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  1. What two conditions stimulate secretion of ANP?
    • Stretch
    • Increased Na intake.
  2. How does ANP stimulate natri and diuresis?
    • Dilation of afferent arteriole
    • Constriction of efferent arteriole.
  3. Where is ADH synthesized, released?
    • Hypothalamus
    • Supraoptic nucleus
    • released from posterior pituitary.
  4. What is the main action of ADH?
    • Increases collecting duct permeability to H2O through V2 receptors
    • Places more water channels in membrane.
  5. What is the cause of central diabetes insipidus?
    Insufficient ADH (synthesis or secretion).
  6. What is the cause of nephrogenic diabetes insipidus?
    • Inability of kidneys to respond to ADH (through V2 receptors)
    • lithium may be a cause.
  7. What are three causes of SIADH?
    • Ectopic production - Small cell lung carcinoma
    • Drug Induced - MDMA
    • Lesion in baroreceptor system.
  8. What is the main factor regulating aldosterone secretion?
    Angiotensin II.
  9. What controls the release of cortisol and adrenal androgens?
  10. What does the adrenal medulla release?
  11. Which hormones are C21, C19, C18?
    • C21: Aldosterone and cortisol (+pathways)
    • C19: Adrenal Androgens, Testosterone
    • C18: Estrogens.
  12. What inactivates and makes cortisol water soluble, where?
    • Glucoronide Group
    • Liver.
  13. What is the major secreted form of adrenal androgens, converted into?
    • DHEA
    • converted into testosterone and DHT (more powerful).
  14. How are adrenal androgens (DHEA) water solubolized?
    Sulfate group is added.
  15. What enzyme converts androgen into estrogen?
  16. What is the first step in the synthesis of all steroid hormones, what enzyme?
    • Cholesterol -> Pregnenolone
    • Desmolase.
  17. What enzyme bridges the zona glomerulosa (aldosterone) pathway to the the zona fasciculata (cortisol) pathway?
    17-alpha-hydroxylase (17-a-OH).
  18. What enzyme bridges the zona fasciculata (cortisol) pathway to the zona reticularis (androgen) pathway?
    17,20 lyase.
  19. What is the result of a deficiency in 21-b-OH?
    steroids pushed toward androgen production.
  20. What steroid is responsible for the main negative feedback on hypothalamus and pituitary of ACTH?
  21. What are the four stress hormones, and what do they do?
    • Growth Hormone: mobilizes fat stores via lipolysis
    • Glucagon: mobilizes glucose via glycogenolysis
    • Cortisol: mobilizes fat, protein, and carbohydrate
    • Epinephrine (exercise): mobilizes fat and glucose.
  22. What do all stress hormones do?
    Increase plasma glucose.
  23. What are the two mechanisms by which cortisol increases blood glucose?
    • Inhibits glucose uptake in most tissues
    • Stimulates gluconeogenesis in the liver
    • -- allows for increased substrate for nervous tissue.
  24. What are the permissive actions of cortisol?
    Enhance capacity of glucagon and epinephrine.
  25. What time is the peak release of CRH (corticotropin releasing hormone), low?
    • Peak: Early morning
    • Low: Late evening.
  26. What is the name of excessive ACTH secretion, what does it cause?
    • Addison's disease
    • Darkening of the skin - increased melanocyte stimulation.
  27. Where and what are the main actions of aldosterone?
    • Kidneys - principal cells
    • Increase reabsorption of Na+ (along with water)
    • K+ secretion
    • H+ secretion.
  28. How does aldosterone promote metabolic alkalosis?
    By secretiion of H+, an HCO3- is moved to ECF.
  29. Where is Renin released, what does it act on?
    • Juxtaglomerular cells of Kidney
    • Angiotensinogen -> angiotensin I
    • Angiotensinogen produced in liver.
  30. Where is ACE found, what does it do?
    • Endothelium of pulmonary vessels
    • Angiotensinogen I -> angiotensinogen II.
  31. What does angiotensinogen II do?
    • Potent secretor of aldosterone
    • Arteriolar vasoconstriction.
  32. What is Cushing's syndrome?
    Hypercortisolism from any cause.
  33. What is Cushing's Disease?
    Hypercortisolism from microadenoma in anterior pituitary.
  34. What is low dose dexamethozone suppression test?
    • Should decrease cortisol in normal individuals
    • Does not decrease cortisol in hypercortisolism -> Cushing's syndrome.
  35. What is high dose dexamethazone suprression test?
    • Should decrease cortisol in Cushings disease/microadenoma
    • Does not decrease cortisol in ectopic ACTH production (small cell lung Ca)/ adrenal tumor.
  36. What is Addison's Disease?
    Primary hypocortisolism from primary adrenal insufficiency.
  37. What is Conn's syndrome?
    • Primary hyperaldosteronism
    • Usually a small unilateral adenoma.
  38. What is an important clinical feature of hyperaldosteronism?
    Hypertension with Hypokalemia.
  39. An increase in 11-deoxycorticosterone leads to?
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kaplan endo
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