hormones of the adrenal cortex n.
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HORMONES OF THE ADRENAL CORTEX. Prof.Dr .Arzu Seven. HORMONES OF THE ADRENAL KORTEX. The adrenal c ortex makes 3 kinds of hormones : Mineralocorticoids Glucocorticoids Androgens.

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slide3

The adrenal cortexmakes 3 kinds of hormones:

  • Mineralocorticoids
  • Glucocorticoids
  • Androgens
slide4

There is an overlap of biologicalactivity, allnaturalglucocorticoidshavemineralocoticoidactivityandvice varsa

  • H + R (intracellular)gene expression
chemical structure of steroid hormones
Chemicalstructure of steroidhormones:
  • 17-C cyclopentanoperhydrophenanthrenestructurewithfourringslabeled A_D
  • Additionalcarbons can be added at positions 10 or 13 or a sidechainattachedto C17
  • Asymetriccarbonatomsallowforstereoisomerism
slide7

Glucocorticoids21C

  • Mineralocorticoids21C
  • Androgens19C
  • Estrogens18C
synthesis of glucocorticoids
Synthesis of glucocorticoids
  • C17
  • C21
  • C11
  • 17
  • 21
  • 11

hydroxylations

Endoplasmicreticulum

mitochondria

slide10

Cortisolis themajorglucocorticoid , synhesized in the adrenal cortex

  • It is underthedirectcontrol of pituitary ACTH
  • Cholestrol is theprecursorforallseroidhormones
  • Theconversion of cholestroltopregnenolone is the rate limiting step
slide11

Cleavage of thecholestrolsidechainliberatesC-21 corticosteroids, furthersidechaincleavageyields C-19 androgens, aromatization of ring A results in C-18 estrogens

slide13

Plazma concentrationshows a pronounceddiurnalrhythm, being 10 timeshigher at 08.00 hrthan at 24.00 hr

  • Thisparallelsthemarkeddiurnalrhythm of ACTH secretion
  • 95% of cortisol in plasma is boundtoproteins, mainlycorticosteridbindingglobulin(CBG) ortranscortin
slide14

CBG is produced in liver

  • Itssynthesis , like TBG, is increasedbyestrogens
  • Freefractionrepresentsthebiologicallyactivecortisol
  • Half life ~ 100 minutes
slide15

Inplasma :80% 17-OH corticoids, 20% cortisoneand 11-deoxycortisol

metabolized in theliverbyreduction, sidechaincleavageandconjugationreactionslipophilicsteroidmoleculebecomeswatersolubleandexcretable

slide16

Inhumansmost of theconjugatedsteroids,thatentertheintestinebybiliaryexcretion,arereabsorbedbytheenterohepaticcirculation

  • Conjugatedsteroidsareexcreted :
  • 70% in theurine
  • 20%in thefeces
  • skin
slide17

Glucocorticoidhormonesaffectbasalmetabolism, hostdefencemechanism, bloodpressureandresponsetostress

slide19

Cortisolworks in tandem withinsulinand GH in regulatingintermediarymetabolism

clinical disorders of cortisol secretion hypofunction
Clinicaldisorders of cortisolsecretionhypofunction:
  • Hyposecretion of cortisolmayoccur as a result of hypothalamic,pituitaryor adrenal failure
  • Diagnosis:
  • Clinicalpresentation
  • Timedmeasurement of cortisoland ACTH
  • Extent of cortisolresponsetosynthetic ACTH

(synacthen)

addison disease adrenal insufficiency
Addisondisease(adrenal insufficiency)
  • Primary adrenal failure

autoimmune/infection(tbcorcytomegalivırus)

  • Secretion of all adrenal hormones
biochemical features
Biochemicalfeatures
  • Hyponatremia
  • Hyperkalemia
  • Acidosis
  • Urea
  • İmpairedcortisolresponsetosynacthen, togetherwith ACTH
  • Darkeningof skin andmucousmembranes
  • Hypovolemiaandhypotensionstimulate AVP secretionwaterretention
synacthen tests short or long
Synacthentests(shortorlong)
  • Synacthen is a synthetic,1-24 analogue of ACTH, adminsteredIV at a dose of 250µg
  • Cortisol is measured at 0,30,60 min
  • EquivocalorinadequateresponsestoSST (shortsynacthen test) mayrequire LST to be performed in ordertoestablishwhether adrenal insufficiency is primaryorsecondarytopituitaryorhypothalamicdisease.DepotSynacthen (1mg) is given IM for 3 days SST repeatedon the 4th day
slide26

A normal responsemakesprimary adrenal insufficiencyunlikely

  • LST may not be neededwhen ACTH is measured
slide28

Therapy:cortisolreplacament , usuallytogetherwith a mineralocorticoid

  • Addison’sdisease can be associatedwithelevated TSH whichrevolveswithglucocorticoidtherapy
hyperfunction
hyperfunction
  • Hypersecretion of cortisolresults in Cushing’ssyndrome
  • Prolongeduse of exogenousglucocorticoids (iatrogenic)
  • Disordersthehypothalamus, pituitary (80%) or adrenal gland(15%)
  • Ectopic ACTH syndrome
slide33

Cortisolexcessproduces DM andhypertension, andusuallysuppressesthehypothalamicgonadalaxis (amenorrhea)

diagnosis
diagnosis
  • Randommeasurement of cortisol is of littleusebecause of thepronouncedcircadianvariation
  • 24 hoururinaryfreecortisolorcortisol/creatinineratio in an earlysample is a commonscreening test
  • Repeatedlyhighearlymorningurinecortisol /creatinineratiosindicatefurtherinvestigations
  • Ifthe test is negative on 3 occasionsexcludeCushing’ssyndromefromdifferentialdiagnosis
slide35

Cortisolconcentrations at 08.00 and 22.00 normallyshows a circadianrhythmwitheveningsamplehaving a lowervaluethan in themorning

  • Loss of thisrhythmindicatesCushing’ssyndrome
  • Failure of 1 mg dexamethasonetaken at 23.00 tosupress serum cortisollevel at 08.00 thefollowingmorning, orfailuretosupressurinarycortisolsecretionovernight (cortisol/creatinine) is anotherindicator of Cushing’ssyndrome
slide36

Failure of serum cortisoltoriseafterinsulin_inducedhypoglycaemia(0.15 unitsinsulin /kg) is a characteristicfeature of Cushing’ssyndrome

  • InpatientswithpitiutarydependentCushing’sdisease , serum urinarycortisolwill be partiallysupressedafter 2 days of dexamethasone, 2.0 mg q.i.d. (syntheticglucocorticoid)
  • Failuretosupresssuggestseitherectopic ACTH productionorautonomoussecretion of cortisolby an adrenal tm