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Endocrine 1

Lou Clark REN Inglés 200 fichas

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  1. 1What are the properties of endocrine secretion (as compared to exocrine)?Hormonal mediators released directly into the blood (glands are ductless) that can target cells/tissue some distance away.
  2. 2What are the four types of intercellular messengers in the body?1. Endocrine
    2. Autocrine & paracine
    3. Neuroendocrine
    4. Neurotransmitter
  3. 3What are autocrine and paracrine messengers?Autocrine: substance that self-targets, bathing the cell within interstitial fluid
    Paracine: effects on neighbouring cell by movement through interstitial fluid
  4. 4Give an example of a hormone that can act as an autocrine?Prostaglandin
  5. 5Give an example of a hormone that can act as a paracrine?Somatostatin: released from Islet of Langerhans acts on neighbouring cells to secrete insulin
  6. 6What are neuroendocrine hormones?Hormone that is synthesised and released by a neuroendocrine cell into the circulation
  7. 7Give two examples of neuroendocrine hormones?1. Oxytocin
    2. Vasopressin (ADH)
  8. 8What are neurotransmitter messengers?Synthesised and released from a neurone acting on a neighbouring neurone via the synapse
  9. 9Give three examples of neurotransmitters?1. ACh
    2. NA
    3. A
    4. Glutamate
    etc etc
  10. 10What are the four types of hormone defined by what they are composed of?1. Peptide hormones
    2. Steroid hormones
    3. Hormones derived from tyrosine (simple hormones)
    4. Eicosanoids
  11. 11Name one simple and two complex peptide hormones?1. TRH (3 AA)
    2. LH and FSH (180 AA)
  12. 12What endocrine glands are peptide hormones released from?1. Hypothalamus
    2. Ant. & pos. pituitary
    3. Pancreas
    4. GIT
  13. 13What are steroid hormones derived from?Cholesterol
  14. 14Name three types of steroid hormones and where they are derived from?1. Cortisol = adrenal cortex
    2. Aldosterone = adrenal cortex
    3. Sex hormones = gonads
  15. 15What hormones are derived from tyrosine?1. Thyroid hormones
    2.Catecholamines = adrenal medulla
  16. 16Name an eicosanoid hormone?Prostaglandin
  17. 17During peptide hormone synthesis what is the mRNA translated to form, where does this occur?Preprohormone
    Occurs mainly of RER
  18. 18What is structure of the preprohormone?A very large molecule with a hydrophobic signal peptide that signals that the protein needs to be processed, packaged and exported.
  19. 19Where is the "pre-" (hydrophobic signal peptide) cleaved from the preprohormone? What can now occur?At RER.
    Protein can now undergo processing
  20. 20What processing alterations might the prohormone undergo?1. Protein folding
    2. Disulphide bonding
    3. Glycosylation
  21. 21Where does the final processing and packaging of the prohormone occur, what does this form?Golgi apparatus.
    Forms mature hormone which is stored in vesicles (secretory granules)
  22. 22To increase the circulating levels of a peptide hormone what would occur at the cells of the endocrine gland?Increased release of stored hormone via exocytosis
  23. 23Where does enzymatic conversion reactions of cholesterol to form steroid hormones occur within the cell?Generally in cytoplasm
  24. 24Why can't steroid hormone be stored?Highly lipophilic so readily crosses cell membrane via simple diffusion
  25. 25How are steroid hormones transported around the body?Often bound to plasma proteins (to improve solubility)
  26. 26To increase circulating levels of a steroid hormone what occurs at the cells of the endocrine gland?Increase in production of steroid hormone from cholesterol which is immediately released
  27. 27What is the half life of peptide hormones?Minutes
  28. 28What is the half life of steroid hormones?Hours/ days
  29. 29Why is half life of steroid hormones greater than that of peptide hormones.=?Proteases in the blood readily breakdown peptide hormones (free hormones). The plasma proteins that transport steroid hormones offer some protection from immediate degradation.
