Endocrine Day 5- Adrenal and Ca Flashcards Preview

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Flashcards in Endocrine Day 5- Adrenal and Ca Deck (36)
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What is the master stress hormone of the body?

Where is it released from?

What does it stimulate?

  • CRH= master sex hormone
  • Released from PARAventricular nucleus
  • Stimulates corticotrophs to release ACTH


What is effect of ACTH?

  • ACTH causes adrenal cortex to release hormones
    • cortisol (type of glucosteroid)
    • aldosterone (mineralocorticoid)
      • allows us to increase Na/h2o reabsorption from tubule
      • cortisol can also act like aldosterone at kidney, causing increase H2O/Na reabsorption
    • androgen precursor
    • angiotensin


What is ACTH?

  • Adrenocorticotropic Hormone derived from precursor pro-opiomelanocortin (POMC) from pit corticotroph cells by enzymatic clevage of precursor products
  • POMC--> ACTH intermediate--> ACTH
    • ACTH can be further cleaved into MSH and CLIP (only mention MSH)
  • MSH can cause increase melanin release by bindign to melanin receptors
    • ACTH is very similar to MSH so it can also bind to receptors in very high concentrations


What are the cellular zones of the adrenal cortex?

  • C=connective tissue capsule
  • ZG=zona glomerulosa produces aldosterone (mineralocorticoids)
  • ZF=zona fasciculata produces cortisol (glucocorticoids)
  • ZR=zona reticularis produces adrenal androgens
  • M=adrenal medulla produces norepi and epi (most central area)


What are 2 major enzymes involved in synthesis of cortisol, aldosterones, and androgens by the cortex? What can happen if you're deficient in either enzyme?

  • Two major enzymes
    • 21 alpha hydroxylase
    • 11 beta hydroxylase
  • If deficient in either enzyme, won't be able to make mineralocorticoids (aldosterone) or glucocorticoids (cortisol)
  • This will force the pathway into andonergic pathway, causing increase in systemic androgens


What can stimulate ACTH secretion (also increase CRH)

  • Cortisol decrease
    • adrenalectomy
  • sleep-wake transition- need cortisol to get out of bed
  • stress
    • hypoglycemia
    • anesthesia
    • sx- contributing factor to puffiness post op is excess cortisol
    • trauma
    • infection
    • pyrogens
  • Psych disturbance- both anxiety/depression can increase cortisol and incrase cortisol can cause anxiety/depression
    • anxiety
    • depression
  • alpha agonists- NE/E incrase cortisol
  • beta adrenergic antagonist
  • serotnin
  • ADH- stress hormone
    • causes constriction of vessels, raising BP
    • corticotorphs also have ADH receptors
  • gaba


What inhibits ACTH secretion?

Cortisol increase





What time of day is largest release in ACTH/cortisol?

8 am

  • Helps when glycogen stores decreased after sleep
  • BP may be a bit lower, surge of cortisol helps compensate


Low cortisol level is ____

High cortisol level is____

anabolic; catabolic

  • Low levels cortisol are anabolic and promote gluconeogenesis and storage of glucose as glycogen
  • Higher livels of cortisol are catabolic and promote breakdown of muscle/fat (proteolysis and lipolysis)
    • glycogenolysis also occurs in liver in order to increase substrates glucose, aa, ffa, aa for use in stress response


What is RAAS system role in aldosterone production?

RAAS system produces angiotensin II which increases aldosterone which increases Na/H2O reabsorbtion and K secretion


What is cushing disease?

  • Cushing disease is due to pituitary tumor over-secreting ACTH and causing excess cortisol secreiton
  • Causes
    • swelling on face
    • body fat redistrubted to back of neck and trunk
    • proteolysis of connective tissue collagen elements, leading to appearance of purple striae
    • hyperglycemia
    • impaired immune response


What is cushing's syndrome?

  • Another version cushing disorder but called cushing syndrome
  • due to adrenal cortical tumor over-producing cortisol
  • excess cortisol drives same s/s as seen in previous cuhsing's disease


What is congenital adrenal hyperplasia?

