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Endocrine system


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Endocrine system

  1. 1. Under the guidance of: Dr. Sandeep Tandon Professor and Head of Dept. of Pedodontics Dr. Ambika Singh Rathore Dr. Rinku Mathur1 Dr .Shantanu Jain Dr. Tripti Sharma Ra
  2. 2. CONTENT: Introduction Evolution of Endocrine system Chemical characteristics of Hormones Regulation of Hormone Release Hypothalamus & its Hormone Various glands and their importance Disorders of Endocrine system common in Children References 2
  3. 3. INTRODUCTION: Constant internal environment (i.e., homeostasis) should be maintained. Two systems help ensure communication: NERVOUS HORMONAL SYSTEM NeuroendocrineRapid transmission Long-lasting regulatory action Both systems interact: Stimuli from the nervous system can influence the release of certain hormones and vice versa. 3
  4. 4. EVOLUTION OF ENDOCRINE SYSTEM The nervous system coordinates rapid and precise responses to stimuli using action potentials. The endocrine system maintains homeostasis and long- term control using chemical signals. The most primitive endocrine systems seem to be those of the neurosecretory type, in which the nervous system either secretes neurohormones directly into the circulation or stores them in neurohemal organs (neurons whose endings directly contact blood vessels, allowing neurohormones to be secreted into the circulation), from which they are released in large amounts as needed. True endocrine glands probably evolved later in the evolutionary history of the animal kingdom as 4 separate, hormone-secreting structures.
  5. 5. CONVERGENT EVOLUTION:Similarities among the endocrine systems of crustaceans, arthropods, and vertebrates.The vertebrate endocrine system consistsof glands (pituitary, thyroid, adrenal), anddiffuse cell groups scattered in epithelial tissues.Endocrine glands arise during development for all three embryologic tissue layers (endoderm, mesoderm, ectoderm). The type of endocrine product is determined by which tissue layer a gland originated in. Glands of ectodermal and endodermal origin: peptide and amine hormones; Mesodermal-origin glands: hormones based on lipids. 5
  6. 6. WHAT ARE HORMONES????? ( “TO SPUR ON”) Hormones are molecules that are produced by endocrine glands:i. The hypothalamus,ii. Pituitary gland,iii. Adrenal glands,iv. Gonads, (i.e., testes and ovaries),v. Thyroid gland,vi. Parathyroid glands, and 6vii. Pancreas
  7. 7.  The term “endocrine” implies that in response to specific stimuli, the products of those glands are released into the bloodstream. The hormones then are carried via the blood to their target cells. The target cells for each hormone are characterized by the presence of docking molecules (i.e., receptors) for the hormone that are located either on the cell surface or inside the cell. The interaction between the hormone and its receptor triggers a cascade of biochemical reactions in the target cell that eventually modify 7 the cell’s function or activity.
  8. 8. CHEMICAL CHARACTERISTICS OF HORMONES Amines (from tyrosine) I. hydroxylation - catecholamines II. iodination - thyroid hormones Peptides/proteins Steroids (from cholesterol) I. adrenocorticoids II. sex hormones III. active metabolites of vitamin D Their mechanisms of action (e.g., whether they can enter their target cells and how they 8 modulate the activity of those cells) also differ.
