Adrenal medulla and adrenaline stress axis Flashcards by Issy Garratt

acute stress

rapid
sympathetic
release of adrenaline and noradrenaline

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chronic stress

HPA axis

release of steroids

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adrenal glands

just aboe kidneys
adrenal cortext: secretes steroid hormones
adrenal medulla: adrenaline etc

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structure of adrenal glands

capsule
zona glomerulosa
zona fasiculartis
zona reticuaris
medulla

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zona glomerulosa
small close cells
makes steriods

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biggest part
cells arranged radially in cords
makes steriods too

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small cells

network of interdigitating capillaries

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adrenal medualla

chromaffin cells
dense granules
makes opiods and enkephalins

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chromaffin cells

innervated by preganglia nerves ending in a cholinergic synapse
secrete adrenaline and noradrenaline

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synthesis of adrenaline and noreadrenaline

synthesized in the medulla in an enzymatic pathway – – converts the amino acid tyrosine into a series of intermediates then epinephrine.

Tyrosine is first oxidized to L-DOPA, which is subsequently decarboxylated to give dopamine. - Oxidation gives norepinephrine.
methylation of the primary amine of norepinephrine using PNMT

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release of adrenaline and noradrenaline

Adrenocorticotropic hormone (ACTH) and the sympathetic nervous system stimulate the synthesis of adrenaline precursors
ympathetic nervous system, acting via splanchnic nerves to the adrenal medulla, stimulates the release of adrenaline
NO NEG FEEDBACK

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actions of adrenaline

increased HR and BP

increased metabolism

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three types of adrenaline receptor

A1: intestine leading to contractions
A2: decreases insulin
B1: increased HR and skin contraction

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example of an effect of adrenaline

mobilisation of energy in the form of glucose

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define catecholamines

dopamine
adrenaline
noreadrenaline

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what hormones does the arenal cortext make?

cortisol, aldosterone, androgens

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whats the roleof cortisol

glucocortiocoid

action of carbohydrate metabolism and the response to stress

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role of aldosterone

regulates salt and water balance

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glucocortiocoid

cortisol

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mineralcoirtiocoid

aldosterone

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describ the hypothalamopituitary axis

organises appropriate hormonal responses by the pituitary to signals made by higher centres in the brain
pit connected to hypothalamus, blood flow in hypophyseal portal transports releasing factors to the pit where its stimulated to make relevant hormones

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which cells in the ant pit are we looking at here

adrenocortiotrophs

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describe the HPA stress axis

stress related stimuli leads to secretion of corticotrophin releasng hormone from hypothalamus
stimulates pituitary to secrete ATCH, adrenlocortioctophic hormone
this stimulate the adrenal cortext to make cortisol

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describe ATCH

a peptide hormone in the family of melanocortins

made as a large precursor and browen down into ATCH and POMC

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role of ZG

secretes aldosterone

role of ZF

secretes cortisol

role of ZR

secretes sex steriods/androgens

what does ATCH do when it reaches the adrenal gland

stimulates the adrenal cortext | - conversion of cholesterole to prenelalone in ZF and ZR

negative feedback on HPA axis

cortisol exerts neg feeback to turn off secretion of CRH and ATCH (pituitary and hypothalamus neg feedback)

circardian rhythms and cortisol

plasma cortisol low around midnight, ax day time but slowly falls throughout the day

transport of cortisol

complexed with corticosteroid binding globulin

main effects of cortisol

- catabolic homrone modules carb, fat and protein metabolism increasing blood glucose

other extra effects of cortisol

stimulates appetite | anti-inflmatory

dysfunctions of cortisol

over production- cushings syndrome

cushings syndrome

over production of cortisol | can be due to steriod medication

cushings disease

benign tumour of ptuitary leading to excess cortisol | it is CRH producing

symptoms of too much cortisol

central obesity due to cortisol stimulating appetite thinning of skul bruising hypertension

diangosis of cushings syndrome

measurement of cortisol/ATCH in urine or plasma

what do normal or low ATCH conc in urine or plasma mean

cushings sundrome but adrenal tumour or steriod medication is leading to the disease

what do high ATCH level in urine or plasma show

ectopic ATCH producting tumour

dexametasome text

low dose will supress ATCH in normal patients but not in cushings disease

treatment of cushings

reduce steriod meds removal of tumor adrenalecomy

under production of cortisol

complicated and presents as addinsons disease

long term stress response of glucocortiocoids

cortisol | fats and proteins broken down into glucose

long term stress mineralocoriocoids

retention of Na and water by kidneys | increased blood vol and BP

short term stress adrenaline and noreadrenaline

glygocen broken down, increased blood glucose | incrased BP and breathing rate and metabolic rate

where is aldosterone made

in the zone glomerulosa

what does aldosterone affect?

distal tubule and collecting ducts of kidney | increases Na resorption

how does aldosterone lead to more Na resorption

intracllular binding leads to transcription of gene | NA transporter protein made and moved to kidney

low sodium diet

higher aldosterone

high sodium diet

lower adosterone and thinner ZG in adrenal gland

what is the rennin-angiotensin system

hormone system that regulates blood pressure and fluid balance.

describe the renin-angiotensin system

renal blood low flow juztaglomerular cell convert pre-renin to renin and secrete into blood this then convers antiotensin to angiotensin 1 which then converts angiotensin 1 into 22 by using ACE

role of angiotensin 2

potent vasoconstrictor peptide that causes blood vessels to narrow inceasing blood pressure also stimulates aldosterone secretion

how do aldosterone and renin-angiotensin work together?

renin-angiotensin system work to stimulate aldosteron to be secreted and then both work togther to increase extracellular fluid volume which will increase the blood pressure. angiotensin also constricts blood vessels to raise BP

excessive mineralcortiocoid

adrenal tumour making alodsterone excessive renin excess ATCH stimulating steriodogenesis

symptoms of excess mineralocortiocoid

too much Na retention leads to hypertention - raised BP burry vision

conns syndrome

aldosterone secreting tumour, adenoma of adrenal cortext | causes hyper-aldosteronism ( high aldosterone)

addinsons disease

adrenal failure | might be autoimmune or inflamatory or heamahaggic

why is addinsons complex

``` lack of all - glucocortiocoids - mineralcoiroiods - adrenal adrogens leads to lots of varied symptoms ```

treatment for addinsons

hydrocortiosone to replace cortisol | administration of mineralicorticoids to replace loss