  • Cuased by 21-alpha hydroxylase deficiency
  • blocks biosynthetic pathway to produce cortisola nd aldosterone
  • forced substrates into androgen pathway
  • lack of cortiosl negative feedback causes excess ACTH release that stimulates excess androgen production
    • has virilizing effect


What is treatment for congenital adrenal hyperplasia?

  • Give cortisol
  • Not having cortisol is life-threatening
  • by reinstating negative feedback, ACTH levels drop and reduce andronergic pathway


What is addion's disease?

  • Autoimmune attack on adrenal cortex destorys cells making cortisol
  • develops cortisol deficiency
    • increased output ACTH from pituitary from loss negative feedback
      • can't survive without cortisol
  • Highly pigmented skin due to melatonin from stimulation of MSH/increased ACTH levels
    • not hazardous but diagnostic tool


What does calcium regulation look like in body?

  • 1000 mg calcium ingested daily
    • GI tract net uptake= 175 mg
    • Bone net even (500 mg in, 500 mg out)
    • Kidney excretes 175 mg from kidney
  • insures that amount Ca in blood remains constant around 900 mg in ECF


What are the 3 main types of bone cells


  • Osteoblasts
  • Osteoclasts
  • Osteocytes (which are absorbed osteoblasts)


What are osteoblasts?

  • osteoblasts are found on surface of bone
  • deposit Ca and phosphate into bone
  • involved in movment of Ca PO4 out of bone, into fluid and into circulation


What are osteoclasts?

  • liberate ca/phosphate from bone aka breakdown bone


What are osteocytes?

  • Absorbed osteoblasts


What are the osteocystic/osteoblastic membranes role in Ca regulation?

  • membrane is target for PTH and calcitiol (active form of VIt D)
    • acts on membrane to cause rapid movmeent of Ca of PO4 into blood= rapid phase Ca/Po4 mobilization
  • To replace bone fluid Ca and PO4 later, PTH stimulates slow phase of Ca mobilization by activating osteoclasts that will digest (reabsorb) bone and liberate Ca PO4 into bone fluid


What exists outside of calcified bone?

  • Bone fluid exists between blasts and bone


What is parathyroid hormone?

  • peptide hormone synthesized by parathyroid glands 
    • 4 parathyroid glands embedded posteirorly in 4 lobes thyroid gland


What cell scretes PTH?

Chief cells in parathyroid gland


What is the main target of PTH?

  • Osteoclasts of bone (although indirectly)
    • PTH actually binds to osteoblasts, in turn osteoblasts secrete cytokines and stimulate osteoclasts to digest bone, which moves Ca/PO4 out of bone and into blood stream
  • kidney tubules
  • gut (via D3)

INCREASES the availability of Ca in blood


What happens with removal of parathyroid glands?

  • Loss of ability to regulate Ca which untreated, will result in rapid death
    • (just need to supplement with external Ca)


What cells monitor Ca concentrations?

Chief cells

  • When Ca levels decline in blood, chief cells increase output of PTH to restore Ca concentration
  • Ca and PTH have inverse relationship


What is the summary of  sites of action of PTH?

  • Bone: promote Ca and phosphate resorption (into blood)
    • increases remodeling of bone
  • Kidney: calcium reabsorption, phosphate excretion (need to decrease phosphate levels so crystals dont' form in blood)
    • involved in final hydroxylation of 25-hydroxy vit d3
  • Intestine: indirect effects via dihydroxy vit D3



What is PTH's effect on plasma calcium and phosphate?

Increase Ca, decrease phosphate


What is pathway for formation of VIt D3?

  • 7-Dehydrocholesterol in skin changes sturcutre when exposed to UV light
  • Vit D3 is delivered to liver, acted on by 25-hydroxylase
  • then taken to kidney
    • PTH activates enzyme 1-hydroxylase
    • creates active form VIT D3 aka calcitriol
      • main target is GI tract to stimulate uptake of ca/po4 from gut, into circulation