The thyroperoxidase iodinates the tyrosyl residues of the thyroglobulin within the colloid. The thyroglobulin was synthesised in the ER of the follicular cell and secreted into the colloid.5. Thyroid-stimulating hormone (TSH) released from the pituitary gland binds the TSH receptor ( a Gs protein-coupled receptor) on the basolateral membrane of the cell and stimulates the endocytosis of the colloid. IUPAC name (2S)-2-amino-3- [4-(4-hydroxy-3-iodo-phenoxy)- 3,5-diiodo-phenyl]propanoic acid 6. The endocytosed vesicles fuse with the lysosomes of the follicular cell. The lysosomal enzymes cleave the T4 from the iodinated thyroglobulin.7. These vesicles are then exocytosed, releasing the thyroid hormones. In the follicular lumen, tyrosine residues become iodinated. This reaction requires hydrogen peroxide. Iodine bonds carbon 3 or carbon 5 of tyrosine residues of thyroglobulin in a process called organification of iodine. The iodination of specific tyrosines yields monoiodotyrosine (MIT) and diiodotyrosine (DIT). One MIT and one DIT are enzymatically coupled to form T3. The enzyme is thyroid peroxidase.
39.
40. T3 (and T4) are very lipophilic and able to pass through the phospholipidbilayers of target cells.
41. The lipophilicity of T3 (and T4) requires their binding to the protein carrier thyroid-binding protein (TBG) for transport in the blood.
42. The thyroid receptors bind to response elements in gene promoters, thus enabling them to activate or inhibit transcription.
43. The sensitivity of a tissue to T3 is modulated through the thyroid receptors.Effects of T3 T3 increases the basal metabolic rate and, thus, increases the body's oxygen and energy consumption. The basal metabolic rate is the minimal caloric requirement needed to sustain life in a resting individual. T3 acts on the majority of tissues within the body, with a few exceptions including the spleen and testis. It increases the production of the Na+/K+ -ATPase and, in general, increases the turnover of different endogenous macromolecules by increasing their synthesis and degradation. ProteinT3 stimulates the production of RNA Polymerase I and II and, therefore, increases the rate of protein synthesis. It also increases the rate of protein degradation, and, in excess, the rate of protein degradation exceeds the rate of protein synthesis. In such situations, the body may go into negative ion balance.
44. GlucoseT3 potentiates the effects of the β-adrenergic receptors on the metabolism of glucose. Therefore, it increases the rate of glycogen breakdown and glucose synthesis in gluconeogenesis. It also potentiates the effects of insulin, which have opposing effects. LipidsT3 stimulates the breakdown of cholesterol and increases the number of LDL receptors, therefore increasing the rate of lipolysis. T3 also affects the cardiovascular system. It increases the cardiac output by increasing the heart rate and force of contraction. This results in increased systolic blood pressure and decreased diastolic blood pressure. The latter two effects act to produce the typical bounding pulse seen in hyperthyroidism. T3 also has profound effect upon the developing embryo and infants. It affects the lungs and influences the postnatal growth of the central nervous system. It stimulates the production of myelin, neurotransmitters, and axon growth. It is also important in the linear growth of bones. NeurotransmittersT3 may increase serotonin in the brain, particularly in the cerebral cortex, and down-regulate 5HT-2 receptors, based on studies in which T3 reversed learned helplessness in rats and physiological studies of the rat brain
45.
46. It acts to reduce blood calcium (Ca2+), opposing the effects of parathyroid hormone (PTH).It has been found in fish, reptiles, birds, and mammals.
47. Its importance in humans has not been as well established as its importance in other animals, as its function is usually not significant in the regulation of normal calcium homeostasisNMR solution structure of salmon calcitonin in SDS micelles Biosynthesis Calcitonin is formed by the proteolytic cleavage of a larger prepropeptide, which is the product of the CALC1 gene (CALCA). The CALC1 gene belongs to a superfamily of related protein hormone precursors including islet amyloid precursor protein, calcitonin gene-relate peptide, and the precursor of adrenomedullin
65. Hypothyroidism is a deficiency of thyroid hormone in humans and other vertebrates.
66. It can be due to an abnormality in the thyroid gland, or less commonly, the pituitary gland or hypothalamus.
67. It can result from a lack of a thyroid gland due to iodine-131, used to treat thyroid cancer and hyperthyroidism, its surgical removal, or its absence at birth.