  9. 9. MECHANISM OF ACTION:STEROIDS: produced by gonads; structure similar to cholesterol.Enter their target cells and interact with the cytoplasm or in the cell nucleusHormone-receptor complexes bind to certainregions of the cell’s genetic material (i.e., theDNA)Regulating the activity of specific hormone- 9 responsive genes
  11. 11.  Amino acid derivatives:are modified versions of building blocks of proteins. thyroid gland & adrenal glands (i.e., the adrenal medulla) Enter the cell, where they interact with receptor proteins that are already associated with specific DNA regions. The interaction modifies the activity of the affected genes. Polypeptide and protein hormones:found primarily in the hypothalamus, pituitary gland, and pancreas Because of their chemical structure, the polypeptide and protein hormones cannot enter cells. Instead, they interact with receptors on the cell surface. 11
  12. 12. REGULATION OF HORMONE RELEASE Constant feedback from the target glands to the hypothalamus and pituitary gland ensures that the activity of the hormone system involved remains within appropriate boundaries.To maintain the body’s homeostasis Negative feedback mechanism Short-loop feedback Positive-feedback mechanisms 12
  13. 13. Negative Feedback Loop 13
  14. 14. Positive Feedback Loop 14
  15. 15. THE HYPOTHALAMUS AND ITS HORMONES Why is the Hypothalamus so Important? Eating and drinking, Sexual functions and behaviors, Blood pressure and heart rate, Body temperature maintenance, The sleep-wake cycle, and Emotional states (e.g., fear, pain, anger, and pleasure) 15
  16. 16. Neurosecretory cells 16
  18. 18. hypothalamic nucleisuperiorhypophysealartery superficial capillary plexustrabecular artery deeplong portal veins capillary plexus inferior 18 hypophyseal artery
  19. 19. hypothalamic nucleisuperiorhypophysealartery superficial capillary plexustrabecular artery deeplong portal veins capillary plexus short portal veins inferior 19 hypophyseal artery
  20. 20. hypothalamic nucleisuperiorhypophysealartery superficial capillary plexustrabecular artery deeplong portal veins capillary plexus short portal veinsadeno-secondaryhypophysealcapillaryplexuscapillaryplexus inferior 20 hypophyseal artery
  21. 21. hypothalamic nucleisuperiorhypophysealartery superficial capillary plexustrabecular artery deeplong portal veins capillary plexus short portal veinsadeno-hypophysealcapillaryplexus inferior 21 hypophysealhypophyseal vein artery
  22. 22. HYPOTHALAMIC HORMONES RELEASING INHIBITING Corticotrophin (CRH) Somatostanin ACTH Gonadotropin (GnRH) Dopamine LH & FSH Thyrotropin (TRH) TSH Growth-Hormone (GHRH) GH 22
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  25. 25. INTERMEDIATE LOBE There is also an intermediate lobe in many animals, but is rudimentary in humans. For instance, in fish, it is believed to control physiological color change. In adult humans, it is just a thin layer of cells between the anterior and posterior pituitary. The intermediate lobe produces melanocyte- stimulating hormone (MSH), although this function is often (imprecisely) attributed to the 25 anterior pituitary.
  26. 26. GROWTH HORMONE Most abundant of the pituitary hormones Pivotal role in controlling the body’s growth and development.1. Stimulates the linear growth of the bones;2. Promotes the growth of internal organs, fat (i.e., adipose) tissue, connective tissue, endocrine glands, and muscle; and3. Controls the development of the reproductive organs.4. GH affects carbohydrate, protein, and fat (i.e., lipid) metabolism. GH levels in the blood are highest during early 26 childhood and puberty and decline thereafter.
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  29. 29.  Two hypothalamic hormones control GH release: (1) GHRH: stimulates GH release, (2) Somatostatin: inhibits GH release.Short-loop feedback component:GH acts on the hypothalamus to stimulate somatostatin release.In addition, GH release is enhanced by Stress, such as low blood sugar levels (i.e., hypoglycemia) or severe exercise, and by the onset of deep sleep. Acute and chronic alcohol consumption have been shown to reduce the levels of GH and IGF-1 in the blood. 29
  30. 30. PROLACTIN. Central role in the development of the female breast and in the initiation and maintenance of lactation after childbirth. Factors control Prolactin release:1. Response to the rise in estrogen levels in the blood that occurs during pregnancy.2. In nursing women, Prolactin is released in response to suckling by the infant.3. Dopamine, which has an inhibitory effect.4. Alcohol consumption by nursing women can influence lactation both through its effects on the release of prolactin and oxytocin. 30
