Adrenal Glands and Addison's

8/13/2019 Adrenal Glands and Addison's

1/6

ADRENAL GLANDS Adrenal glands have

a)Cortexcortex has two functional parts:

1)Zona fascicular/reticularissecretes glucocorticoids and androgens

2)Zona Glomerulosasecretes mineralocorticoidsb) Medullasecrets adrenaline and noradrenalin

Control of the adrenal glands is gien the !ox"

S#nthesis of adrenal hormones


2/6

Glucocorticoids$

Cortisol is the major glucocorticoids in the humans.

Cortisol levels are highest in the morning and lowest in the night.

Glucocorticoids increase or stimulate follo%ing

luconeogenesis

l!cogen deposition

"rotein catabolism

#at deposition


3/6

Mineralocorticoids$

Aldosterone is the predominant mineralocorticoid.

Aldosterone increases the $a%reabsorbtion and increases &%and ' %excretion.

Aldosterone is important is blood pressure regulation( and is controlled b! the AA*

s!stem

Androgens$ Androgens are important for pubert!.

Androgens are regulated b! the same '"A axis.

Catecholamines$

+nl! small portions of catecholamines are secreted b! the adrenal medulla( the! are

mainl! secreted b! the nerve endings.

ADD&S'N(S D&SEASE

Etiolog#

Clinical features$

Asthenia is the cardinal s!mptom. wea,ness( anorexia ma! be other features.

-nexplained weight losss

$ausea( vomiting( chronic diarrhea

'!perpigmentation .

/t commonl! appears as a diffuse brown( tan( or bron0e dar,ening of parts such as

the elbows or creases of the hand and of areas that normall! are pigmented suchas the areola about the nipples.

luishblac, patches ma! appear on the mucous membranes.

'!per pigmentation is due to AC' excess( so h!per pigmentation is not feature

of secondar! adrenal in sufficienc!

3itiligo ma! paradoxicall! be present in patient with autoimmune Addison4s disease

)rimar# *+AC,-.

Autoimmune *poradic(

"ol!glandular s!ndromes

uberculosis

'/35A/6*

7etastatic carcinoma

ilateral adrenalectom!

Rare causes 8!mphoma

/ntraadrenal haemorrhage

Corticosteroid !ios#nthetic en#me defects

Congenital adrenal h!perplasias

6rugs met!rapone( ,etocona0ole (etc

Secondar# *0AC,-.

ithdrawal of suppressive glucocorticoids

therap!

'!pothalamic or pituitar! disease


4/6

Arterial h!potension with postural accentuation is fre;uent . "ostural h!potension is

usuall! ver! earl! sign

Axillar! and pubic hair ma! be decreased esp. in women.

Clinical features of acute Addison(s disease are:

1. unconsciousness2. Circulator! shoc, with h!potension.

3. 3omiting and diarrhoea.

&nestigations$

1. AC,- stimulation test:

his test is done to confirmadrenal insufficienc!

2


5/6

'/3 I8/*A.

/maging of the adrenals b! C or 7/ to identif! metastatic malignanc!

Management$

reatment of adiisons disesease is life long replacement of glucocorticoids.

eplacement doses and advice to patient of Addison4s disease are

"rednisolone B.< mg dail! 9< mg on wa,ing( 2.


6/6

+ral replacement medication is then started( unless unable to ta,e oral medication(

initiall! h!drocortisone 2= mg( Fhourl!( reducing to 2=>= mg in divided doses

over a few da!s.

C'NGEN&,AL ADRENAL ->)ER)LAS&A*CA-. +ne of the important cause of h!poadrenalism.

CA' is autosomal recessive disorder( deficienc! of en0!mes of cortisol s!nthesis.

Commonest deficienc! is 21h!drox!lase resulting in reduced levels of cortisol and

increased of AC'.

Clinical features

1. ;emales: ambiguous genitalia( clitoromegal! and h!poadrenalism.

2. Males$ enlarged penis and increased pubic hair and h!poadrenalism.

3. 6eficiencies of 11 h!drox!lase and 1B h!drox!lase present with h!pertension.

&nestigations$ educed levels cortisol and increased levels of 1B h!drox!progesterone and AC'.

+ther investigations are same as Addison4s disease.

Management$

eplacement of glucocorticoids is the main sta! therap!. aim is to suppress the

AC'.

6oses of steroids are same as addisons but higher dose is re;uired in the night and

lower in the morning

Documents

Adrenal Glands and Addison's