  30. 30Although steroid hormone is immediately released into the circulation upon synthesis the body still has a reservoir of hormone. How?Binding of plasma proteins delays both its metabolism and renders it biologically inactive, therefore acting as a circular reservoir
  31. 31Where are receptors for peptide hormones located?On plasma membrane of target cell
  32. 32What are two types of peptide hormone receptors?1. G-protein coupled receptor
    2. Tyrosine kinase linked receptor
  33. 33Give an example a peptide hormone and its G-coupled receptor?Glucagon (Gs receptor)
  34. 34Give an example of a hormone that binds to a tyrosine kinase linked receptor?Insulin
  35. 35What are the two types of receptors for steroid hormones normally located?1. Nuclear receptor
    2. Cytosolic receptor
    = intracellularly
  36. 36Where are the majority of hormones metabolised?Liver, kidney and/or blood.
    (small amount by target tissues)
  37. 37How are metabolites of hormones removed from circulation?Excreted in urine and/or faeces
  38. 38What are the two types of negative (or in theory positive) feedback?1. Simple
    2. Endocrine axis
  39. 39Give an example of a simple negative feedback system?Beta-cells secrete insulin promoting glucose uptake, which suppresses the activity of the beta-cells
  40. 40What are the feedback loops involved in the endocrine axis?Long loop: peripheral hormone regulates hypothalamus and pituitary
    Short loop: tropic hormone regulates hypothalamus
  41. 41What regulates cortisol release?Neuroendocrine reflex:
    input from higher centres activate the endocrine axis
  42. 42What hormone expresses circadian rhythm of release?Cortisol:
    high during beginning of day, lowest at night
  43. 43What are three possible mechanisms displayed due to endocrine disorders?1. Hypersecretion
    2. Hyposecretion
    3. Decreased target-cell responsiveness
  44. 44What are the two potential causes of hypersecretion of hormone?1. Tumour
    2. Immunological factor
  45. 45What are the potential causes of hyposecretion of a hormone?1. Genetic
    2. Immunological attack of gland
    3. Destruction by disease
    4. Surgical removal
  46. 46Describe primary and secondary endocrine disorders?Primary = dysfunction of peripheral endocrine gland
    Secondary = Dysfunction at the level of the hypothalamus, pituitary or an independent primary defect
  47. 47What test would you use if hormone insufficiency was suspected?Simulation test (would fail to stimulate hormone production)
  48. 48What test would you use if you suspected hypersecretion of a hormone? What would the results indicate?Suppression test
    Failure to suppress = autonomous secretion via tumour
  49. 49What are the alternative names for the anterior and posterior pituitary?Anterior: adenohypophysis
    Posterior: neurohypophysis
  50. 50What are the 3 parts of the anterior pituitary?1. Pars distalis
    2. Pars tuberalis
    3. Pars intermedia
  51. 51What are the 3 parts of the posterior pituitary?1. Pars nervosa
    2. Infundibular stem
    3. Median eminence
  52. 52What is the embryological origin of the anterior pituitary?Ectodermal upgrowth (Rathke's pouch) from roof of primitive mouth
  53. 53What is the embryological origin of the posterior pituitary?Neuroectodermal downgrowth of the brain
  54. 54What occurs if there is inappropriate detachment of the Rathke's pouch from the primitive mouth?Pharyngeal hypophysis (ectopic pituitary tissue within the sphenoid bone near to the roof of the mouth
  55. 55What arteries supplies the posterior pituitary? How is blood received to the anterior pituitary?Superior hypophyseal artery and inferior hypophyseal artery.
    Blood flows from superior hypophyseal artery to anterior lobe via portal vessels
  56. 56How is blood drained from the pituitary?Inferior hypophyseal veins drain both anterior and posterior pituitary
  57. 57What nuclei are associated with hormone release from the adenohypophysis?1. Arcuate nucleus
    2. Ventromedial nucleus
    3. Preoptic nucleus
  58. 58What is the mechanism for control of hormonal release from the adenohypophysis?Nuclei secrete releasing/inhibitory factors that enter the infundibulum plexus and pass along portal vessels to the anterior lobe. They then control the secretion of hormones into the capillary network of the anterior lobe.
