THE ADRENALS - UMF IASI 2015
THE ADRENALS
Anatomy of the adrenal glands:
Adrenal glands, which are also called suprarenal glands, are small, triangular glands located on top of both kidneys. An adrenal gland is made of two parts: the outer region is called the adrenal cortex and the inner region is called the adrenal medulla.
ADRENAL CORTEX: is formed in the weeks V-VI:
Cells are derived from the cells derived from genital crest which will form sterodegenetic cell from adrenal glands and gonads. They develop under the control of genes SF- 1, DAX
ADRENAL MEDULLA: is of neuroectodermic origin
Fetal adrenal glands are formed of 3 zones:
• “definitive” under the capsulla (it produces mineralocorticoids )
• of transition ( glucocorticoids)
• fetal zone has the most important area during fetal life and produces androgens - DHEA-S which are transformed within e placenta into estrogens
• zona glomerulosa and fasciculata are completely formed at 3 years, and zona reticularis at 15 years
The anatomy of the adrenal glands.
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STERODOGENESIS IN THE ADRENAL CORTEX
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Pattern of sterodogenesis within the adrenal cortex
Glucocorticoid synthesis is produced into yona fasciculata
1. Cholesterol is converted into pregnenolone due to an enzyme that produces the clivage of lateral chain of cholesterol and StAR – steroidogenetic acute regulatory protein
2. Pregnenolone is transformed into 17 hydroxi-pregnenolone due to enzyme 17 hydroxilase (C17)
3. 17 hydroxi-pregnenolone in transformed into 17 hyroxiprogesterone due to 3β hydroxysteroid dehydrogenase
4. 17 hyroxiprogesterone is transformed into 11 deoxy-cortisole by 21 hydroxilase
5. 11 deoxy-cortisole is converted into cortisole by 11 β hydroxilase
Androgen synthesis is produced into zona reticularis
1. Cholesterol is converted into pregnenolone due to an enzyme that produces the clivage of lateral chain of cholesterol and StAR – steroidogenetic acute regulatory protein
2. Pregnenolone is transformed into 17 hydroxi-pregnenolone due to enzyme 17 hydroxilase (C17)
3. 17 hydroxi-pregnenolone is transformed into dehydroepiandrosterone due to 17-20 lyase
4. Dehydroepiandrosterone is coverted into androstendione due to 3β hydroxysteroid dehydrogenase
5. a small fraction of androstedione is transformed into testosterone and most of it is transformed into testosterone within peripheral tissues.
Mineralocorticoid bysinthesis
1. Cholesterol is converted into pregnenolone due to an enzyme that produces the clivage of lateral chain of cholesterol and StAR – steroidogenetic acute regulatory protein
2. Pregnenolone is transformed into progesterone due to enzyme 3β hydroxysteroid dehydrogenase
3. Progesterone is converted into deoxycorticosterone under the action of 21 hydroxilase
4. Deoxycorticosterone is convertes into corticosterone due to 11 β hydroxilase
5. Corticosterone is transformed into 18 hydroxi-corticosterone due to 18 hyroxilase (corticosterone methyl oxidase I)
6. 18 hydroxi-corticosterone is converted into aldosterone due to 18 hydrogenase (corticosterone methil oxidase II)
Plasma circulation of adrenal steroids
|Steroid |Production rate |Carrier protein |% free fraction |Plasma concentration |
| | | | |ng/ml |
|Cortisole |8-25 mg/24 h |Corticosteroid-binding | |20-140 (F) |
| | |Globulin (CBG) |3-10 % |40-180 (M) |
| | |Transcortin – 90 % | | |
| | |albumin | | |
|Aldosterone |0.15 mg/24 ore |Transcortin: |40 % aldo |0,15 - 0,17 |
|DOC |0,6 mg /14 ore |20 % aldo and % DOC |24 % DOC |0,15 – 0,17 |
| | |Albumin: | | |
| | |40 %aldo nd %DOC | | |
|DHEA |0,7 mg /14 ore (F) |SHBG | |5,34 ± 1,57 |
|DHEA-S |6-8 mg /24 ore |TeBG | |1130 (F), 1260 (M) |
|Testosterone |0,23 mg/24 ore (F) |Sex hormone – binding | |0,48 ± 0,14 (F) |
| | |globulin | |5,59 ± 1,51 (B) |
|Progesterone | |Transcortin | |11,8 ± 7 (F) |
|Estradiol | |SHBG | |0,18 ± 0,1 (M |
|(conversion | | | | |
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Glucorticoids control
CRH – 41 amino acids and is derived from pre-pro CRH with 192 amino acids
• CRH secreting neurons are located into paraventricular nucleus and have projections to median eminence
• CRH was identified in stomach, pancreas, placenta, adrenals, adrenal medula with unknown actions
• CRH modulates CNS response to stress, norepinephrine liberation and glucagon response
• CRH has excitatory effects on CNS
• CRH through cAMP and vasopresin through PI3 –DAG – PK C stimuleaza concomitent ACTH
• CRH is negatively controlled by cortisole
• CRH stimuleaza secretia de fond a ACTH
• Vasopressin stimulates ACTH response to stress
ACTH
• Immediate sctions: increases cortisole level and that of andrenal androgens
• Long term action: stimulates all steps in the pattern of cortisole synthesis and liberation
• ACTH has lypolitic action and opioid-like actions
• ACTH and melanocortin (MSH) control learning process
• Melanocortin inhibits apetite
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ACTH secretory characteristics
- Nictemeral rhythm : is produce by light/dark exposure
CRH-ACTH-Cortizole are minimal between 0 -3 a.m. and maximum between 6-8 a.m.