68. Cretinism is a form of hypothyroidism found in infants.CHILD SUFFERING FROM HYPOTHYROIDISM Signs and symptoms In adults, hypothyroidism is associated with the following symptoms:
88. Factors such as iodine deficiency or exposure to iodine-131 from nuclear fallout, which is absorbed by the thyroid gland like regular iodide and destroys its cells, can increase that risk. There are a number of causes for hypothyroidism.
91. The first phase is typically hyperthyroidism; the thyroid then 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 life-long treatment.
94. Both synthetic and animal-derived thyroid tablets are available and can be prescribed for patients in need of additional thyroid hormone.
95. Thyroid hormone is taken daily, and doctors can monitor blood levels to help assure proper dosing. There are several different treatment protocols in thyroid replacement therapy:
96. T4 only This treatment involves supplementation of levothyroxine alone, in a synthetic form. It is currently the standard treatment in mainstream medicine.
97. T4 and T3 in combination-This treatment protocol involves administering both synthetic L-T4 and L-T3 simultaneously in combination.Desiccated thyroid extract Desiccated thyroid extract is an animal based thyroid extract, most commonly from a porcine source.
98.
99. It is thought that many cells responsible for forming connective tissue react to increases in TSH levels.
101. Thus, in addition to the inflammation within the thyroid any cell that expresses the TSH receptor will likely experience lymphocytic infiltrates as well.
102. The inflammation can cause tissue damage and scar tissue formation explaining the deposition of glycosaminoglycans.
107. Symptoms of Hashimoto's thyroiditis include weight gain, depression, mania, sensitivity to heat and cold , paresthesia, fatigue, panic attacks, bradycardia, tachycardia, high cholesterol, reactive hypoglycemia, constipation, migraines, muscle weakness, cramps, memory loss, infertility and hair loss.
108.
109. A tablet taken once a day generally keeps the thyroid hormone levels normal.
110. In most cases, the treatment needs to be taken for the rest of the patient's life. In the event that hypothyroidism is caused by Hashimoto's Thyroiditis, it is recommended that the TSH levels be kept under 3.0.
111.
112. Graves' disease is an autoimmune disease where the thyroid is overactive, producing an excessive amount of thyroid hormones (a serious metabolic imbalance known as hyperthyroidism and thyrotoxicosis).
113. This is caused by autoantibodies to the TSH-receptor (TSHR-Ab) that activate that TSH-receptor (TSHR), thereby stimulating thyroid hormone synthesis and secretion, and thyroid growth (causing a diffusely enlarged goiter).
114. The resulting state of hyperthyroidism can cause a dramatic constellation of neuropsychological and physical signs and symptoms, which can severely compromise the patients’ ability to maintain jobs and relationshipsLADY SUFFERING FROM GRAVE’S DISEASE
121. In severe cases, the optic nerve may be compressed and acuity of vision impaired.
122. Occasionally loss of vision.Treatment It is yet unknown how to interrupt the autoimmune processes of Graves' disease, which means treatment has to be indirect. The link that is targeted is the thyroid gland, via three different methods (which have not changed fundamentally since the introduction of antithyroid drugs and radioactive iodine in the 1940s). These are the use of antithyroid drugs (which reduce the production of thyroid hormone), partial or complete destruction of the thyroid gland by ingestion of radioactive iodine (radioiodine) and partial or complete surgical removal of the thyroid gland (thyroidectomy)
125. The inner part (medulla) of the adrenal glands secretes hormones, such as adrenaline (epinephrine), that help control blood pressure, heart rate, sweating, and other activities also regulated by the sympathetic nervous system.
126. The outer part (cortex) secretes different hormones, including corticosteroids (cortisone-like hormones, such as cortisol) and mineralocorticoids (particularly aldosterone, which controls blood pressure and the levels of salt and potassium in the body).
127.
128. The hypothalamus, a small area of the brain involved in hormonal regulation, produces corticotropin-releasing hormone and antidiuretic hormone.
129. These two hormones trigger the pituitary gland to secrete corticotropin (also known as adrenocorticotropic hormone or ACTH), which stimulates the adrenal glands to produce corticosteroids.
