Adrenal and Thyroid Glands

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iloveyoux143
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Adrenal and Thyroid Glands
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2015-11-03 18:30:30
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Endocrinology
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Exam of 11/4/2015
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  1. What makes up the adrenal gland?
    • the cortex and medulla
    • each make different hormones, yet there is an influence of one over the other
  2. Embryological development of adrenal gland
    • cortex: typical epithelial tissue- glandular
    • medulla: derived from neuroectoderm- neural tissue, near sympathetic ganglia
  3. Control of the medulla
    it is under direct nervous control
  4. Development of adrenal gland- birth
    by the time of birth, the cortex envelopes the medulla but the medulla receives sympathetic NS impulses (stress- fight/flight) and is also influenced by endocrine system.
  5. Communication between medulla and cortex
    there is a portal blood system- direct blood from the cortex to the medulla + the hydrocortisone from the cortex stimulates epinepherine synthesis in the medulla from norepinepherine by inducing the PNMT enzyme
  6. Hormones of the adrenal cortex
    • all steroid hormones- made from cholesterol
    • main hormones are hydrocortisone and aldosterone
    • also a small amount of sex steroids
    • hormones are made in specific zones of the cortex
  7. Zones of the adrenal cortex from outermost to innermost
    • outermost: Zona glomerulosa- makes mineralocorticoids (aldosterone)
    • middle: Zona fasciculata- makes glucocorticoids (hydrocortisone)
    • innermost: Zona reticularis- makes adrenal androgens (male sex steroids)- mainly dehydroepiandosterone (androstenedione and testosterone) and small amount of estrogen
  8. which hormones are catecholemines?
    • dopamine
    • epinepherine
    • norepinepherine
  9. steps of molecules in epinepherine synthesis
    • 1. Phenylalanine
    • 2. Tyrosine
    • 3. Dopa
    • 4. Dopamine
    • 5. Norepinephrine
    • 6. Epinephrine
  10. synthesis of epinepherine (conversion steps)
    • 1. start with phenylalanine which gets converted to tyrosine by phenylalanine hydroxylase
    • 2. Tyrosine is converted to Dopa by tyrosine hydroxylase which is stimulated by the sympathetic NS
    • 3. Dopa is converted to dopamine by aecarboxylation by L-aromatic amino acid decarboxylase 
    • 4. Dopamine (the parent catecholamine) is converted to norepinepherine by dopamine beta hydroxylase
    • 5. Norepinepherine is converted to epinepherine by phenylethanolamine N-Methyltransferase (PNMT enzyme- enduced by hydrocortisone from cortex that travels via portal blood)
  11. PNMT
    • An enzyme induced by hydrocortisone from the adrenal cortex in adult mammals
    • travels to medulla via portal blood to convert norepi to epi
  12. What happens after norepi and epi are made?
    • they are metabolized by 2 enzymes: monoamine oxidase and catecholo-methylatransferase
    • metabolization occurs mostly in the liver/kidney
  13. what are the waste products after norepi and epi are metabolized
    • vanillymandelic acid and metaneephrine
    • these are excreted into the urine
  14. what is the rate limiting step in the synthesis of epi and norepi?