  59. 59What nuclei are involved in hormonal secretion from the posterior pituitary?1. Paraventricular nucleus
    2. Supraoptic nucleus
  60. 60Describe the mechanism for control of hormonal secretion from the posterior pituitary.Nuclei send neural fibres via the hypophysial tract to the capillary network of the posterior lobe, they are neuroendocrine fibres that directly secrete hormone into the blood supply
  61. 61Which lobe of the pituitary would appear more vascularised in histology?Anterior lobe
  62. 62What oval nuclei are seen in a histological stain of the posterior pituitary?Pituicites: specialised form of glial cells
  63. 63What are Herring bodies?Terminal ends of axons of hypothalamus found in the posterior pituitary that are often seen as filled with neurosecreotry granules.
  64. 64What are the four broad categories of cells found in the anterior pituitary using histology?1. Acidophils
    2. Basophils
    3. Cells secreting glycoproteins
    4. Chromophobes
  65. 65What colour do 1. acidophils; 2. basophils and 3. chromophobes appear using histological staining?1. pink
    2. purple
    3. pale staining
  66. 66What percentage of secreting cells do each of the broad categories of cells of the anterior pituitary make up?Acidophils = 40%
    Basophils = 10%
    Cells secreting glycoproteins = 10%
    Chromophobes = 40%
  67. 67What are the two types of acidophils of the anterior pituitary? What do they secrete?1. Somatotrophs = GH
    2. Mammotrophs (lactotrophs) = Prolactin
  68. 68What are the two types of basophils found in the anterior pituitary? What do they secrete?1. Corticotrophs = ACTH
    2. Thyrotrophs = TSH
  69. 69What cells secrete glycoproteins in the anterior pituitary? What hormones do they secrete?Gonadotrophs = LH & FSH
  70. 70What are chromophobes likely to be (in anterior pituitary)?Immature secretory cells or secretory cells that have recently released all of their contents. Or cells that are waiting in reserve.
    Overall they have none or little secretory product present.
  71. 71What cells make up the majority of anterior pituitary tumours?Chromophobes (display low levels of granules and hormone)
  72. 72What features might be observed of a cell of the anterior pituitary using the electron microscope?1. Pale staining nucleus with prominent nucleoli (multiple)
    2. Storage + secretory granules
    3. Many mitochondria
    4. Many endoplasmic reticulum
  73. 73Are pituitary tumours often benign or invasive?Benign = adenomas
  74. 74What can be caused by a pituitary tumour exerting pressure of the optic chiasm?Bilateral hemianopia (tunnel vision)
  75. 75What is GH?Growth hormone
  76. 76What is ACTH?Adrenocorticotropic hormone
  77. 77What is TSH?Thyroid stimulating hormone
  78. 78What is growth hormone involved in?Growth and development of soft and skeletal tissue. Particularly linear growth.
    Has affects on metabolism
  79. 79What is the effect of prolactin?Simulates lactation of breasts, promotes growth and development of breasts.
  80. 80What is the effect of prolactin on FSH and LH?At high levels prolactin inhibits GnRH which prevents synthesis of LH and FSH (no menstrual cycle)
  81. 81What is the effect of ACTH?Stimulates synthesis and release of cortisol
  82. 82What is the effect of TSH?Stimulates synthesis and release of thyroid hormones
  83. 83What is the effect of LH?Stimulate steroid hormone synthesis from ovaries/ testes.
    Causes ovulation + formation of corpus luteum
  84. 84What is the effect of FSH?Stimulates follicular development and spermatogenesis
  85. 85What does "tropic" refer to?Affecting activity of endocrine glands
  86. 86What does "trophic" refer to?Promote growth or tissue integrity
  87. 87What is CRH? What is its effect?Corticotropin-releasing hormone.
    Stimulates released of ACTH
  88. 88What is GnRH? What is its effect?Gonadotropin-releasing hormone.