- Nictemeral rhythm in impaired by stress,
- depression impaires this rhythm and produces an increased level of both CRH and ACTH permanently
- Rhythm associated with food intake: CRH and ACTH increase before meals
• both CRH and ACTH increase during stress
• cortisole inhibits both CRH and ACTH in the feed-back system controle
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Stress induced CRH-ACTH secretion due to hypoglycemia
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Control of adrenal androgen secretion
ALDOSTERONE
• increases cell membrane permeability for Na and conductance of Na chanels
• stimulates activity of Na/Potassium pump
• stimulates potassium excretion and Na retention in the kidney
• aldosterone produces potassium excretion and Na retention in the small bowel, colon, salivary glands
Control of mineralocorticoid secretion
• RENIN: proteolytic enzyme produced by juxtaglomerullar aparatus and in small amounts in zona glomerulosa with paracrine action
• Renin is increased by sodium loss, low blood pressure, upright position, vasodilatatory drugs, beta stimulation
• Renin acts on renin substrate – angiotensinogen produced by the liver to liberate angiotensin 1 which is converted by the angiotesnin converting enzyme into angiotensin 2 which stimulates aldosterone secretion and produces constriction of arteries
• Potassium ions directly stimulate aldosterone production
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Assessment of adrenal function
|Blood |Urine |Dynamic tests |
|Cortisole |17 OH-CS |ACTH stimulation test |
|Aldosterone |17 KS |DXM inhibition test |
|DHEA, DHEA-S |Free urinary cortisole |OGTT |
|17 – OH progesterone |Aldosteone |Hypoglicemia |
|Testesterone |Pregnandiole |Metopirone test |
| | |CRH stimulating test |
The assessment of adrenal function
Is based on basal and functional tests
The main basal hormones produced by hypothalamic –pituitary –adrenal axis , their values and functional tests are presented in the tables below..
|Assessed hormone |Determination |Normal values |Clinical relevance |
|Plasma cortisole |RIA (radio immuno-|5-20 (g/dl at |Decreased in adrenal insufficiency and congenital adrenal hyperplasia |
| |assay) |h.8 a.m. |Increased in Cushing’s syndrome, stress, depression, alcohol consumption, |
| |enzyimo | |kidney and liver failure |
|Salivary |RIA |Depends of the |Same variation as free crotisole. Good method for children |
|cortisole | |method | |
|17-hidroxi |RIA enzymo |Depends of the |Increased in congenital adrenal hyperplasia (CAH) due to 21 hydroxilase and 11 |
|progesterone | |method |hydroxilase deficiency |
|11 deoxi |RIA |Depends of the |Increased in CH due to 11 hydroxilase defficiency |
|cortisole | |method | |
|Testosterone |RIA enzymo |According to |Increased in CAH due to 21 hydroxilase and 11 hydroxilase deficiency and in |
| | |the sex |androgen-secreting adrenal tumors |
|dehidroepi |RIA |According to |Increased in CAH due to 21 hydroxilase and 11 hydroxilase, 3β OH-DH and in |
|androsterone | |the sex |androgen-secreting adrenal tumors |
|DHEA | | | |
|delta 4 |RIA |According to |Increased in CAH due to 21 hydroxilase and 11 hydroxilase deficiency and in |
|androstendione | |the sex |androgen-secreting adrenal tumors |
|Free urinary |enzymo |25-95 ng/g |Same variation as plama cortisole |
|cortisole | |creatinine | |
|17 OH |fluorimetric |3-7 mg/24 h |incresed: Cushing’s syndrome, obesitaty, alcohol consumtion, depression |
|cortico |Porter-Silber | |decreased: adrenal failure and CAHs |
|steroids | | | |
|17 Ketosteroids |fluorimetric |females: 6-10 |incresed: Cushing’ syndrome, most of CAH syndromes |
| |Zimmerman |mg/24 h |decreased: adrenal insufficiency |
| | |malesi: 16-20 | |
| | |mg/24 h | |
|ACTH |RIA |10-20 pg/ml at | ................
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