    • the conversion of tyrosine to dopa by tyrosine hydroxylase
    • Tyrosine hydroxylase is an enzyme stimulated by the symp NS
  15. How do hormones of the adrenal cortex travel through the blood
    • as steroids they travel attached to protein to keep them soluble
    • for metabolism in liver and excretion in urine they are converted to a salt form
  16. different effects of adrenal hormones
    • hormonal effects: physiological effect (the typical concentration)
    • pharmacological effect: high dosage from drugs or made by body
    • the effects of the two may differ
  17. Glucocorticoids of the adrenal cortex
    • affect glucose by have many other functions
    • main one is hydrocortisone
  18. hydrocortisone
    • a hyperglycemic hormone (like Growth hormone)
    • acts in the liver to convert amino acids to glucose
    • different from other hyperglycemic hormones bc it stimulates glycogen synthesis but it stimulates gluconeogenisis much more
  19. functions of hydrocortisone
    • stimulates gluconeogenesis
    • helps body cope w/ stress
    • stimulates glycogen synthesis
    • affects fat and protein metabolism
    • stimulates PNMT
    • anti-inflammatory function
    • stimulates RBC synthesis
    • affects other corticol hormone (weak)
    • anti-vitamin D affect
    • affects mood
    • increases appetite
    • permissively affects adrenal medulla hormones
    • increases kidney filtration 
    • embryological development
    • negative feedback
  20. hydrocortisone in gluconeogenesis
    • primary function
    • increases blood glucose
  21. hydrocortisone in stress
    helps the body cope with it and helps return the body to homeostasis after a fight/flight response
  22. hydrocortisone in glycogen synthesis
    although it increases blood glucose it also stimulates glycogen synthesis in the liver and muscle
  23. glycogen
    • polysaccharide of glucose
    • a storage molecule
  24. hydrocortisone in fat metabolism
    • affects fat metabolism-varies with the area of the body
    • its primarily lypolitic (mobilizes fats) in appendages and primarlily promotes fat deposit in axial areas (head and torso)
  25. hydrocortisone in protein metabolism
    • its primarily catabolic- decreases protein synthesis and increases protein breakdown, except in the liver where it stimulates synthesis of gluconeogenesis and enzymes (which are proteins)
    • gets protein, breaks it down into amino acids and mobilizes them for conversion to glucose in gluconeogenesis in the liver
  26. hydrocortisone in stimulation of PNMT
    travels via portal blood to adrenal medulla to stimulate this to convert norepi to epi
  27. hydrocortisone in anti-inflammatory functions
    • suppresses the immune system defenses- this is coping with stress to prevent body from going overboard
    • useful theraputically (shot, cream, etc)
    • delays, slows wound healing
    • anti-lymphotic effect- decreases number and function of lymphocytes (important WBC in immune system), decreases antibody formation by lymphocytes and decreases antigen-antibody rxns
    • maintains membrane integrity of lysosomes
    • inhibits enzymes of the inflammatory response
  28. hydrocortisone in stimulation of RBC synthesis
    does this by stimulating synthesis and secretion of erythropoetin in the kidney
  29. hydrocortisone in the effect on other corticol hormones
    has a weak effect on aldosterone, stimulating Na+ reabsorption into the blood from kidney tubules
  30. hydrocortisone in the anti-vitamin D effect
    affects Ca 2+ reabsorption from food
  31. hydrocortisone in affecting mood
    • gives a positive sense of well being
    • if there is a high amount you can get positive or negative mood- depression or euphoria.
  32. hydrocortisone in appetite
    increases appetite (ie exogenous, store prednisone)
  33. hydrocortisone in effects on adrenal medulla hormones
    has a permissive effect on the ability of adrenal medulla hormones to increase blood pressure- done through maintaining the blood vessel muscle tone.
  34. hydrocortisone in affect on kidney filtration
    increases filtration rate of the kidney in making urine
  35. hydrocortisone in embryological development
    • stimulates maturation of the lungs
    • if unusually high level, it can decrease growth b/c it stimulates protein breakdown
  36. hydrocortisone in negative feedback
    • neg feedback on hypothalamus and pituitary- homeostasis in blood but also a daily rhythm
    • highest amounts in the AM before breakfast- lower later in the day- purpose is to keep up blood glucose level
    • follows pattern of ACTH which follows ACTH releasing hormone
    • more can be stimulated under certain circumstances (ie blood sugar lvl too low or stress)
    • if hemmorrage, it can keep up the blood pressure
  37. Feed back regulation of hydrocortisone
    • the hypothalamus makes corticotroph releasing hormone which travels via portal blood to the anterior pituitary gland. This stimulates the corticotrophs to make ACTH which is released from the ant pit into the blood and travels to the adrenal gland. It stimulates the adrenal cortex to make Hydrocortisone