    Stimulates release of LH and FSH
  89. 89What is GHRH? What is its effect?Growth-hormone releasing hormone
    Stimulates release of GH
  90. 90What is TRH? What is its effect?Thyrotropin-releasing hormone
    Stimulates release of TSH
  91. 91What anterior pituitary hormone is under major inhibitory control? What inhibits its release?Prolactin.
    Under inhibition from dopamine form hypothalamus
  92. 92What hormone is involved in a slight stimulatory effect on prolactin release?TRH
  93. 93What is the role of somatostatin in the anterior pituitary?Inhibitory to GH and TSH.
  94. 94What does GH cause to be released in the liver?IGF-1 (insulin-like growth factor)
  95. 95What is involved in the long feedback loop of the endocrine axis?Peripheral hormone negatively regulates (inhibits) anterior pituitary and hypothalamus
  96. 96What is involved in the short feedback loop of the endocrine axis?Tropic hormone (from ant. pit.) negatively regulates (inhibits) hypothalamus
  97. 97What two hormones are secreted by the posterior pituitary?1. Vasopressin (AVP) (ADH)
    2. Oxytocin
  98. 98What stimulates the release of AVP?Increase in body fluid osmality (increase NA+), fall in blood volume/pressure.
    Stress.
  99. 99What us the action of AVP on V1 receptors?Activated at high levels of AVP, cause vasoconstriction to increase BP
  100. 100What is the action of AVP on V2 receptors?Increase permeability and reabsorption of water at distal CT and collecting ducts
  101. 101What is the effect of AVP on hormonal production from the anterior pituitary?Stimulates secretion of ACTH at times of stress (induce cortisol release)
  102. 102What stimulates oxytocin release?Suckling
    Cervical dilation during parturition
  103. 103What is the action of oxytocin?Uterine contraction of SM
    Stimulation of let-down reflex.
    Maternal behaviour/ sexual behaviour/ social bonding
  104. 104What might cause hyposecretion of the pituitary?Surgical damage.
    Genetic disease
    Tumours
  105. 105What causes hypersecretion of the pituitary?Tumours
  106. 106What is the most common cause of pituitary dysfunction?Pituitary adenomas (tumours)
  107. 107What defines a microadenoma or a macroadenoma?Micro-: <10mm
    Macro-: >10mm
  108. 108What effects can a pituitary tumour have on presenting symptoms?1. Hypersecretion of a pituitary hormone
    2. Hyposecretion of another pituitary hormone (tumour impacts on surrounding cells in pituitary)
    3. Local effects on anatomically-related structures
  109. 109What would a prolactinoma of the pituitary cause?Hyperprolactinaemia
  110. 110What would a GH-secreting tumour of the pituitary cause?Acromegaly, gigantism
  111. 111What would an ACTH-secreting tumour of the pituitary cause?Cushing's disease (hypersecretion of cortisol)
  112. 112What effects could a non-functioning pituitary tumour cause?1. Mechanical symtoms
    2. Hypopituitarism
  113. 113What might be the side effects of surgery or radiotherapy on a pituitary tumour?Hypopituitarism
    Damage to surrounding structures e.g. optic pathway
  114. 114What is the preferred treatment method for pituitary tumours?Trans-sphenoidal surgery (enter through sphenoidal air sinus)
  115. 115What are the symptoms of hyperprolactinaemia due to a prolactinoma?1. Loss of fertility/ libido (due to FSH, LH inhibition)
    2. Galactorrhoea
    3. Gynaecomastia (enlargement of male breast)
  116. 116What is the typical treatment of hyperprolactinaemia?Dopamine receptor agonist (inhibitory action), shrink tumour
  117. 117Why would damage to the pituitary stalk cause prolactinaemia?Pathway of pathway from hypothalamus is impaired therefore prolactin is not under inhibition from dopamine and levels rise
  118. 118What is the most common cause of acromegaly?GH secreting tumour
  119. 119What treatment options are used for a GH-secreting tumour?1. Surgery
    2. Radiotherapy
    3. Somatostatin analogue (inhibition)
    4. Bromocriptine (dopamine receptor agonist) - some GH adenomas acquire dopamine receptors
  120. 120What is pan-hypopituitarism?Deficiency of all pituitary tumours
  121. 121What could cause pan-hypopituitarism?1. Pituitary adenoma (compressing cells)
    2. Surgery
    3. Radiotherapy
    4. Damage to pituitary stalk
  122. 122What condition is associated with ADH deficiency?Diabetes insipidis
  123. 123What are the two thyroid hormones?1. Tri-iodothyronine (T3)
    2. Thyroxine (T4)
  124. 124What is produced from the parafollicular cells of the thyroid gland?Calcitonin
  125. 125How does the thyroid gland develop?Endodermal down growth from the floor of the pharynx (between anterior 2/3 and posterior 1/3 of tongue) via foramen caecum between 1st and 2nd pharyngeal arches.
