Endocrine and Stress: adrenals, kidneys, heart

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Endocrine and Stress: adrenals, kidneys, heart
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2010-11-28 10:54:23
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IBHS final 525 ... dr. r (Hormones and stress: acute stress)
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  1. T/F
    "Though connected to the kidneys, the adrenal glands play no role in the functioning or, or health of the kidneys" - wikipedia
    false
  2. 2 organs of stress
    • 1. kidneys
    • -Latin: renes (renal, renin, adrenal, adrenaline)
    • -Greek: nephros (nephron, nephrology, epinephrine)
    • 2. adrenal glands (cortex and medulla)
  3. context: 2 organs of stress
    hormones secreted by kidneys
    • 1. renin (aka - angiotensinogen-ase)
    • 2. EPO (erythropoietin)
    • remember: Ren and Stimpy, REPO Men
  4. context: 2 organs of stress
    hormones secreted by adrenal glands
    • -cortex (endocrine cells):
    • 1. aldosterone
    • 2. cortisol
    • 3. testosterone
    • -medulla (neuroendocrine cells):
    • 1. epinephrine (aka - adrenaline)
    • 2. norepinephrine (aka - noradrenaline)
  5. 2 types of stress
    • 1. acute (aka - alarm phase, Eustress 'good stress')
    • 2. chronic (aka - resistance phase, distress 'bad stress')
  6. context: 2 types of stress
    acute stress
    • aka: alarm phase, Eustress 'good stress'
    • -lasts: seconds --> hours
    • proactive: short term response to protect/maintain homeostasis (alert --> alarm --> panic)
    • evolved to protect us from short term injury (cliffs and bears)
    • quick responses: neurons (neurons --> hormones) and fast acting hormones
    • 1. adrenal gland - epinephrine/norepinephrine (by ACh)
  7. context: 2 types of stress
    chronic stress
    • aka: resistance phase, distress 'bad stress' (failed to escape the stressor and when "fight or flight" via E/NE did not work well enough, "conserve and survive" via cortisol, aldosterone, renin, EPO, more occur)
    • -lasts: hours --> weeks or more
    • reactive: long term response to recover homeostasis
    • evolved to protect us from long term injury (dehydration or starvation)
    • slower responses: hormones (hormones --> hormones)
    • 1. kidneys - renin, EPO
    • 2. adrenal gland - aldosterone (by renin), cortisol (by ACTH)
  8. 5 goals/results of sympathetic stimulation for acute stress (fight/flight)
    • brain: NE -->
    • 1. alert/memory
    • neurons and blood: NE, E/NE -->
    • 2. mobilization of glucose reserves
    • 3. changes in circulation
    • 4. increases in heart and respiratory rates
    • 5. increased energy use by all cells
  9. context: acute stress
    2 branches
    • 1. functions of hypothalamus
    • 2. functions/effects (dominant) of high E/NE
  10. context: acute stress - 2 branches
    2 functions of the hypothalamus
    • 1. releases norepinephrine into brain
    • - increases alertness and memory
    • 2. sends neural signals to organs
    • -ACh --> neurons --> NE directly onto most organs
    • -ACh --> adrenal medulla --> E/NE indirectly to organs via blood
  11. context: acute stress - 2 branches
    high E/NE effects on 4 areas
    • 1. blood vessels
    • -less blood to skin, kidneys, intestines
    • -more blood to lungs, cardiac muscles, skeletal muscles
    • 2. fat tissues and liver
    • -release more glucose into blood
    • 3. lungs and heart
    • -increased oxygen and blood delivery
    • 4. sweat glands
    • -increased body sweating (ACh --> muscarinic receptors)
    • -increased hand/foot sweating (E/NE --> alpha-1 receptors
  12. pathway for creation of epinephrine/norepinephrine by adrenal medulla (middle)
    • adrenal medulla - under neuronal control
    • pathway: tyrosine --(tyrosine hydroxylase)--> dihydroxyphenylalanine (DOPA) --(DOPA decarboxylase)--> dopamine --(dopamine-ß-hydroxylase)--> norepinephrine --(phenylethanolamine-N-methyltransferase)--> epinephrine
  13. context: adrenal medulla creation
    storage of epinephrine and norepinephrine
    in granules
  14. context: adrenal medulla creation
    release of epinephrine and norepinephrine
    • activated by: "stress" --> activate neurons from hypothalamus --> release acetylcholine (ACh) at the adrenal medulla --> immediately releases ~80% epinephrine (binds to adrenergic receptors: a-1, a-2, b-1, b-2) and 20% norepinephrine (binds to adrenergic receptors: a-1, a-2, b-1, b-2) into blood