    • when hydrocortisone levels get too high it causes neg feedback on hypo to shut off releasing hormone and on the ant pit to shut off ACTH (long loop)
    • when ACTH gets too high it can cause neg feedback on hyp to shut off releasing hormone (short loop)
  38. Disorders of the adrenal cortex
    • cushings syndrome
    • congenital adrenal hyperplasia
    • addisons disease
  39. Cushing's syndrome
    hydrocortisone usually seen from exogenous production (hydrocortisone high from HC drug administration)
  40. congenital adrenal hyperplasia
    • genetic condition aka adrenal genital syndrome
    • person lacks the enzyme in the adrenal cortex to make hydorcortisone (not vital for life)
    • adrenal cortex keeps being stimulated by high levels of ACTH (no neg feedback) causing growth of cortex and the pathway to T gets amplified (more T)
    • person is XX- looks and has masculin characteristics but has female reproductive strucutres
    • there will be sexual ambiguity
    • if happens in a male there will be early puberty
  41. Addison's disease
    • opposite of cushings- adrenal cortex failure w/ low hydrocortisone
    • there can also be low aldosterone
    • could be due to infection, a tumor or some sort of congenital or auto immune condition
    • low aldosterone functioning, so decreased Na+ reabsorption into the blood and low H2o reabsorption- these go into the urine causing dehydration and low blood volume and pressure (potentially fatal)
  42. symptoms of Addison's Disease
    • hypoglycemia- low blood sugar
    • weak and fatigued feeling
    • large inflammatory problems (ie arthritis)
    • depression, apathy
    • in extreme cases a person may not be able to handle or survive stress
    • anemia- low RBC synthesis
    • hyperpigmentation- if low HC high ACTH to bind to MSH receptors
  43. Mineralocorticoids of the adrenal cortex
    aldosterone- vital for life
  44. functions of aldosterone
    • stimulates sodium reabsorption
    • stimulates potassium and Hydrogen ion excretion
    • increases blood volume and pressure
    • important in acid base balance
    • stimulates increase in sodium in blood from different sources
    • vasoconstrictor in times of hemmorhage
  45. aldosterone function in sodium reabsorption
    • main function
    • stimulates sodium reabsorption in the kidneys from fluid in the tubules (distal convoluted tubule and collecting duct) into the blood- increasing blood Na+ and decreasing urine Na+
  46. aldosterone function in relation to K+ and H+
    stimulates excretion of potassium and hydrogen ions in the urine
  47. Aldosterone function in blood volume and pressure
    • b/c it causes na+ retention in the body, when na+ builds up in the blood, Cl- will be attracted into the blood from the tubular fluid (so less Cl- in the urine)
    • the buildup of NaCl in the blood will attract H2O by osmosis in to the blood from tubular fluid
    • so you retain Na, Cl and h2o in blood increasing blood volume and pressure
    • important for na+, fluid and BP homeostasis
  48. Aldosterone function in acid base balance
    if excess H+ in blood, aldosterone will stimulate excretion of H+ ions and will reabsorb Na+, replacing acid with salt
  49. What sources do aldosterone stimulate Na+ reabsorption from?
    • GI tract
    • Food
    • Salivary Glands
    • Sweat Glands
  50. Aldosterone in times of hemmorhage
    it acts as a vasoconstrictor in times of hermmorhage to prevent blood loss and increase blood pressure (just like antidiuretic hormone can do)
  51. Atrial Natriuritic Peptide
    • has the opposite function of aldosterone
    • made in atria of heart
    • when increased bp is sensed in heart, this ANP will be released into the blood and will stimulate the kidneys to excrete sodium into the urine (natriuresis)
    • the Na+ excretion will be followed by Cl- and H2O excretion so your losing fluid from the blood, decreasing the blood volume and pressure
    • ANP also important in homeostasis of BP
  52. Conn's Syndrome
    • Hypersecretion (high) aldosterone
    • usuallly this is from a tumor
    • high blood pressure from high Na+, Cl- and H2O retention in the blood
    • high depletion of potassium from blood into urine, causing cardiac arrhythmia (affects heart- irregular heart beats)
    • high depletion of H+ ions from blood making it too basic (alkalosis)
  53. Treatment of Conn's Syndrome
    • Blood pressure medicine to decrease bp and potassium supplements
    • adrenalecotmy- remove adrenal glands followed by hormone replacement
  54. Renin-Angiotensin-Aldosterone System
    • to affect the adrenal cortex, we first affect a kidney hormone, renin, which affects angiotensin
    • helps maintain homeostasis of blood pressure
  55. Stimulus for Renin-Angiotensin-Aldosterone System
    • low blood volume and low blood pressure
    • this is sensed in the juxtaglomerular apparatus of the kidney (baroreceptors sense low blood pressure in blood vessles)