  126. 126What can remnants of the thyroglossal duct form in adult life?Cysts, ectopic thyroid tissue (pyramidal lobe)
  127. 127What is the blood supply to the thyroid in the majority of people?Superior thyroid artery (from external carotid)
    Inferior thyroid artery (from thyrocervical trunk)
  128. 128What veins drain the thyroid gland?Superior thyroid vein (from internal jugular vein)
    Inferior thyroid vein (from brachiocephalic vein)
  129. 129What is the possible third arterial supply to the thyroid? Where can it originate from?Thyroidea ima
    Arch of aorta/ subclavian/ carotid artery
  130. 130Describe the cellular layout of the thyroid gland.Follicles: ring of cuboidal epithelium surrounding colloid.
    (Parafollicular cels are found outside follicles)
  131. 131Where is thyroid hormone stored?Colloid
  132. 132Describe parafollicular cells under a microscope.Large pale-staining cells with an eccentric nucleus and clear unstained cytoplasm.
  133. 133What might be seen histologically when looking at non-secreting inactive thyroid cells?Flattened cells with large amounts of colloid stored.
  134. 134What might be seen in hyperactive cells of thyroid gland?Little colloid stood, hyperactive columnar cells
  135. 135What do the parathyroid glands secrete? What is it involved in?Parathyroid hormone
    Increases Ca2+ in blood
  136. 136What is the effect of calcitonin?Decreases Ca2+ in blood
  137. 137What cells secrete parathyroid hormone?Chief cells
  138. 138What is the precursor to thyroid hormone?Tyrosine
  139. 139What makes up tri-iodothyronine (T3)?Mono-iodotyrosine + di-iodotyrosine
    MIT + DIT
  140. 140What makes up thyroxine (T4)?DIT + DIT
  141. 141Where does iodination occur to form MIT?3' of ring
  142. 142Where does iodination occur to form DIT?3' & 5' of ring
  143. 143In what proportions are T3 and T4 produced from the thyroid gland?T4 = 90-95%
    T3 = 5-10%
  144. 144What does DIT + MIT form?reverse tri-iodothyronine rT3
  145. 145What thyroid hormone is considered biologically inactive?rT3 (can bind to T3 receptor = antagonist)
  146. 146How do people tend to gain a supply of iodide?From water intake
  147. 147How is iodide brought into the follicular cell?Active transport of iodide via an ATP-driven Na+-iodide symporter.
  148. 148How is iodide moved across the apical membrane of the follicular cell?Pendrin transporter
  149. 149What process must iodide undergo before it can combine with tyrosine? What allows this to occur?Oxidation to form IODINE.
    TPO catalyses this oxidation.
  150. 150What is TPO? Where is it found?Thyroid peroxidase
    An intergral membrane protein in the apical membrane of follicular cells
  151. 151What reactions does TPO catalyse?1. Oxidation of iodide
    2. Iodination of tyrosine
    3. Coupling of iodotryosines
  152. 152What large structure is tyrosine stored as?Thyroglobulin (130-140 T per Tg)
  153. 153How does thyroglobulin enter the colloid to be stored?Exocytosis via excretory vesicles
  154. 154What does iodine bind to in the colloid, what does it form? What is the name given to this process?Iodination of tyrosine molecules on thyroglobulin (MIT and DIT within thyroglobulin).
