Ch 16 endocrine Animal Physiology.txt

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rincrocci
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265130
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Ch 16 endocrine Animal Physiology.txt
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2014-03-05 01:58:17
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  1. Ch 16
  2. what are hormones
    • chemical substances produced by secretory cells (ENDOCRINE Glands)
    • Released by non-neuronal endocrine cells OR neurons
    • travel via BLOOD to interact with distant cells
  3. What determines hormones Affectivness
    • Amount of RECEPTOR molecules that can bind
    • Amount of hormone concentration in BLOOD
  4. Types of hormones and method of synth and action
    • 1. Steroid hormones: synth from cholesterol, lipid molecules move thru membrane to act DIRECTLY, long halflife though takes LONGER to get there
    • 2. Peptide or protein: made of aa's, water soluble attach to surface of membrane, act via second messengers, short halflife though action is FAST to initiate
    • 3. Amines: come from aa's (tryp or tyr) thyroid hormones interact as steroid hormones, whereas melatonin and catecholamines act similar to peptide hormones
  5. paracrine or autocrine
    act like hormones: fxn of cells in same tissue WITHOUT going through circ system
  6. Types of endocrine glands
    Discrete, diffuse (scattered populations of endo cells) or intermediate
  7. Endocrine cells two classes
    • 1. Epiethlial endocrine cells: secretions termed HORMONES, usually stimulated by OTHER HORMONES
    • 2. Neurosecretory cells: their endocrine secretions termed NEUROhormones, ALWAYS stimulated by SYNAPTIC INPUT from neurons
    • These can be organized into discrete glands to form epithelial glands and neurosecretory glands
  8. Pituitary gland location and two parts
    • Located just BELOW the hypothalamus
    • 1. Anterior pituitary
    • 2. Posterior pituitary
  9. Posterior pituitary role
    • Where 2 peptide hormones, that came from the hypothalamus and traveled via action potentials, are released into the capillaries
    • 1. vasopressin, aka Antidiuretic hormone (ADH): increases the Reabsorption of H20 from kidney to extracellular fluid
    • 2. oxytocin: causes contractions during birth and ejection of milk by mammary glands
  10. Anterior Pituitary
    • Secretes 2 main groups of hormones from the endocrine cells in its tissues
    • 1. Hormones that exert their effects on NON-endocrine tissue, ie Growth Hormone
    • 2. Hormones that control other ENDOcrine glands (TROPIC), ie Thyroid stimulating hormone (TSH)
  11. Group 1 ant pit hormones
    • hormones exerting effect on NON-endo tissues
    • GH: influences growth on fat and muscle and liver
    • Prolactin: Growth during pregnancy and milk production
    • Melanocyte-stimulating hormone (MSH): Skin DARKENING in amph, reptiles and fish
  12. Group 2 ant pit hormones
    • Hormones that control other ENDOcrine glands, termed TROPIC
    • TSH: causes STIMULATION of Thyroid hormones for metabolism and growth
    • Adrenocorticotropic hormone (ACTH): Act on Adrenal cortex, involved with metabolism and STRESS Response
    • Follicle-stimulating hormone (FSH) and Lutenizing hormone (LH): acts in the gonads, FSH involved in sperm production in males, follicle development in females, LH is a sex hormone
  13. Axis and a type studied
    • Axis: a system when secretions of on endocrine gland ACT ON another in sequence
    • Example: Hypothalamus-Pituitary gland-Adrenal cortex (HPA) axis
  14. Adrenal gland
    Stimulates GLUCOcorticoids: steroid hormone (promote blood GLUCOse concentration)
  15. Example of what is controlled by HPA axis
    Corticotropin-releasing hormone (CRH) released by neurons in the HYPOTHALAMUS and travel to capillaries to the ANTERIOR PITUITARY to stimulate Adrenocorticotropic cells to secrete ACTH into capillaries where it stimulates the ADRENAL CORTEX to secrete glucocorticoids (such as cortisol)
  16. How to modulate hormonal axis (such as HPA) (CH 16 SUMMARY #7 and 9)
    • In patients receiving cortisone drug therapy, Negative feedback: high levels of glucocoritoid can SUPPRESS secretion of CRH by hypothalamus and ACTH by ant pit, and can also reduce responsiveness of ACTH to CRH
    • Normally glucocorticoid secretion results from neurons secreting CRH, stimulating adreno glands to stimulate ACTH, which is carried to the adrenal cortex to stimulate glucocorticoid secretion. ACTH is suppressed due to the negative feedback, therefore resulting in the lack of stimulus to secrete glucocorticoids in the adrenal cortex (SHRINKAGE RESULTS)
  17. Synergism example (CH 16 SUMMARY #10 part1)
    • Enhanced response with both hormones
    • ie: Vasopressin interacts with CRH to increase secretion of ACTH from ant pituitary (Vaso needs CRH to influence ACTH secretion)
  18. Antagonism example (CH 16 SUMMARY #10 part2)
    • action of one hormone opposes action of other
    • IE: Insulin and Glucagon
  19. Permissiveness example (CH 16 SUMMARY #10 part3)
    • One hormone required for other to have effect
    • Cortisol allows epi and norepi to cause constriction, b/c cortisol MUST be present for vasoconstriction to occur, this glucocorticoid must be present with basal levels to regulate blood pressure
  20. Neural modulation (2 ways)
    • Sensory input from neurons to generate input to allow for CRH to secrete in hypothalamus
    • Clocklike mechanism: coritosol levels in blood fall and rise rhythmically in a cycle, driven by circadian clock in brain that sends input to hypothalamic CRH cells
  21. How are hypothalamic and pituitary hormones secreted
    PULSES governed by synaptic input to neurosecretory cells, causing pulsing release of hypothalamus hormones, therefore pulse of release of pituitary hormones

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