    • blood flows through nephrons and main stimuls is bp- when it drops baroreceptors around glomerulus start initial response
    • also if decreased Na+ or increased K+ sensed in mecula densa which is located at begining of the distal convoluted tubules
  56. Process of renin angiotensin aldosterone system
    • low bp, volume or blood na+ (or high k+) is sensed in juxtaglomerular aparatus, by baroreceptors in bvs or macula densa and the kidney secretes renin into the blood
    • the liver secretes angiotensin (a substrate for renin) which is in inactive plasma protein (normally secreted into the blood by the liver- its already in the blood)
    • renin, an enzyme, converts angiotensin (inactive) into angiotensin I (still inactive) by lopping off some amino acids
    • Angiotensin converting enzyme (ACE), an enzyme that is already in the blood (made by the lungs) usually doesn't do anything unless angiotensin I is present. When Angiotenisn I (decapeptide) is formed from angiotensine, ACE converts it to Angiotensin II (active octapeptide)
    • Angiotensin II's main function is stimulating the desmolase reaction in the adrenal cortex zona glomerulosa cells to cause aldosterone to be made and released
    • The zona glomerulosa cells make and release aldosterone after stimulation from angiotensin II which stimulates Na+ reabsorption followed by Cl and water in the kidney which restores blood volume and pressure to normal
    • the other minor function of angiotensin II is vasoconstriction to directly stimulate Na+ reabsorption from distal convoluted tubules to help bring up blodo pressure
  57. What happens after Na+ Cl- is increased in the blood after renin-angiotensin system
    • also increased antidiuretic hormone which increases H20 reabsorption (bc high na and cl affect osmolarity of blood)
    • and increased thirst which increases bodily h2O
    • these also help restore bp and blood volume
  58. Renin
    • made by kidney
    • enzyme that converts angiotensin (normally in blood, a plasma protein made by liver) to angiotensin I (still inactive) by lopping off some amino acids
    • synthesis of renin stimulated by low blood pressure and volume sensed in juxtaglomerular apparatus or baroreceptors in blood vessels
  59. Angiotensin
    • plasma protien made by liver that exists in the blood
    • inactive
  60. Angiotensin I
    • a decapeptide
    • inactive
    • converted to angiotensin II by ACE
  61. ACE
    • enzyme made by lungs
    • naturally exists in blood but does nothing unless there is angiotensin I present
    • converts angiotensin I (inactive) to angiotensin II (active) by lopping off more amino acids
  62. Angiotensin II
    • an octapeptide, active
    • primary functions in stimulate zona glomerulosa cells of adrenal cortex to undergo desmolase reaction (synthesizing aldosterone)
    • also acts as a vasoconstrictor to directly stimulate na reabsorption from distal convoluted tubules helping to bring up bp
  63. When is aldosterone a vasoconstrictor
    • only if youre significantly bleeding
    • angiotensin II however normally is
  64. When are renin and aldosterone made
    • only secreted when you need them, not made automatically
    • once homeostasis is reached, no more hormone is made bc no longer needed
  65. Adrenal Medulla
    secretes epineperine (80%) and norepinepherine (20%) (important as a NT for sympathetic NS for stress, but here it is secreted into the blood as a hormone).
  66. Epinepherine and Norepinephrine- characteristics (shared)
    • water soluble
    • packaged into vessicles by adrenal medulla cells
    • travel freely in the blood but have an extremely short half life (they are metabolized in less than 3 mins)
    • have a short duration of action (theyre slower than NS but faster than other hormones)
  67. mechanism of action for epi and norep
    they have G-protein receptors on the membrane (but different adrenergic receptors)
  68. Effects of Epinepherine
    • hyperglycemic
    • fight or flight response
    • has other metabolic effects
    • cardiovascular effects
    • respiratory effects
    • decreased function in organs
    • affects brain
  69. effects of epinephrine- hyperglycemic
    • increases blood glucose (sugar needs to be available in stress) by glyconeogenesis- especially in liver, also in muscle
    • if there is low blood glucose, it is sensed by hypothalamic cells and hyp will send impulses downt he spinal cord to the symp splancnic nerve which will stimulate the adrenal medulla to secrete epinepherine
    • some effect on gluconeogenesis but mostly glycogen breakdown
  70. Effects of epinepherine- fight or flight
    • key in this response
    • gets the most out of the body in stress
  71. Effects of epinephrine- other metabolic effects
    lipolysis and stimulation of oxygen consumption and energy production- especially in muscle- gets the most out of a muscle in a stress situation
  72. Effects of epinephrine- cardiovascular effects