    ORGANIFICATION
  155. 155What process immediately follows organification of tyrosine molecules?Coupling of iodotryosines (MIT + DIT etc) to form T3 and T4 within iodinated thyroglobulin
  156. 156Where is iodinated thyroglobulin stored?In colloid
  157. 157What occurs when T3 and T4 need to be released into the circulation?Iodinated thyroglobulin is taken up from colloid by endocytosis. It fuses with lysosomal proteases, which releases T3 and T4, which then enter the blood
  158. 158SO what processes are catalyses by thyroid peroxidase?1. Oxidation of iodide
    2. Iodination of tyrosines
    3. Coupling of iodotryosines
  159. 159At which steps of thyroid hormone production and release does TSH have a stimulatory effect?EVERY STEP:
    1. Na+-I symporter
    2. Pendrin transporter
    3. Exocytosis of thyroglobulin
    4. Iodination of tyrosine molecules
    5 Coupling of iodotyrosines
    6. Endocytosis of iodinated thyroglobulin
    7. Lysis of thyroglobulin
    8. Release T3 & T4
  160. 160Which regulatory hormone is involved more in day-to-day control of thyroid hormone levels? Which is involved more in long-range adjustments?Day-to-day: TSH
    Long-range: TRH
  161. 161What is TRH again?Thyrotropin releasing hormone
  162. 162What effects does TSH have on the thyroid gland?Increases size and number of thyroid follicular cells.
    Stimulates release of thyroid hormones
  163. 163Describe the effect of a cold environment on thyroid function in a neonate?Neuroendocrine reflex: cold stimulates high centres of the brain which stimulate TRH = increase TSH = increases T3/T4.
    Increased metabolism and heat production
  164. 164What is the effect of stress (e.g. trauma) on thyroid function?Neuro-endorcine reflex: stress activates higher brains centres causing a release of somatostatin and also directly inhibits TRH. Somatostatin inhibits release TSH = decrease T3/4.
    Conserves energy to produce ATP to deal with the stress situation
  165. 165What three plasma proteins are involved in transport of thyroid hormones in the circulation? What proportion do they transport?1. Thyroxine-binding globulin = 70%
    2. Transthyretin = 10%
    3. Albumin = 20%
  166. 166What % of thyroid hormones are bound to plasma proteins?99%
  167. 167Which thyroid hormone is used as the principle active hormone? Why?T3
    T3 is 4-5 times more potent than T4
  168. 168What catalyses the conversion of T4 to T3 at the target cell (and a small amount to rT3)?Deiodinase enzymes D1 & D2
  169. 169What are the three main actions of thyroid hormones?1. Increase metabolism
    2. Stimulate growth and repair
    3. Synergistic effect on SNS / catecholamine actions
  170. 170What metabolic activity do thyroid hormones stimulate?Increase metabolism of CHOs, proteins, fats.
    Increased O2 consumption
    Increased heat production
    Increased BMR
  171. 171What region is thyroid hormone particularly important in promoting growth and development?CNS
  172. 172How does thyroid hormone act to synergistically effect SNS and catecholamine actions?Increase expression of beta-adrenoceptors (especially in CVS)
  173. 173What effect does T3 have on mitochondria?Binds directly to receptors on mitochondria causing a rapid increase in their metabolic activity
  174. 174Where are the majority of thyroid hormone receptors located in target cells? What does their activation lead to?Nuclear receptors:
    Act as hormone-regulated transcription factors altering gene expression causing protein expression and biological effects
  175. 175What can affect deiodinase activity? What is the often the outcome?Disease (kidney, liver), acute stress (surgery, illness), drugs, diet low in calories (starvation).
    Causes an increase in the conversion of T4 to rT3 = antagonist of T3 receptor decreasing metabolic rate.
  176. 176What is a goitre?Non-specific term for an enlargement of the thyroid gland?