    • -effect peaks at 30 seconds, persists for several minutes
  15. context: adrenal medulla creation
    2 ways for prepare for fight or flight (purpose)
    • 1. accelerate delivery of nutrients/oxygen to cells
    • -increase in HR, SV, BP, Bronchiodilation
    • 2. accelerate conversion of nutrients to ATP
    • -glycogen --> glucose --> ATP (for strength and endurance
    • -lipids --> fatty acids --> ATP (for strenth and endurance)
  16. Name the 13 common adrenergic drugs (generics)
    • 1. Tamsulosin
    • 2. Terazosin
    • 3. Doxazosin
    • 4. Clonidine
    • 5. Tizanidine
    • 6. Atenolol
    • 7. Metoprolol
    • 8. Bisoprolol
    • 9. Propanolol
    • 10. Albuterol
    • 11. Salmeterol
    • 12. Pseudoephedrine
    • 13. Carvedilol
    • *many used for cardiovascular and/or respiratory disorders
  17. context: adrenergic drugs (13)
    Tamsulosin
    • adrenergic receptor: alpha-1
    • endogenous agonist: Epinephrine, Norepinephrine
    • function: antagonist
  18. context: adrenergic drugs (13)
    Terazosin
    • adrenergic receptor: alpha-1
    • endogenous agonist: Epinephrine, Norepinephrine
    • function: antagonist
  19. context: adrenergic drugs (13)
    Doxazosin
    • adrenergic receptor: alpha-1
    • endogenous agonist: Epinephrine, Norepinephrine
    • function: antagonist
  20. context: adrenergic drugs (13)
    Clonidine
    • adrenergic receptor: alpha-2
    • endogenous agonist: Epinephrine, Norepinephrine
    • function: agonist
  21. context: adrenergic drugs (13)
    Tizanidine
    • adrenergic receptor: alpha-2
    • endogenous agonist: Epinephrine, Norepinephrine
    • function: agonist
  22. context: adrenergic drugs (13)
    Atenolol
    • adrenergic receptor: beta-1
    • endogenous agonist: Epinephrine, Norepinephrine
    • function: antagonist
  23. context: adrenergic drugs (13)
    Metoprolol
    • adrenergic receptor: beta-1
    • endogenous agonist: Epinephrine, Norepinephrine
    • function: antagonist
  24. context: adrenergic drugs (13)
    Bisoprolol
    • adrenergic receptor: beta-1
    • endogenous agonist: Epinephrine, Norepinephrine
    • function: antagonist
  25. context: adrenergic drugs (13)
    Propanolol
    • adrenergic receptor: beta-1, beta-2
    • endogenous agonist: Epinephrine, Norepinephrine
    • function: antagonist for both
  26. context: adrenergic drugs (13)
    Albuterol
    • adrenergic receptor: beta-2
    • endogenous agonist: Epinephrine, Norepinephrine
    • function: agonist
  27. context: adrenergic drugs (13)
    Salmeterol
    • adrenergic receptor: beta-2
    • endogenous agonist: Epinephrine, Norepinephrine
    • function: agonist
  28. context: adrenergic drugs (13)
    Pseudoephedrine
    • adrenergic receptor: alpha/beta
    • endogenous agonist: Epinephrine, Norepinephrine
    • function: agonist
  29. context: adrenergic drugs (13)
    Carvedilol
    • adrenergic receptor: alpha/beta
    • endogenous agonist: Epinephrine/Norepinephrine
    • function: antagonist
  30. 4 goals/results of chronic stress
    • 1. prevention of dehydration and hypotension
    • 2. delivery of more oxygen
    • 3. prevention of starvation
    • 4. prevention of excessive inflammation
  31. context: 4 goals of chronic stress
    prevention of dehydration and hypotension
    • via hormone: renin, angiotensin, aldosterone, ADH
    • Process: low BV or BP stimulate kidneys to release renin into blood --> renin converts angiotensinogen to angiotensin I --(ACE in lungs)--> angiotensin I converted into angiotensin II --> angiotensin II stimulates:
    • 1. posterior pituitary to release ADH (ADH makes kidneys more permeable to water)
    • 2. adrenal cortex to release aldosterone (aldosterone stimulates kidneys to hold onto Na+)
    • -Less water out of kidneys = more water in blood
    • Pathophysiology: chronic psychological stress --> hypertension
    • Pharmacology: treat the psychological problem
  32. context: 4 goals of chronic stress
    delivery of more oxygen
    • via hormone: erythropoietin (EPO)
    • Process: low erythrocytes, plasma, and/or oxygen --> kidneys release EPO --> EPO stimulates RBC production by bone marrow
    • Pathophysiology: -
    • Pharmacology: patients with anemia (due to chemotherapy, athletes