    • overall epi increases cardiac output- gets the most out of the heart
    • there is both an increase in contraction force and an increase in heart rate
    • its a vasodilator- widens blood vessels (vs norepi which is a vasoconstrictor)
    • increased cardiac output and vasodilation= increased blood flow to organs, esp muscle
    • increases the systolic pressure, not diastolic (diastolic is affected by blood vessels themselves which are widened) (norepi affects both)
  73. blood pressure
    • normal 120/80
    • top#: systolic pressure when heart contracts
    • bottom#: diastolic pressure when heart is relaxed
  74. Effects of epinephrine- Respiratory effects
    dilates bronchial passageways to increase O2 influx into the body
  75. Effects of epinephrine- decreased function in some organs
    (ie digestive) that are not critical for stress
  76. Effects of epinephrine- effects on brain
    body is more alert, aware and anxious in stress due to a heightened reticular activating system
  77. Norepinepherine functions
    • not important in metabolic effects
    • more significant as a NT in the symp NS than as a hormone but it is a hormone and both are involved in stress
    • major effects on cardiovascular system
    • affects mood and brain
  78. norepi effects on cardiovascular system
    a pressor effect- increases bp bc it stimulates cardiac output but is a vasoconstrictor
  79. norepi effects on mood and brain
    more aroused, alert and sometimes more aggressive due to it
  80. Differences between epi and norepi is due to what?
    • different adrenergic receptors
    • alpha1, alpha2, beta1, beta2 and beta3- all cause diff effects on the target cells
    • epinepherine effects beta2 receptors (more than norepi) which causes bronchodilation, vasodilation and metabolic effects in liver
    • epi and norepi effect beta3 receptors (invovled in cardiac functions) equally
    • epi and norepi somewhat equal on alpha 1 and alpha2 involved in blood pressure, vasoconstriction (more norepi), sweating, pupi dilation
    • (sometimes one more than the other effects a specific receptor)
  81. Medical application of epinephrine
    • giving epi and affecting receptors are the 2 medical applications
    • epi pen
    • beta blockers
  82. epi pen
    • in severe allergies there is anapheliectic shock 
    • heart can stop, respiratory passages close up
    • epinepherine counteracts these effects
    • can also be given just if heart stops
  83. beta blockers
    • given for high blood pressure
    • prevent high heart contraction and rate
  84. Disorders of the Adrenal Medulla
    Pheochromocytoma
  85. chromaffin cells
    make catecholamines in adrenal medulla
  86. Pheochromocytoma
    • usually from a tumor
    • there is an increase in more nor epi but also more epi
  87. symptoms of pheochromocytoma
    • high blood pressure
    • short term panic attacks (caused by norepi and epi)
    • heart palpatations/chest pain
    • headaches
    • sweating
    • pale skin (from constricted bvs)
    • a stress (like surgery) can cause even higher bp
  88. treatment for pheochromocytoma
    • 1st you need to control blood pressure bc surgery will cause even higher bp
    • control receptor by receptor agaonist (beta blocker) then remove tumor in surgery
  89. High blood pressure medicine
    • can affect renin-angiotensin-aldosterone system
    • if its a type of diuretic: increases water excretion so decreased fluid in blood so decreasd blood vol and pressure
    • ACE inhibitors: in inhibitor that inhibits the enzyme that allows angiotensin II to be made- no angiotensin to stimulate production of aldosterone or to stimulate vasoconstriction- decreases nacl + h2o reabsorption and they are excreted instead lowering blood vol and pressure
  90. How do hormones from the adrenal gland influence blood pressure
    • many do
    • can do this by acting at the heart (ex- epi and nor epi), changing blood vessel constriction or changing blood volume
  91. Salt and water balance
    there are 3 natriuritic peptides- they all function to decrease blood pressure when it gets too high
  92. 3 natriuritic peptides, and what is their stimulus
    • atrial natriuritic peptide: found in heart
    • brain natriuritic peptide: found in brain + heart
    • C-type natriuritic peptide: found in brain and lining of blood vessels
    • stimulus is stretch due to increased blood volume and pressure and response is to excrete na+ which is followed by cl- and water causing lower blood vol and pressure
    • all are vasodilators- if you widen the bvs gives more room lowering bp (Secondary function)
  93. Two main types of cells of the Thyroid gland
    • follicle cells
    • parafollicle cells
  94. Follicle cells
    • make thyroid hormone
    • there is a single layer of epithelial cells
    • larger when active, flat when inactive
    • stimulated by TSH and become large and active
    • colloid in center- stores thyroid hormone as a protein (thyroid globulin)
  95. Parafollicle cells
