Download MBBS Adrenal Cortex Lecture PPT

Download MBBS (Bachelor of Medicine and Bachelor of Surgery) Latest Adrenal Cortex Lecture PPT


ADRENAL CORTEX
Anatomy of Adrenal gland

? The 2 adrenal gland wt. about 4gm lies at the

superior pole of the two kidney.

? Each gland composed of two distinct parts ,

the adrenal medulla, and the adrenal cortex.

? Adrenal medulla secretes Catecholamines

and Adrenal cortex steroid hormones.

? Blood supply by superior, middle and inferior

adrenal arteries

Histology and Develpoment

? The adrenal cortex in adult comprises 3

distinct zone:

? Zona glomerulosa(outermost), 15%

? Zona fasciculata(middle zone),50%

? Zona reticularis(innermost zone),7%

? The adrenocortical cells contains abundant

lipids, especially in outer portion of zona fasci

culata.
Section of Adrenal gland showing

medulla & zones of cortex
Contd.

? Fetal adrenal gland begins developing 3-4 wks of gestation

? At 6-8wks ,there is rapid enlargement of adrenal gland.

? Cells of cortex differentiate to form `fetal zone' and an

outer layer called definitive zone

? Fetal zone is capable of synthesizing steroids at 8-10 wks.

? At birth : Fetal cortex, 80% of the gland with 20% true

cortex.

? Within 1 months after birth: fetal cortex 50% and adrenal

medulla increases in size.

? ACTH regulates growth and development of adrenal gland
Adrenal cortex

? Secretes two major hormones

:mineralocorticoids and glucocorticoids, and

small amounts of sex steroids especially

androgenic hormones.
Structure of Adrenocortical hormones

? The hormones of adrenal cortex are

derivatives of cholesterol.

? Contains Cyclopentanoperhydre

phenanthrene nucleus like cholesterol, bile

acid ,vit.D, ovarian and testicular steroid
Contd.

? Gonadal and adrenocortical steroids are of 3

types: C21,C19,C18 steroids

? The adrenal cortex secretes primarily C21 &C19

steroids.

? C19 steroids have keto group at position 17 ,so

called 17-ketosteroid,they have androgenic

activity.

? C21 steroid have hydroxyl group at position 17 in

addition to side chain , hence called 17-

hydroxysteroid.have both moneralocorticoid and

glucocorticoid activity.
Basic structure of adrenocortical and

gonadal hormone
Steroid Biosynthesis

? The precursor of all steroids is cholesterol.
? Some is synthesized, but most are taken up

from LDL in the circulation.

? LDL receptors are especially abundant in

adrenocortial cells.

? ACTH facilitates cortisol synthesis by

activating enzyme cholesterol ester hydrolase.

Synthesis of mineralocorticoids

? Mineralocorticoids are formed in zona

glomerulosa of adrenal cortex.

? The conversion of cholesterol to pregnenolone is

stimulated by ACTH and angiotensin II.

? Aldosterone synthesis is limited to this zone b'coz

aldosterone synthase is found only in cells of

zona glomerulosa.

? Zona glomerulosa lacks enzyme 17-hydroxylase,

hence glucocorticoids and sex steroid are not

formed here.
Cholesterol

ACTH,ANG II

Pregnenolone

Progesterone

Deoxycorticosterone

Corticosterone

Aldosterone synthase,

18-Hydroxycorticosterone

Ald . synthase

Aldosterone
Function of mineralocorticoid-

Aldosterone

? Aldosterone is very potent and accounts for

about 90% of mineralocorticoid activity.

? Deoxycorticosterone is 1/30 as potent as

aldosterone ,but very small quantity secreted..

? Aldosterone increases renal tubular

reabsorbtion of Na+ and secretion of K+

especially in the principal cells (P cells)of

collecting tubules, and lesser extent in DT and

collecting ducts.
Functions of aldosterone

? Aldosterone is very essential for life.
? It maintains the osmolarity and volume of ECF.
? Main function of aldosterone are:

?Reabsorbtion of Na+ from renal tubules

?Excretion of K+ and through renal tubules

? Secretion of H+ into renal tubules.

?Also es Na+ reabsorbtion from sweat ,

Saliva , and contents of colon.
MOA Of Aldosterone

? Like other steroids. Aldosterone binds to

cytoplasmic receptor.

? HR complex moves to nucleus.

? Transcription of mRNA.

? production of proteins that alter cell functions.