  33. context: 4 goals of chronic stress
    prevention of starvation
    • via hormone: glucocorticosteroids/glucocorticoids/corticosteroids (cortisol)
    • Process: mobilization of glucose from reserves for wound healing and maintaining glucose to CNS:
    • -adipose --> fatty acids + glycerol into blood
    • -skeletal muscle --> amino acids into blood
    • -stimulate liver --> convert glycerol and a.a. to glucose
    • -non-CNS tissues --> use fatty acids not glucose
    • Pathophysiology: disorders of cortisol
    • -problem with hypothalamus, pituitary, or adrenal gland
    • -Addison's Disease/Syndrome: absent cortisol (less mobilization of energy stores during stress)
    • -Cushing's Disease/Syndrome: copious cortisol (excess mobilization of energy stores during stress, increased infections)
    • Pharmacology: -
  34. context: 4 goals of chronic stress
    prevention of excessive inflammation
    • via hormone: glucocorticosteroids/glucocorticoids/corticosteroids (cortisol)
    • Process: inhibit:
    • -WBC proliferation
    • -WBC migration
    • -WBC inflammatory mediators
    • Pathophysiology: -
    • Pharmacology: glucocorticoids can be used to inhibit dangerous inflammation
  35. context: Glucocorticosteroid Therapy
    2 uses of glucocorticosteroid
    • 1. adrenal insufficiency
    • 2. suppression of immune system
    • -autoimmune disorders, allergies, asthma, transplants
    • -any acute/chronic symptom of inflammation/pain
  36. context: Glucocorticosteroid Therapy
    7 ways of administrations
    • 1. I.V.
    • 2. I.M.
    • 3. S.C.
    • 4. oral
    • 5. topical
    • 6. inhaled
    • 7. intra-articular
  37. context: Glucocorticosteroid Therapy
    Name 10 synthetic glucocorticosteroids
    • 1. Cortisol (hydrocortisone)
    • 2. Prednisone
    • 3. Prednisolone
    • 4. Methylprednisolone
    • 5. Triamcinolone
    • 6. Dexamethasone
    • 7. Betamethasone
    • 8. Fluticasone
    • 9. Mometasone
    • 10. Budesonide
  38. context: 10 synthetic glucocorticosteroids
    Cortisol (hydrocortisone)
    • half-life: <1.5 hours
    • potency: 1x
    • Top 200 listing: -
  39. context: 10 synthetic glucocorticosteroids
    Prednisone
    • half-life: 2-5 hours
    • potency: 4x
    • Top 200 listing: generic
  40. context: 10 synthetic glucocorticosteroids
    Prednisolone
    • half-life: 2-5 hours
    • potency: 4x
    • Top 200 listing: -
  41. context: 10 synthetic glucocorticosteroids
    Methylprednisolone
    • half-life: 2-5 hours
    • potency: 5x
    • Top 200 listing: generic
  42. context: 10 synthetic glucocorticosteroids
    Triamcinolone
    • half-life: >5 hours
    • potency: 5x
    • Top 200 listing: generic, Nasacort AQ™
  43. context: 10 synthetic glucocorticosteroids
    Dexamethasone
    • half-life: >5 hours
    • potency: 20-50x
    • Top 200 listing: Tobradex™ (2 agents)
  44. context: 10 synthetic glucocorticosteroids
    Betamethasone
    • half-life: >5 hours
    • potency: 20-50x
    • Top 200 listing: generic (2 agents)
  45. context: 10 synthetic glucocorticosteroids
    Fluticasone
    • half-life: -
    • potency: ?
    • Top 200 listing: Flonase™, Flovent™
  46. context: 10 synthetic glucocorticosteroids
    Mometasone
    • half-life: -
    • potency: ?
    • Top 200 listing: Nasonex™
  47. context: 10 synthetic glucocorticosteroids
    Budesonide
    • half-life: -
    • potency: ?
    • Top 200 listing: Rhinocort AQ™
  48. Chronic Stress diagram
    • Hypothalamus:
    • -psycho or physio distress
    • -renin, ADH, ACTH
    • Blood loss:
    • -direct: renin, EPO
    • Goals:
    • -recover blood cells
    • -retain fluid --> BV, BP
    • -regulate energy
    • -suppress WBCs
    • Diuretics:
    • -increase fluid loss
    • -to lower blood pressure
    • -to decrease heart's effort
    • Types of diuretics:
    • 1. ACE inhibitors
    • 2. Angiotensin II receptor antagonists
    • 3. Aldosterone receptor antagonists
    • 4. many others that work directly on the kidneys
  49. The heart as an endocrine gland
    -over-hydration is also a form of biological stress
    • 5 step process:
    • (1) blood volume increases --> (2) atria chamber of heart stretches --> (3) triggers release of Atrial Natriuretic Peptides (ANP) --> (4) ANP triggers Na+ and water loss via kidneys --> (5) blood volume decreases

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