  32. 32. VASOPRESSIN Vasopressin (arginine vasopressin, AVP; anti- diuretic hormone, ADH) is a peptide hormone formed in the hypothalamus, then transported via axons to, and released from, the posterior pituitary. Two principles site of action: KIDNEY & BLOOD VESSEL 32
  33. 33. MECHANISMS REGULATING THE RELEASE OF AVP Hypovolemia: decreased central venous pressure, the decreased firing of atrial stretch receptors leads to an increase in AVP release. Hypotension, which decreases arterial baroreceptor firing and leads to enhanced sympathetic activity, increases AVP release. Angiotensin II receptors located in a region of the hypothalamus regulate AVP release – an increase in angiotensin II simulates AVP release. Increased sympathetic activation stimulates AVP release 33
  34. 34. OXYTOCIN HORMONEI. Stimulates the contractions of the uterus during childbirth.I. In nursing women, the hormone activates milk ejection in response to suckling by the infant(i.e., the so-called let-down reflex). 34
  36. 36.  Action of Cortisol:1. Cortisol increases glucose levels in the blood by stimulating gluconeogenesis in the liver and promotes the formation of glycogen in the liver.2. Reduces glucose uptake into muscle and adipose tissue,3. Promotes protein and lipid breakdown into products (i.e., amino acids and glycerol, respectively) that can be used for gluconeogenesis.4. Protect the body against the deleterious effects of various stress factors.5. Suppress tissue inflammation in response to injuries and to reduce the immune response to foreign molecules. 36
  37. 37. ACTION OF ALDOSTERONE: Regulate the body’s water and electrolyte balance. Conserve sodium and to excrete potassium from the body. Reducing water excretion and increasing blood volume. Decreases the ratio of sodium to potassium concentrations in sweat and saliva, thereby preventing sodium loss via those routes. Controlled primarily by another hormone system, the reninangiotensin system, which also controls kidney function. 37
  41. 41. ACTION OF THYROID HORMONE Stimulates the production of certain proteins involved in heat generation in the body, a function that is essential for maintaining body temperature in cold climates. Promotes other metabolic processes involving carbohydrates, proteins, and lipids that help generate the energy required for the body’s functions. Plays an essential role in the development of the central nervous system during late fetal and early postnatal developmental stages. Required for the normal development of teeth, skin, and hair follicles as well as for the functioning of the nervous, cardiovascular, and 41 gastrointestinal systems
  42. 42.  Parafollicular C cells) in the thyroid gland produce calcitonin, a hormone that helps maintain normal calcium levels in the blood. Specifically, calcitonin lowers calcium levels in the blood by reducing the release of calcium from the bones; inhibiting the constant erosion of bones (i.e., bone resorption), which also releases calcium; and inhibiting the reabsorption of calcium in the kidneys. 42
  44. 44. ROLE OF PARATHYROID HORMONE Increases calcium levels in the blood, helping to maintain bone quality and an adequate supply of calcium. Causes re-absorption of calcium from and excretion of phosphate in the urine. Promotes the release of stored calcium from the bones as well as bone resorption. PTH stimulates the absorption of calcium from the food in the gastrointestinal tract.Functions facilitated by a substance called 1,25-dihydroxycholecalciferol, a derivative of vitamin D. 44
  48. 48. INSULIN & GLUCAGON Beta cells of Islet Alpha cells of IsletBlood sugar-lowering Increases blood glucose levels hormone Actions opposite to insulinEffect of Insulin:1. Inhibits gluco-neogenesis2. Insulin promotes the formation of storage forms of energy (e.g., glycogen, proteins, and lipids) and suppresses the breakdown of those stored nutrients. 48
  50. 50. THE GONADS AND THEIR HORMONESOVARIES AND TESTESThey produce the germ cells.Synthesize steroid sex hormones that are necessary for the development and function of both female and male reproductive organs and secondary sex characteristics.Affect the metabolism of carbohydrates and lipids, the cardiovascular system, and bone growth and development. 50
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  52. 52. DIABETES Type 1 diabetes is growing by 5% per year among pre-school children in India. It is estimated that 70,000 children, who are under 15 years, develop juvenile type 1 diabetes each year (almost 200 children a day!).“Symptoms of Diabetes in Children: Stomach pains, Headaches Behaviour problems Weight loss, thirst, tiredness and frequent urination. Detected through the presence of ketoacidosis 52