    • in betweein follicle cells
    • make calcitonin
  96. Thyroid hormone
    has 2 types: T3 and T4
  97. T4
    • Thyroxine-tetraiodothyronine 
    • 4 iodines in it
  98. T3
    • tri-iodothyronine 
    • 3 iodines
  99. Relationship between t4 and t3
    T3 is several times more active than T4 but more t4 is made but it gets converted to T3 after its released from the thyroid or when it enters the target cell
  100. Synthesis of Thyroid hormone (T3 and T4)
    • made from iodine and the amino acid tyrosine
    • iodine is trapped by the thyroid gland- you already have it there and more gets taken up (taken up against the conentration gradient); iodine also taken up from food very easily
    • synthesis occurs inside thyroid globulin (the storage protein or colloid) inside the follicle
    • in that molecule there are about 134 tyrosines in it and about 25-30 of them go to form the hromone- these ones become iodinated
    • thyroglobulin is phagocotyzed (engulfed) by follicle cells
  101. Phagocytosis of thyroglobulin in synthesis and release of thyroid hormone
    • once it is in the cells, theres proteolysis by proteases in lysososmes (breaking apart of the peptide chain) and diodonasis to remove some iodine
    • and from that thyroglobulin you end up with a mixture of free iodine, free tyrosine, T3 and T4 
    • any free iodine and tyrosine that are released can be reused to form DIT and MIT
  102. What happens when T3 and T4 are released into the blood?
    • most are bound to protein for solubility (even tho theyre made from amino acids they arent freely soluble)
    • and bc their very small so being bound to protein protects these hormones from metabolism and excretion
  103. Protein carriers of T3 and T4
    • mainone- thyronine binding protein
    • also albumin and prealbumin
    • t3 and t4 are released from these proteins to be able to be taken up by these target cells
  104. Regulation of the thyroid gland
    • TSH from anterior pituitary is the main regulator of the thyroid (it is water soluble)
    • it works by a cyclic AMP mechanism
    • increases TH synthesis
    • increases uptake of iodine by thryoid cells
    • increases all aspects of synthesis
    • stimulates increase in phagocytosis of thyroglobulin and discharge of t3 and t4 into the blood
    • increases growth and vascularity of the thyroid gland
  105. How is Thyroid hormone
    overall metabolized by the liver and kidney
  106. Feedback and regulation and homeostasis of thyroid hormone
    • The hypothalamus makes thyrotropin releasing hormone which travles via portal blood to the anterior pituitary where it stimulates the thyrotrophs to make thyroid stimulating hormone (TSH)
    • TSH is released into the the blood which travels to the thyroid gland to stimulate the thyroid gland to make T3 and mostly t4
    • When T4 and T3 get too high both cause - FB (t3 more strongly does) on both the hypothalamus to stop TSH releasing hormone and the ant pit to stop TSH (feedback on ant pituitary is more important)
    • also when TSH gets to high there is a minor effect by sympathetic nerves and TSH has -FB on the hypothalamus
  107. Thyroid hormone in relation to receptors
    T3 has a stronger affinity to the receptors which is why it causes feedback stronger
  108. How are thyroid cells regulated
    • primary regulated by TSH but somewhat responsive to nervous (a neuroendocrine response)
    • theres more endocrine effect than gland
  109. Mechanism of action of T4 and T3
    • They are small molecules that can pass through the membrane
    • t3 has a stronger affinity than t4 for receptors
    • receptors are located in nucleus of cell
    • these hormones will (like steroids) will end up affecting transcription and translation- activating or supressing genes
  110. receptors of thyroid hormone
    • there are at least 3 receptors
    • 2 are general receptros
    • 1 is for -FB on the hyp and ant pit
  111. functions of Thyroid hormone
    • affects most cells of the body
    • critical for growth and development in the body- reaching adult form
    • metabolic affects for all ages
    • muscle effects
    • cardiovascular effects
    • other physiological effects
  112. Thyroid hormone function in growth and development of the body
    • it is synergistic with growth hormone, estrogen and testosterone in this function
    • important in adult height, organ growth, reproductive development (including puberty changes), and brain development and functioning 
    • brain critically develops in the fetus, and post birth for 2 years- laying down neurons (which wont undergo mitosis anymore after 3-4 years)
  113. thyroid hormones in metabolic effects
    • affects all ages
    • TSH stimulates the basal metabolic rate (the lowest metabolism you need to live while not doing anything)
    • increases the speed of cell rxns
    • increases O2 consumption and energy and heat production
    • stimulates both anabolism and catabolism- glucose absorption, utilization (breakdown), glycogenolysis and gluconeogenesis