134. Situated along the perimeter of the adrenal gland, the adrenal cortex mediates the stress response through the production of mineralocorticoids and glucocorticoids, including aldosterone and cortisol respectively.
135. It is also a secondary site of androgen synthesis.Layers of cortex.
136. Layers Notably, the reticularis in all animals is not always easily distinguishable and dedicated to androgen synthesis. In rodents, for instance, the reticularis also generates corticosteroids (specifically corticosterone, not cortisol). The two layers are collectively referred to as the fasciculo-reticularis. Female rodents also exhibit another cortical layer called the "X zone" whose function is not yet clear.
137.
138. Progesterone -> (hydroxylation at C21) -> 11-Deoxycorticosterone -> (two further hydroxylations at C11 and C18) -> Aldosterone
143. The primary mineralocorticoid is aldosterone. Its secretion is regulated by the oligopeptideangiotensin II (angiotensin II is regulated by angiotensin I, which in turn is regulated by renin).
144. Aldosterone is secreted in response to high extracellular potassium levels, low extracellular sodium levels, and low fluid levels and blood volume.
148. It increases water retention and blood volume.Mode of action The effects of mineralocorticoids are mediated by slow genomic mechanisms through nuclear receptors as well as by fast nongenomic mechanisms through membrane-associated receptors and signaling cascades.
149.
150. The opposite mechanism is called transrepression. The hormone receptor without ligand binding interacts with heat shock proteins and prevents the transcription of targeted genes.
164. Dissociation The ordinary glucocorticoids do not distinguish among transactivation and transrepression and influence both the "wanted" immune and "unwanted" genes regulating the metabolic and cardiovascular functions. Intensive research is aimed at discovering selectively acting glucocorticoids that will be able to repress only the immune system. Genetically modified mice which express a modified GR which is incapable of DNA binding are still responsive to the antiinflammatory effects of glucocorticoids while the stimulation of gluconeogenesis by glucocorticoids is blocked. This result strongly suggests that most of the desirable antiinflammatory effects are due to transrepression while the undesirable metabolic effects arise from transactivation, a hypothesis also underlying the development of selective glucocorticoid receptor agonists.
165.
166. Androgen, also called androgenic hormones or testoids, is the generic term for any natural or synthetic compound, usually a steroid hormone, that stimulates or controls the development and maintenance of male characteristics in vertebrates by binding to androgen receptors.
167. This includes the activity of the accessory male sex organs and development of male secondary sex characteristics.
173. Spermatogenesis During puberty, androgen, LH and FSH production increase and the sex cords hollow out, forming the seminiferous tubules, and the germ cells start to differentiate into sperm. Throughout adulthood, androgens and FSH cooperatively act on Sertoli cells in the testes to support sperm production. Exogenous androgen supplements can be used as a male contraceptive. Elevated androgen levels caused by use of androgen supplements can inhibit production of LH and block production of endogenous androgens by Leydig cells. Without the locally high levels of androgens in testes due to androgen production by Leydig cells, the seminiferous tubules can degenerate resulting in infertility. For this reason, many transdermal androgen patches are applied to the scrotum. Inhibition of fat deposition Males typically have less adipose tissue than females. Recent results indicate that androgens inhibit the ability of some fat cells to store lipids by blocking a signal transduction pathway that normally supports adipocyte function.Also, androgens, but not estrogens, increase beta adrenergic receptors while decreasing alpha adrenergic receptors- which results in increased levels of epinephrine/ norepinephrine due to lack of alpha-2 receptor negative feedback and decreased fat accumulation due to epinephrine/ norepinephrine then acting on lipolysis-inducing beta receptors.
174.
175.
176. It is located at the center of the gland, being surrounded by the adrenal cortex.
177. It is the inner most part of the adrenal gland, consisting of cells that secrete epinephrine, norepinephrine, and a small amount of dopamine in response to stimulation by sympathetic preganglionic neurons.Medulla labeled at bottom right.
178.
179. Composed mainly of hormone-producing chromaffin cells, the adrenal medulla is the principal site of the conversion of the amino acid tyrosine into the catecholamines adrenaline (epinephrine), noradrenaline (norepinephrine), and dopamine.
180. Because the ANS exerts direct control over the chromaffin cells the hormone release can occur rather quickly. In response to stressors such as exercise or imminent danger, medullary cells release catecholamines into the blood in a 17:3 ratio of adrenaline to noradrenaline.