  177. 177What are the two types of goitre? What can cause them?Diffuse: over-stimulation of gland due to TSH or TSI
    Nodular: thyroid tumour
  178. 178What is the most common cause (90%) of primary hypothyroidism?Hashimoto's thyroiditis
  179. 179What would cause secondary hypothyroidism?Failure of hypothalamus or anterior pituitary (causing low TSH/TRH)
  180. 180What is the most common GLOBAL cause of hypothyroidism?Lack of dietary iodine (not common in west)
  181. 181List the possible causes of hypothyroidism?1. Primary failure of thyroid
    2. Secondary failure of hypo. or ant. pit.
    3. Lack of dietary iodine
    4. Drug-induced
    5. Radioactive iodine therapy
    6. Surgery
    7. Thyroid hormone resistance
  182. 182What is Hashimoto's thyroiditis?Chronic autoimmune disease against thyroglobulin and other components of the thyroid gland e.g. TPO.
  183. 183What are the symptoms of hypothyroidism?General decrease in BMR and metabolism:
    weight gain
    myxodena (puffy)
    dry and thickened skin
    hoarse voice, slow speech
    cold intolerance
    menstrual changes
    constipation
    lowered HR / BP
    depression, confusion, poor memory
  184. 184What does hypothyroidism cause in children?Cretinism (dwarfism and mental retardation)
  185. 185Describe the plasma levels of relevant hormones under primary hypothyroidism (eg. Hashimoto's thyroiditis).Decreased T3/T4
    Increased TSH
  186. 186Is a goitre present in Hashimoto's thyroiditis?Yes = elevated TSH causes proliferation of thyroid
  187. 187Describe the plasma level of relevant hormones under secondary hypothyroidism?Decreased T3/T4
    Decreased TSH
  188. 188Is there a goitre present with secondary hypothyroidism?No
    = lack of TSH (may see atrophy of gland)
  189. 189Describe the plasma levels of relevant hormones under iodine deficiency related hypothyroidism.Decreased T3/ T4
    Increased TSH
  190. 190Is there a goitre present in iodine-deficiency related hypothyroidism?Yes
    TSH levels are high
  191. 191What tests could be performed to test for Hashimoto's thyroiditis?Test for thyroid antibodies
    e.g. anti-microsomal for TPO
    anti-thyroglobulin for Tg
    (10-15% of patients don't have the antibodies)
  192. 192What treatment is given for hypothyroidism?Synthetic thyroid hormone:
    Levothyroxine (T4)
    Liothyronine (T3)
  193. 193What is the drug of choice for treating hypothyroidism? Why?Levothyroxine (T4)
    Easy to manage doses, where as liothyronine (T3) is far more potent and needs careful monitoring of dose
  194. 194What is the most common cause of hyperthyroidism?Graves' disease
  195. 195What would cause secondary hyperthyroidism?Excess hypothalamic and/or anterior pituitary secretions (increased TRH / TSH)
  196. 196What are the possible causes of hyperthyroidism?1. Graves'
    2. Secondary hyperthyroidism
    3. Hyper-secreting thyroid tumour (primary)
    4. Iatrogenic (drugs)
  197. 197What is Graves' disease?Autoimmune disease whereby thyroid stimulating immunoglobulins (TSI) activate TSH receptors in the thyroid causing excess production of T3/T4.
  198. 198What are the common symptoms associated with hyperthyroidism?1. Weight loss
    2. Sweating
    3. Heat intolerance
    4. Diarrhoea
    5. Palpitations (HR and BP)
    6. Tremor
    7. Anxiety, emotional, irritable, restlessness
  199. 199What symptom is unique to Graves' disease? What causes it?Exophthalmos = bilateral protrusion of the eyeball due to glycoproteins deposits by infiltrating lymphocytes on the back of the eye.
  200. 200Describe the plasma level of relevant hormones under Graves' disease.High T3/T4
    Low TSH (due to -ve feedback)

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REN Fichas sobre Endocrine 1, creado por Lou Clark el 20/01/2017.
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