    • stimulates fat synthesis and breakdown
    • stimulates protein synthesis (contributing to growth) and breakdown
    • decreases blood cholesterol
  114. Does thyroid hormone affect blood glucose?
    • generally it doesnt increase or decrease blood glucose level in any specific way
    • only significantly changes it if there is a pharmocological effect where you have high TH level-increases blood glucose by breaking down glycogen
  115. Thyroid hormone in muscle effects
    increases muscle tone and contraction
  116. thyroid hormone in cardiovascular effects
    • increases force and rate of heart contraction- therefore increases cardiac outbput
    • its a vasodilator and increases blood flow to organs
  117. other physiological effects of thyroid hormone
    • in general it has a positive effect on normoal functioning of orgnas and normal activity levels of enzymes (ex- brain in regulating normal patterns in functioning in sleep and eating cycles)
    • --> digestion, immune function, kidney function, temperature balance
    • stimulates synthesis of active vitamin A for nutrition from beta carotene
  118. Formation of T3 and T4
    • happens in thyroglobulin storage in the follicle
    • start with tyrosine (which can be made from phenylalanine) which undergoes iodination to form monoiodotyrosine (has one iodine)
    • monoiodotyrosine is then iodinated to form diiodotyrosine (DIT)- 2 iodines
    • next there is condensation/coupling where 2 DITs come together to form T4 OR a DIT and an MIT come together to form T3
  119. iodination
    • organifaction of iodine- changes to the organic form
    • the iodination process (adding iodine to molecule) has to be coupled to make t3 and t4
    • coupling is where 2 DITs come together to form or when MIT and DIT come together
  120. types of t3
    • there is the active form where the DIT is on the right and MIT and OH is on the left
    • the inactive form has the DIT and OH on the left and the MIT on the right
  121. Where is thyroid hormone synthesized
    occurs within the backbone of the polypeptide chain of thyroglobulin in the follicle cells of the thyroid gland
  122. Thyroid disorders
    • after diabetes mellatus, they are the most common endocrine disorders
    • goider
    • hypothyroidism
    • hyperthyroidism
  123. goiter
    • an enlarged thyroid gland- can occur in any of 3 possible situations 
    • 1. a person is hypothyroid
    • 2. a person is hyperthyroid
    • 3. a person is euthyroid (normal TH)-eg nodules or excess growth without affecting TH- goiter will likely be small
    • you can also have disorders without goiter
  124. history of goiters
    • in ancient egypt they noticed many people had goiters (from iodine deficiency- hypothyroidism)
    • they had endemic goiters
  125. endemic goiter
    • widespread in populations
    • happens in populations that live away from the ocean bc not only do marine fish and seafood have a good source of iodine, but foods grown near the ocean have iodine from the soil
  126. Iodized salt
    • a way to fortify the diet with iodine
    • it contains both nacl and KI (potassium iodide)
  127. why do people have a goiter if they have low iodine in diet?