184. It increases heart rate, contracts blood vessels, dilates air passages and participates in the fight-or-flight response of the sympathetic nervous system.Chemically, epinephrine is a catecholamine, a monoamine produced only by the adrenal glands from the amino acids phenylalanine and tyrosine.
185. The term adrenaline is derived from the Latin roots ad- and renes and literally means on the kidney, in reference to the adrenal gland's anatomic location on the kidney. (R)-(–)-L-Epinephrine or (R)-(–)-L-adrenaline Systematic (IUPAC) name (R)-4-(1-hydroxy-2-(methylamino)ethyl)benzene-1,2-diol
186.
187. These extracts, which he called "nadnerczyna", contained epinephrine and other catecholamines.Japanese chemist JokichiTakamine and his assistant Keizo Uenaka independently discovered adrenaline in 1900.
188.
189. Chemical synthesis Epinephrine may be synthesized by the reaction of catechol with chloroacety chloride, followed by the reaction with methylamine to give the ketone, which is reduced to the desired hydroxy compound. The racemic mixture may be separated using tartaric acid. Formula for the synthesis of adrenaline
190.
191. As a stress hormone, norepinephrine affects parts of the brain where attention and responding actions are controlled.
192. Along with epinephrine, norepinephrine also underlies the fight-or-flight response, directly increasing heart rate, triggering the release of glucose from energy stores, and increasing blood flow to skeletal muscle.
193. Norepinephrine can also suppress neuroinflammation when released diffusely in the brain from the locus ceruleus.IUPAC name 4-[(1R)-2-amino-1-hydroxyethyl]benzene-1,2-diol
194.
195. Norepinephrine is synthesized from dopamine by dopamine β-hydroxylase. It is released from the adrenal medulla into the blood as a hormone, and is also a neurotransmitter in the central nervous system and sympathetic nervous system where it is released from noradrenergic neurons. The actions of norepinephrine are carried out via the binding to adrenergic receptors.Origins Norepinephrine is released when a host of physiological changes are activated by a stressful event. In the brain, this is caused in part by activation of an area of the brain stem called the locus ceruleus. This nucleus is the origin of most norepinephrine pathways in the brain. Noradrenergic neurons project bilaterally (send signals to both sides of the brain) from the locus ceruleus along distinct pathways to many locations, including the cerebral cortex, limbic system, and the spinal cord, forming a neurotransmitter system. Norepinephrine is also released from postganglionic neurons of the sympathetic nervous system, to transmit the fight-or-flight response in each tissue respectively. The adrenal medulla can also be counted to such postganglionic nerve cells, although they release norepinephrine into the blood.
216. Surgery or radiation therapy may be needed to remove or destroy a pituitary tumor.
217. Tumors of the adrenal gland (usually adenomas) can often be removed surgically.
218. Both adrenal glands may have to be removed if these treatments are not effective or if no tumor is present.
219. People who have both adrenal glands removed, and many people who have part of their adrenal glands removed, must take corticosteroids for life.
220. Tumors outside the pituitary and adrenal glands that secrete excess hormones are usually surgically removed.
221.
222. In Addison's disease, the adrenal glands are underactive, resulting in a deficiency of adrenal hormones.
223. Addison's disease may be caused by an autoimmune reaction, cancer, an infection, or some other disease.
224. A person with Addison's disease feels weak, tired, and dizzy when standing up after sitting or lying down and may develop dark skin patches.
225. Doctors measure sodium and potassium in the blood and measure cortisol and corticotropin levels to make the diagnosis.
226. People are given corticosteroids and fluids.ADDISON’S DIESEASE - HYPERPIGMENTATION INVOLVING PALM OF THE HAND.
227.
228. In 70% of people with Addison's disease, the cause is not precisely known, but the adrenal glands are affected by an autoimmune reaction (see Autoimmune Disorders) in which the body's immune system attacks and destroys the adrenal cortex.
229. In the other 30%, the adrenal glands are destroyed by cancer, an infection such as tuberculosis, or another identifiable disease.
230.
231. These problems may develop gradually and insidiously. People with Addison's disease develop patches of dark skin.
232. The darkness may seem like tanning, but it appears on areas not even exposed to the sun. Even people with dark skin can develop excessive pigmentation, although the change may be harder to recognize.
