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Flashcards in Adrenal Gland Deck (18):
1

name the 3 zones of the adrenal cortex, the hormones secreted and what they are regulated by

  • z. glomerulosa
    • secretes aldosterone
    • regulated by AG II
  • z. fasiculata
    • secretes mainly cortisol + some androgens
    • regulated by ACTH
  • z. reticularis
    • secretes mainly androgens
    • regulated by ACTH

2

what does the medulla secrete and what regulates it

  • medulla
    • secretes: epi + norepi
    • regulated by sympathetic control

3

describe CRH

  • released by PVN cells in the hypothalamus 
  • stimulates ACTH synthesis and release from AP

4

describe CRH signalling pathway

cAMP

5

what is ACTH derived from?

POMC

6

ACTH contains _____ in its sequence

  • alpha-MSH is contained in the sequence of ACTH
    • excess ACTH secretion results in hyperpigmentation

7

the precursor for all steroid hormones is _____

most of the cholesterol for synthesis comes from _____

adrenocortical cells have ____ which promotes ___ entry into cells

they are stored as _____ in the cell

the precursor for all steroid hormones is cholesterol

most of the cholesterol for synthesis comes from circulating cholesterol in LDL

adrenocortical cells have lipoprotein receptors which promotes cholesterol entry into cells

they are stored as lipid droplets in the cell

8

describe the MoA of ACTH

  • ACTH binds to receptor and causes increase in cAMP 
  • StAR (steroidogenic active regulatory protein) becomes activated and promotes entry of cholesterol into mitochondria, where cholesterol is turned into pregnenolone
  • also promotes steroidogenic enzymes DNA transcrption 

9

name the short term and long term effects of ACTH

  • short term
    • increases conversion of cholesterol into pregnenolone
  • long term
    • increases number of LDL receptors
    • increases transcription of synthesis enzymes which requires chronic exposure to ACTH
      • clinical application: patients on long term corticosteroid therapy require gradual withdrawal of steroids otherwise they will experience severe glucocorticoid deficiency

10

describe the function of aldosterone synthase (aka CYP 11B)

  • rate limiting step of aldosterone synthesis
  • converts corticosterone into aldosterone in the z. glomerulosa

11

describe the signaling pathway of AG II

IP3/DAG, activates aldosterone synthesis

12

describe the signaling pathway of potassium on aldosterone

Increased ECF K concentration causes depolarization of the cell, which causes release of Ca and activation of aldosterone synthesis

13

describe the signaling pathway of aldosterone at target tissues

Enters the cell nucleus to modulate gene expression, which leads to an increase in enzymes/transport proteins

14

describe the MoA of aldosterone at the target tissue

  • target tissue = distale tubule and collecting duct principal cells
  • adds more Na and K channels at the lumen
    • more Na is reabsorbed (+ H2O)
    • more K is excreted into urine

15

what causes aldosterone release?

  • JGA releases renin based on fluid status (hypovolemic, or hyponatremic)
  • JGA releases renin (ENZYME)
  • renin acts on angiotensinogen and converts it into AG I
  • AG I -> AG II via ACE in the lungs
  • AG II promotes aldosterone in z. glomerulosa

16

describe hyperaldosteronism

  • increased Na and H2O retention in the ECF and excretion of K into urine
  • leads to hypertension because of the increase in ECF
  • H+ from ECF is exchanged for ICF K (for lost K) 
    • alkalosis
    • hypokalemia causing muscle weakness and arrhythmias 
  • hypertension is transient because of renal compensation

17

describe the types of hyperaldosteronism

  • 2 types of hyperaldosteronism
    • primary (Conn's syndrome) caused by an adrenal tumor or hyperplasia of z. glomerulosa
      • decrease in renin (because of negative feedback)
    • secondary causes = hypovolemic states
      • increase in renin

18

describe hyposecretion of aldosterone

 

  • hyperkalemia
    • decreased K excretion
  • increase in ECF K will make cells take up extra K, exchanging for H+ 
    • causes metabolic acidosis
  • Hyponatermia
    • decreased ECF volume and shock