  53. 53. CAUSES: Type I (Juvenile Diabetes): body’s inability to produce insulin Genetic factors; environmental factors Increased Type 2 Diabetes: linked overwhelmingly to lifestyle changes that have contributed to increased weight problems and lack of activity in children. 53
  54. 54. TREATMENT: INSULIN: The advent of insulin pumps for administration has allowed many children added flexibility in their daily lives. Monitoring blood sugar levels Crucial factor Diet: reduced consumption of fats and sugars, intake fibers, vegetables and fruits. Exercise: helps in lowering blood glucose levels of the body 54
  55. 55. COMPLICATIONS Sudden hypoglycemia & hyperglycemiaImmediately giving the child a glucose tablet or glucose beverageLONG-TERM COMPLICATIONS Problems of the kidney, heart, lungs, eyes, feet and nerves. High blood sugar or high cholesterol levels 55
  56. 56. GIGANTISM Gigantism refers to abnormally high linear growth due to excessive action of insulin-like growth factor-I (IGF-I) while the epiphyseal growth plates are open during childhood. Acromegaly is the same disorder of IGF-I excess when it occurs after the growth plate cartilage fuses in adulthood. Robert Wadlow, called the Alton giant, who stood 8 feet 11 inches tall at the time of his death in his mid-20s 56
  57. 57. CAUSES Causes of excess IGF-I action may be divided into 3 categories: Those originating from primary GH excess released from the pituitary; Those caused by increased GH-releasing hormone (GHRH) secretion or hypothalamic dysregulation; and Hypothetically, those related to the excessive production of IGF-binding protein, which prolongs the half-life of circulating IGF-I. 57
  58. 58.  Most people with giantism have GH-secreting pituitary adenomas or hyperplasia.TREATMENT Medical Carei. Surgery clearly fails to cure a notable number of patients with IGF-I excessii. Long-acting somatostatin analogs and dopamine agonists improve adherence and efficacy.iii. Octreotide are the most effective medical therapies for GH excess. Bromocriptine are best used as adjuvant treatments. 58
  59. 59. PITUITARY DWARFISM The achondroplastic dwarf has an orthopedic reason for having short limbs and a short spinal colum. The pituitary dwarf lacks growth hormone (an endocrine reason). SYMPTOMS: GH Deficiency Low blood sugar 59
  60. 60. RISK FACTORS: Disease of the hypothalamus of the brain Disease of the front of the pituitary gland in the brain Newborns who had some type of serious medical event (such as a lack of oxygen) happen in the perinatal period, are at risk for the type of growth hormone deficiency caused by damage to the hypothalamus.TREATMENT:Treatment with human growth hormone theoretically corrects the deficiency, but is most successful when the child is young. It must be given by injection. 60
  61. 61. PRECOCIOUS PUBERTY Precocious puberty describes puberty occurring at an unusually early age.CAUSES:Central: damage to the inhibitory system of the brain hypothalamic hamartoma produces pulsatile gonadotropin-releasing hormone (GnRH) Langerhans cell histiocytosis 61
  62. 62. PERIPHERAL CAUSES Secondary sexual development induced by sex steroids from other abnormal sources is referred to as peripheral precocious puberty.Causes can include: Endogenous sources  gonadal tumors (such as arrhenoblastoma)  adrenal tumors  germ cell tumor  congenital adrenal hyperplasia  McCune–Albright syndrome Exogenous hormones  Environmental 62  As treatment for another condition
  63. 63. TREATMENT GnRH agonists stimulate the pituitary to release Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH). One possible treatment is with anastrozole. Histrelin acetate. 63
  64. 64. PEDIATRIC CUSHING’S SYNDROME(CS) Rare in childhood and adolescence. Caused by prolonged exposure to excessive glucocorticoids which can be secreted endogenously or administered exogenously. Supra-physiological doses of exogenous gluco- corticoids in the form of topical, inhaled or oral corticosteroids. Eczema and asthma are common conditions in childhood often requiring treatment with corticosteroids. 64
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  66. 66. 66
  67. 67. TREATMENT Primary adrenal lesionsSurgical excision is the first-line therapy for a cortical-secreting ACT.Mitotane therapy appears to be the treatment of choice Cushing’s diseaseMedical therapies such as Metyrapone and Ketoconazole to lower serum cortisol levels can be used as a short-term measure, but cannot be recommended as long-term therapy. 67