233. Black freckles may develop over the forehead, face, and shoulders, and a bluish black discoloration may develop around the nipples, lips, mouth, rectum, scrotum, or vagina.Most people lose weight, become dehydrated, have no appetite, and develop muscle aches, nausea, vomiting, and diarrhea. Many become unable to tolerate cold. Unless the disease is severe, symptoms tend to become apparent only during times of stress.
234.
235. If Addison's disease is not treated, severe abdominal pains, profound weakness, extremely low blood pressure, kidney failure, and shock may occur (adrenal crisis).
236.
237. Usually, treatment can be started with hydrocortisone or prednisone (a synthetic corticosteroid) taken by mouth.
238. However, people who are severely ill may be given cortisolintravenously or intramuscularly at first and then hydrocortisone tablets.
239. Because the body normally produces most cortisol in the morning, replacement hydrocortisone should also be taken in divided doses, with the largest dose in the morning. Hydrocortisone will need to be taken every day for the rest of the person's life.
240. Larger doses of hydrocortisone are needed when the body is stressed, especially from an illness, and may need to be given by injection if the person has severe diarrhea or vomiting.
241. Most people also need to take fludrocortisone tablets every day to help restore the body's normal excretion of sodium and potassium.
252. Other cells in the adrenal cortex produce testosterone and small amounts of estrogen, both necessary for sexual maturation in men and women, and aldosterone, a hormone involved in blood pressure regulation and water and electrolyte balance. Now about he disease…….here we discussed 2 diseases which were….cushing syndrome and addison’s syndrome. These 2 disease are caused due to the increased or the decreased level of adrenal gland…..
259. The tubules are lined with a layer of cells (germ cells) that from puberty into old age, develop into sperm cells (also known as spermatozoa or male gametes).
260. The developing sperm travel through the seminiferous tubules to the rete testis located in the mediastinum testis, to the efferent ducts, and then to the epididymis where newly-created sperm cells mature (see spermatogenesis).
261. The sperm move into the vas deferens, and are eventually expelled through the urethra and out of the urethral orifice through muscular contractions.Amphibians and most fish do not possess seminiferous tubules.
262. Instead, the sperm are produced in spherical structures called sperm ampullae. These are seasonal structures, releasing their contents during the breeding season, and then being resorbed by the body.
263.
264. Sertoli cells - the true epithelium of the seminiferous epithelium, critical for the support of germ cell development into spermatozoa. Sertoli cells secrete inhibin.
265. Between tubules (interstitial cells) Leydig cells - cells localized between seminiferous tubules that produce and secrete testosterone and other androgens important for sexual development and puberty, secondary sexual characteristics like facial hair, sexual behavior and libido, supporting spermatogenesis and erectile function. Testosterone also controls testicular volume.
270. Estrogen is responsible for the appearance of secondary sex characteristics of females at puberty and for the maturation and maintenance of the reproductive organs in their mature functional state.
271.
272. granulosa cells - surrounding follicular cells have change from flat to cuboidal and proliferated to produce a stratified epithelium
278. Dioscorea produces large amounts of a steroid called diosgenin, which can be converted into progesterone in the laboratory.Systematic (IUPAC) name pregn-4-ene-3,20-dione
279.
280. It increases core temperature (thermogenic function) during ovulation.
281. It reduces spasm and relaxes smooth muscle. Bronchi are widened and mucus regulated. (Progesterone receptors are widely present in submucosal tissue.)
282. It acts as an antiinflammatory agent and regulates the immune response.
284. It normalizes blood clotting and vascular tone, zinc and copper levels, cell oxygen levels, and use of fat stores for energy.
285. It may affect gum health, increasing risk of gingivitis (gum inflammation) and tooth decay.
286.
287.
288. The three major naturally occurring estrogens in women are estrone (E1), estradiol (E2), and estriol (E3). Estradiol (E2) is the predominant form in nonpregnant females, estrone is produced during menopause, and estriol is the primary estrogen of pregnancy. In the body these are all produced from androgens through actions of enzymes.
289. From menarche to menopause the primary estrogen is 17β-estradiol. In postmenopausal women more estrone is present than estradiol.
290. Estradiol is produced from testosterone and estrone from androstenedione by aromatase.
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