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Adrenal Gland Final 2

Adrenal Gland Final 2

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Published by: Std Dlshsi on Feb 13, 2011
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07/12/2013

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SUBJECT: PHYSIOLOGY
 
TOPIC: Adrenal GlandLECTURER:
DR. VIC MENDOZA
DATE:
FEBRUARY 2011
Adrenal Gland
 
Remember:
the
blood supply
of the adrenalgland is designed in such a way that theblood passing through the cortex will also bethe same blood that will pass through themedulla
 
o
 
This means that the medulla is alsoexposed to the hormones producedby the adrenal cortex!
 
 
Embryologically 
 
The cortex is
mesodermal,
whereas themedulla is
neuroectodermal 
in origin.
Adrenal Cortex
 
About 80‐90% of the weight of the gland
 
Secretes 3 classes of steroid hormones
[notstored but synthesized as needed]
o
 
Because there is no storage, thereare no pre‐formed hormones thatcan be secreted right away.Although it takes longer, steroidhormones have a longer‐lastingeffect compared to other hormonesanyway.
 
Glucocorticoids, mineralocorticoids and sexhormones
 
Recall Histology:
3 layers of the cortex 
 
o
 
Zona Glomerulosa, Fasciculata andReticularis
o
 
Glomerulosa: synthesis andsecretion of 
mineralocorticoids
 
o
 
Fasciculata:
glucocorticoids
 
o
 
Reticularis:
sex hormones
 
 
Also, recall that the
rate‐limiting step
in theformation of steroid hormones is the
conversion of cholesterol to pregnenolone.Mineralocorticoids
 
For regulation of water and sodium,potassium ion concentrations
 
Regulation of normal acid‐base balance
 
Main mineralocorticoid:
ALDOSTERONE
 
Aldosterone
 
A steroid hormone responsible forregulating
sodium reabsorption
in the distaltubule and the cortical collecting duct
 
 
Target cells:
Principal [P] Cells
 
Stimulates the synthesis of Na/K‐ATPasepump
 
Furthermore,
ALDOSTERONE
:
 
Promotes the retention of sodium and water[hand‐in‐hand]
o
 
Chloride is also retained togetherwith bicarbonate
(This consequently affects acid‐basebalance.)
 
Promotes the loss of potassium through thekidneys and hydrogen ion
(These are also responsible for how Aldosteroneaffects acid‐base balance)
 
 
 
Direct stimulators:
o
 
Increased extracellular potassium
o
 
Decreased osmolality
 
Indirect stimulators [RAAS]
o
 
Decreased blood pressure
Reduction in kidney perfusion thusresulting in INCREASED Renin production, which acts on Angiotensinogen to eventually yield  Angiotensin II. This can then stimulatethe adrenal cortex to produce morealdosterone.
o
 
Decreased macula densa blood flow
 
RAAS: Renin Angiotensin‐Aldosterone System
Glucocorticoids
 
3 classes of glucocorticoids:
o
 
Cortisol [major glucocorticoid!]
o
 
Corticosterone
o
 
Cortisone
 
CORTISOL
o
 
A steroid hormone that is plasmabound to
corticosteroid bindingglobulin
[CBG or transcortin]
o
 
Essential for life
o
 
Net effects of cortisol are
catabolic 
:
prevents hypoglycemia
 (very low glucose in the bloodstream)
 
A person cannot survive for a long timewithout glucocorticoids in the body.
If adrenal glands are removed, there will be aneed for exogenous supply
Net effects of cortisol are
catabolic
They circulate bound to a globulin but being steroid hormones, they are capable of crossing cell membranes. When they detach to CBG, they cancross the cell membrane because of receptors insidethe cell membrane. Once they enter the nucleus of the cell, they can promote transcription.
 
 
Physiological actions:
(how it prevents hypoglycemia)
 
 
Promotes gluconeogenesis
[primarily amino acids coming from catabolismof skeletal muscle thus providing substrates for gluconeogenesis]
 
 
Promotes breakdown of skeletal muscleprotein
 
Enhances fat breakdown [lipolysis]
 
Suppresses immune system
[at pharmacological doses: reduces phagocyticactions of WBCs]
 
 
Breakdown of bone matrix
[High doses; like when exogenous glucocorticoidshad been administered. Fracture is therefore aside‐effect of prolonged use of high doseglucocorticoids.]
 
Reduces fever
 
Suppresses allergic reactions
 
Widespread therapeutic use
[Primarily because it CAN suppress immuneresponse. Disease entities promoted by inflammation will be affected, such as bronchial asthma or lupus, or patients who haveundergone a transplant. Suppression of immunesystem is needed so that the body will not reject the transplanted organ.]
 
 
Decreases formation of connective tissue
 
[Thus weakening it. Eg capillaries with CT in itswalls. High doses of glucocort can cause thesupporting CT to disappear leading to
easy bruisability 
 ]
 
 
Enhance vascular responsiveness tocatecholamines
 
Inhibit bone formation
 
Increase GFR
[Can promote free water clearance in thekidneys]
 
 
Decrease REM sleep
[Modulates wakefulness of a particular person]
 
 
Influences brain function: states of cortisolexcess or deficiency cause mood changesand memory and learning alterations
Cortisol Effects:
 
Regulation of Cortisol Release
 
Cortisol release is regulated by the
ACTH
[secreted by the anterior pituitary;
pulsatilesecretion
; diurnal rhythm]
 
Release follows a daily pattern—Circadian
Since ACTH secretion is pulsatile, it follows that cortisol seems to have a similar pattern.
 
Negative feedback by cortisol inhibits thesecretion of ACTH and CRH [regulation of their relationship]
 
Cortisol also promotes negative feedback tothe hypothalamus
 
CRH acts on Anterior Pituitary; it stimulatessecretion of ACTH

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