    bc not enough TH (its low) so -FB isnt happening causing high TSH which keeps causing growth of the gland even though it cant make Thyroid hormone bc of the low iodine
  128. Hypothyroidism
    • too low TH
    • multiple types
  129. types of hypothyroidsm
    • creatinism 
    • adult hypothyroidism
  130. cretinism and types
    • low TH in children, 3 types
    • goitrous cretinism
    • athyrotic cretinism
    • genetic disorders
  131. goitrous creatinism
    • due to low iodine in the diet so low TH in critical periods of development causing decreased growth of body and barin and decreased mental facility
    • reversable if done early and fast enough-up to 2 years old, but can be perminent
  132. athyreotic cretinism
    • congenital- people are born without a thyroid or it degenerates
    • rare
    • treated with Thyroid Hormone administration
  133. Genetic disorders in cretinsim
    a person may lack an enzyme requiered for Thyroid hormone synthesis
  134. Adult hypothyroidism
    • a simple goiter is caused by low iodine in diet
    • there can be genetic issues that affect TSH itself or the receptor (rare) 
    • hahimoto's disease is most common type of adult hypothyroidism
  135. hashimotos disease
    an autoimmune disease- the lymphocytes destroy thyroid tissue (b/c the body sees it as foreign) and converts it to fibrous tissue
  136. symptoms of hypothyroidism
    • not all hypothyroid people will have all symptoms-can be mild to severe
    • only a goiter after a while, after you have hormone changes, not instantanious
  137. hypothyroidism symptoms list
    • low metabolic rate
    • low cardiac output- weak and slow
    • low muscle tone
    • increased blood cholesterol
    • sensitive to cold (bc body making less heat)
    • slower mental function (but not as bad as in child)
    • may have reproductive problems (menstrual, pregnancy, etc)- can affect fetus in most severe cases
    • increased weight gain even tho no increased eating (bc slow metabolism)
    • low energy
    • increased susceptability to infection bc all rxn types decreased
    • sleepy
    • slower digestion
    • constipation
    • slower physically
    • myxedema
  138. myxedema
    puffy thick skin in face due to deposit of mucopolysaccharides (a carbohydrate) in intestinal fluid- causes fluid retention
  139. Treatment of hypothyrodism
    • thyroid pill T4 reverses symptoms, decreases TSH
    • if a problem with TSH you can give it, but not if its a receptor issue
  140. Primary endocrine disorder
    something wrong with the gland that makes the problem hormone
  141. secondary endocrine disorder
    result of something else, doesnt originate in the organ where you have too much or too little of the hormone
  142. Hyperthyroidism
    • aka thyrotoxicosis
    • too high Thyroid hormone
    • there are a number of possible causes
  143. Possible causes of hyperthyroidism
    • a generally overactive thyroid
    • tumor
    • excess tsh
    • lack of ability to respond to neg feedback
    • graves disease
  144. generally overactive thyroid in causing hyperthyroidism
    • gland is generally overactive with hyperplasia (multiplying cells) but not cancer
    • causes growth and possible goiter
  145. tumor in causing hyperthyroidism
    • goiter from increased cells
    • cancerous 
    • can have cancer of thyroid with increased TH or of pituitary causing increased TSH, both result in goiter
  146. excess tsh in causing hyperthyroidism
    from genetic disorder can be a cause
  147. lack of ability to respond to neg feedbck in causing hyperthyroidism
    if you lack receptors you will keep making tsh bc the feedback is not regulated and the hormone wont bind receptors to cause neg feedback
  148. graves disease in causing hyperthyroidism
    • most significant cause of hyperthyroidism
    • there are thyroid stimulating antibodies produced by lymphocytes that bind TSH receptors and mimic TSH giving you excess thyroid hormone and there is no neg feedback regulation
    • TSH and antibodies stimulate growth and thyroid hormone production can cause goiter
  149. overall treatment of hyperthyroidism
    • depends on cause of increased thyroid hormone
    • tumor- gland can be removed by surgery and they can give replacement tH
    • destroy tumor-drink radioactive iodine
    • give antithyroid medicine
    • antiinflammatory meds
    • beta blocker
  150. destroying tumor by drinking radioactive iodine
    will go to thyroid and destroy tissue- preferential to tumor but can affect the whole gland, in which youd need to administer TH
  151. antithyroid medicine
    • thyouracil
    • an antithyroid hormone, this can counteract effects
  152. anti inflammatory meds in treating hyperthyroidism
    • given for eye symptoms
    • this medication or surgery can be done to remove extra tissue
  153. beta blocker in treating hyperthyroidism
    • given for cardiac symptoms
    • even tho the beta adrenergic receptor is related to adrenal functioning, this can be given
  154. symptoms of hyperthyroidism
    • often a goiter (from cancer, not cancer, excess growth stimulation, etc)
    • exopthalamus
    • increased metabolic rate
    • increased cardiac output (increased heart rate, pulse, possibly increased bp and maybe irregular heartbeat)
    • increased body temp- ppl have intolerence to heat, feel hot
    • may have nerbous energy-anxious, excitable, restelss, feel excess energy
    • may be quick mentally
    • weight loss even tho no change in eating
    • menstrual irregularites
    • can but not always have higher blood glucose

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