  68. 68. THYROID DISORDERS Thyroid disease occurs less frequently in children than in adults, the signs and symptoms can be similar.Congenital hypothyroidism Affects infants at birth, and occurs in about 1 in 4000 live-born babies. Loss of thyroid function, due to the thyroid gland failing to develop normally. Enzyme defect leading to deficient hormone production, iodine deficiency and a brain pituitary gland abnormality. 68
  69. 69.  Within the first week of life, a heelprick blood sample is taken to assess an infants thyroid hormone level. Infant is immediately given thyroid hormone replacement therapy (T4 — thyroxine). Normal growth and development should then continue, with no adverse effects on the childs mental capacity.Subtle symptoms: Severe:1. Poor feeding Poor growth and development2. Constipation Dry skin & hair3. Low body temperature Slow tendon reflex4. Slow pulse Enlarged tongue5. Prolonged jaundice, Umbilical hernia6. Increased sleepiness Puffiness & swelling7. Decreased crying. 69
  70. 70. HYPERTHYROIDISM IN NEWBORNS Overactive thyroid gland: referred to as NEONATAL HYPERTHYROIDISM.If the mother has Graves disease, the thyroid- stimulating antibodies in her blood can cross the placenta and stimulate the unborn childs thyroid gland, thus producing too much thyroid hormone. Some newborns may hardly be affected if the levels of antibodies are low. No treatment may be necessary as the mothers antibodies will soon clear from the babys bloodstream, usually within 2 to 3 months. 70
  71. 71. NEWBORNS WITH ADVANCED HYPERTHYROIDISM • EXTREMELY FAST PULSE IRRITABILITY FLUSHED MOIST SKIN • INFANT TENDS TO BE THIN & LONGTREATMENTAnti-thyroid drugs is safe and effective, and will only be needed for a short period of time, until the stimulating antibodies pass from the babys bloodstream.If the mother is on a high dose of anti-thyroid medication, the diagnosis can be delayed by about a week until the infant clears the anti-thyroid medication. 71
  72. 72. HASHIMOTOS THYROIDITIS The most common cause of hypothyroidism in children and adolescents is Hashimotos thyroiditis, an autoimmune disease. As the thyroid gland becomes increasingly underactive, physical and mental changes will become more obvious. Symptoms of hypothyroidism develop very slowly 72
  73. 73. SIGNS AND SYMPTOMS The first sign is that the childs growth rate decreases unexpectedly and skeletal development is delayed. Decreased GOITRE Energy Lethargy Dry Itchy Skin WEIGHT & GAIN Constipation Poor 73 Concentration
  74. 74. TREATMENT Thyroid hormone replacement is taken daily for life. The dosage of thyroid hormone needs to be age- appropriate, as the bodys demands for thyroid hormone vary with age.SIDE-EFFECTS:In children who have had long-standing hypothyroidism, ultimate height potential may be partly lost. As the child regains normal thyroid function, behavioural problems may arise as their 74 physical and mental processes speed up
  75. 75. GRAVES DISEASE The most common cause of hyperthyroidism in children and adolescents is an autoimmune condition called Graves disease. In Graves disease the body produces antibodies that stimulate the thyroid gland uncontrollably, to make too much thyroid hormone. 75
  76. 76. SIGNS AND SYMPTOMS Increased Energy, hyperactive, restless, Easily distracted Enlarged Thyroid Gland, fast pulse, nervousness, heat intolerance, weight loss Accelerated growth rate, Shaky hands Muscle weakness, diarrhoea, and Sleep & behavioural disturbances. 76
  77. 77. TREATMENT Propylthiouracil (PTU) or Carbimazole. Period of block and replace therapy (anti-thyroid drugs as well as thyroxine) is useful. Throughout a childs treatment, thyroid hormone levels will need to be monitored regularly, along with their clinical symptoms. SIDE EFFECTS Anti-thyroid drugs can, however, occasionally stop the production of white blood cells or platelets. Sore throats, mouth ulcers, excessive bruising or skin rashes can indicate this. 77 The only safe action is to stop the medication until after the result of the blood test.
  78. 78. REFERENCES: Susanne Hiller-Sturmhöfel and Andrzej Bartke. The Endocrine Syste An Overview. Alcohol Health & Research World; Vol. 22(3):1998; 153-64 Ashley B. Grossman, Martin O. Savage.Pediatric Cushing’s Syndrome: Clinical Features, Diagnosis, and Treatment. Arq Bras Endocrinol Metab 2007;51/8:1261-1271) Kim E. Barrett, Susan M. Barman. Ganong’s Review of Medical Physiology;Vol.23:451-568 Arthur C. Guyton. Textbook of Medical Physiology 10th edi;993- 1019 K. Sembulingham. Essentials Of Medical Physiology;3rd edi;667-714 78
  79. 79. Presented by: Dr. Ruby Kharkwal1st year postgraduate studentDepartment of Pedodontics 79