Contd.

Aldosterone stimulated proteins leads to:
Genomic actions like
? es activity of ENaCs (epithelial Na+ channels),a

rapid action.

? Slower effect is that it increases the synthesis of

ENaCs , by ing the mRNA activity for synthesis of

proteins.

? es insertion of these channels on cell membrane.
? Gene activated by aldostrone is sgk gene ,a serine-

threonine protein kinase.

? Non-Genomic Actions: mediated by IP3

? Nongenomic actions occurs rapidly.

? It es activity of Na+K+exchangers,which

Increases intracellular accumulation of Na+
What is Aldosterone escape

phenomenon ?

? When there is aldosterone excessive

secretion the ECF expands due to Na+ and

water retention , but when the ECF expansion

passes a certain point ,Na+ excretion is

usually ed inspite of continued action of

mineralocorticoids on renal tubules.
Mechanism

? Mineralocorticoid/aldosterone excess.

? ECF expansion(due to Na+ & water retension).

? BP rises leading to distention of atria.

? Secretion of ANP(atrial natriuretic peptide).

? ANP causes profound natriuresis and diuresis.
Contd.

? ECF returns back to normal.

?Due to this phenomenon edema is not

produced by mineralocorticoids in normal

individual and in patients of

hyperaldosteronism.
Regulation of Aldosterone Secretion

? Aldosterone secretion is regulated mainly by

3 important stimuli:

1. ACTH

2. Angiotensin II

3. Plasma K+ conc.

RAAS system
RAAS system

? Angiotensinogen

Renin(JGA)

Angiotensin

ACE(lungs)

Angiotensin II

Adrenal cortex

Aldosterone

Na+ and water retention,es ECF volume
ACTH

? Cells of zona glomerulosa have ACTH

receptors.

? ACTH mediates aldosterone secretion by

cAMP& Protein kinase.

? Effect of ACTH on aldosterone secretion is

temporary , aldosterone secretion declines

even if ACTH secretion is elevated ,due to

decrease renin secretion.
Plasma K+ Conc.

? Plasma K+ level need increase only 1meq/L to

stimulate aldosterone secretion.

? Like angiotensin II, K+ stimulates the conversion

of cholesterol pregnenolone ,&

deoxycortecosteronealdosterone.
? ECF K+ Activate voltage gated Ca channel

cytosolic Ca

aldosterone secretion
Dysfunction Of Aldosterone

Primary
? Hypersecretion
Secondary
Primary Hyperaldosteronism
? The cause of excess aldosterone secretion is

due to adrenal disease : Adrenal adenoma

? Adrenal hyperplasia

?Adrenal carcinoma
Conn's Syndrome

? Major cause of primary hyperaldosteronism.
? Occurs due to the tumor(adenoma) of zona

glomerulosa of adrenal cortex.

? Clinical features: Hypertension

? Muscle weakness

? Polyuria

? Edema is absent

? Hypokalemia

? Hypernatremia
? Low renin level

? Metabolic alkalosis
Secondary Hyperaldosteronism

? ed aldosterone secretion is due to activation

of RAAS .

? Occurs in cirrhosis, heart failure, nephrosis,

renin secreting tumor.

? renin in plasma.
? Edema is a usual feature.
Hyposecretion of Aldosterone

Addison's disease/Primary Adrenal Insufficiency
? Occurs due to autoimmune inflammation of

adrenal gland, tuberculosis.

? Deficiency of mineralocorticoids occurs.Leading

to hyponatremia , hyperkalemia, ECF,

metabolic acidosis, cardiac output,BP.

? Also there is glucocorticoid deficiency, so patient

is unable to maintain blood glucose conc.

Contd.

? Circulating ACTH levels are elevated, leading to

melanin deposition , so there is pigmentation of

palm creases, lips ,gums etc.

? Untreated patient may die in 4days-2wks.
? Treatment: Mineralocorticoid & Glucocorticoids

replacement.

?Addisonian Crisis : Glucocorticoid level does not

during stress in addison's disease patients e.g.;

trauma, surgery etc leading to severe debility.


Contd.

? Secondary adrenal insufficiency: caused

by pituitary disease and decrease ACTH

secretion.

? Tertiary adrenal insufficiency : caused by

hypothalamic disorders disrupting CRH

release.

? Pseudohypoaldosteronism : produced when

there is resistence to action of aldosteronism.

This post was last modified on 30 November 2021