ADRENAL

Anatomy
A pair of triangular structures
Superomedial of the kidney
Cortex and medulla

The adrenal cortex

from mesodermal splanclic
steroidogenesis

The adrenal medullla

from neural crest cells
cathecolamines
GLOMERULOSA FASCICULATA RETICULARIS

Cholesterol Cholesterol Cholesterol

Regnenolone Pregnenolone Pregnenolone

Progesterone 17-OH- 17-OH-

pregnenolone pregnenolone

Deoxycortico- 17-OH-
sterone progesterone

Dehydroepi-
Corticosterone 11-deoxycortisol androsterone

aldosterone cortisol androstenedione

Glucocorticoid

Steroid adrenal, main effect : carbohydrate metabolism

In human : cortisol (hydrocortison) has a role in almost

all glucorticoid activity

Secretion : 20 mg/day

Corticosterone : a weak glucocorticoid

cortisol has metab effect for almost all tissues

Effect of ACTH

The adrenal cortex :

Activate adenylate cyclase & c-AMP

cholesterol synthesis; uptake protein by cortex

adrenal; RNA. DNA & protein synthesis

Chronic stimmulation of ACTH hyperplasia &

hyperthrophic of adrenal cortex

Extra adrenal effect :

Secretion MSH (melanocyte stimmulating hormone)
Cortisol secretion

1. Diurnal variation :

2. Cortisol feed-back :
Blood GCC ACTH
Exogenous GCC ACTH

3. Stress (physical & psychological) :

sress ACTH cortisol

GCC effects :

- Gluconeogenesis
- lipid & protein catabolism
- redristribution & depostition of body fat in adipose tissue
- lysis of lymphoid system lymphocytes in circulation
- eosinophil & basophil suppression
- neutrophil
- osteoporosis (osteoblast activity)
- GCC : - sufficient amount : normal muscle function
- hypo- / hyper- : muscular weakness
- Pharmacological dose : potent effect to inflammatory &
immune respons.
- High dose : suppress the inflammatory & immune response
Cortisol transportation

Mostly bound to CBG = corticosteroid-binding globulin

(α-glob, produced by liver) and to albumin.
Small amount : free cortisol

estrogen CBG circ. cortisol :

free cortisol : N

liver disease
CBG circ. cortisol :
nephrotic syndr free cortisol : N
Cortisol catabolism

Half life : ± 90 mnts

it’s bound to CBG

Catabolism : in the liver

Excreted : urine (17- hydroxycorticosteroids)

CUSHING ‘S SYNDROME
Hypercortisolism (cortisol )

Cushing disease : primary hypercortisolism

(from pituitary)
Etiology :
-Exogen : administration of supraphysiologic doses of CS
in long term
-Endogen : - pituitary tumor ( 60-70%)
- adrenal tumor (20%)
- nonendocrine tumors ACTH-like substance :
> Oat cell Ca (lung tumor)
> Carcinoid bronchial adenoma
> Prostat / Ovarium Ca
> Pancreas Ca
Cushing’s syndrome
Clinical manifestations :

1. Habitus : obesity (trunk, buffalo hump, supracavicular

and abdominal), moon face
2. Hypertension (mineralocorticoid effect & increase sensitivity
to catecholamine)
3. Muscular weakness
4. Easy bruising, skin hyperpigmentation
5. Osteoporosis
6. Glucose intolerance
7. Androgen acne, hirsutism, amenorrhoe
8. Striae lividae
9. Psychiatric manifestation
Cushing’s disease
Diagnosis :
Clinical app : habitus, striae, aosteoporosis, hypertension

1. Exogenous : history of usage of CS drugs

blood cortisol & ACTH at 8.0 a.m
2. Endogenous : 2 steps
a) screening test : dexamethasone test
1 mg of dexamethasone at 10 p.m (po)
morning at 8 a.m : blood cortisol level
Normal response : cortisol < 5 µg/dl
Cushing’s disease : no cortisol suppression
Diagnosis :
Liddle test :
0.5 mg (po) dexamethasone every 6-h intervals – 48 h
24-h urine samples for 17-OCHS
(before and during dexamethasone administration)

Normal : urine 17-OCHS

Cushing’s dis: fail to suppress

b) Definitive test
1. Cortisol & ACTH level without dexamethasone adm
2. Metyrapone test
Diagnosis :

Radiologic diagnosis :
1. X- ray : sella turcica
2. Adrenal angiography & venography :
uni/bilateral ?
3. Scanning

Treatment :
1. Surgery
2. Pituitary irradiation
3. Drugs : metyrapone ( inhibits 11-β hydroxylase )
- pre-operative
- inoperable adrenal Ca
- ectopic tumor with unknown sites or has
already metastated