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What is the average size of the adrenal gland ( width,length,thickness and weight)?

2-3cm wide. 4-6cm long. 1cm thick. Average weight of 4g


What are the 3 layers of the adrenal cortex?

Zona glomerulosa. Zona fasciculata, Zona reticularis.


What are the relative proportions(%) of the outer cortex and central medulla of the adrenal gland?

~90% and ~10% respectively


Which hormones are secreted by the medulla?

Adrenaline(80%) and noradrenaline(20%)


What does the adrenal cortex produce?

Steroid hormones


What does each layer of the adrenal cortex produce specifically?

zona fasciculata= glucocorticoids( so makes cortisol)
zone reticularis= androgens
zona glomerulosa= mineralocorticoids


Which enzyme is absent in each of the 3 layers of the adrenal cortex specifically?

zona fasciculata= lacks aldosterase synthase
zona reticularis= lacks aldosterase synthase
zona glomerulosa= lacks 17 alpha hydroxylase


Describe the regulation of synthesis for cortisol.

The hypothalamus releases CRH. This stimulates the corticotrophs of the anterior pituitary to release ACTH.
ACTH stimulates the adrenal cortex to synthesize and release cortisol.
Negative feedback mechanism for control: cortisol feeds back to the corticotrophs to decrease acth release and on the hypothalamus to inhibit release of CRH.


What is ACTH derived from

Pro-opiomelanocortin (POMC)


Name 2 factors that stimulate hypothalamus to produce CRH

cicardian rhythms


What is the half life of cortisol?



What is the half life of aldosterone ?



What is the role of steroid receptors in bringing about increased protein synthesis?

Steroid hormones interact with nuclear receptors. Steroid hormones enter cells by diffusion and bind to the cytoplasmic receptor, leading to dissociation of heat shock protein( hsp90) from the receptor. The hormone-receptor complex dimerises and is translocated to nucleus. The complex binds to hormone responsive element (HRE) on DNA which leads to an increase in mRNA production and therefore increased protein synthesis.


What is the general effect of glucocorticoids?



What is the role of the mineralcorticoid receptor in preventing cortisol activation?

Once cortisol binds to the receptor, it is converted to an inactive form called cortisone. The enzyme beta-HSD is needed for this conversion.


What are the two isoforms of 11beta-HSD , where are they expressed and what do they do?

11Beta-HSD1 : expressed in liver,adipose, muscle. Converts cortisol to cortisone

11Beta-HSD2 : expressed in aldosterone sensitive tissues.(kidney,colon,salivary glands)


What are some adverse effects of glucocorticoids

-suppression of response to infection.
-suppression of endogenous glucocorticoid production.
-metabolic effects
-iatrogenic Cushing's syndrome


What are some of the characteristics of Cushing's syndrome?

Red cheeks, moon face, fat pads, bruisality/ecchymoses, hypertension, thin skin, red striation, thin arms and legs,pendulous abdomen, poor wound healing,osteoporosis, negative nitrogen balance, increased appetite, obesity,increased susceptibility to infection,neuropsychiatric effects, menstrual disorders, impotency,glucose intolerance, diabetes


What is Cushing's syndrome

A hormonal disorder caused by prolonged exposure of the body's tissues to high levels of cortisol


How can we treat Cushing's syndrome?

-METYRAPONE: 11Beta hydroxylase inhibitor
-KETOCONAZONE: (withdrawn in europe) inhibits steroid biosynthesis
-PASIREOTIDE (somatostatin analogue) SSTR5 agonist.
-CABERGOLINE( dopamine D2 agonist)
-MIFEPRESTONE (glucocorticoid receptor antagonist,progestogen receptor antagonist)


What is Addison's disease.

'Chronic adrenal insufficiency'
hypocortisolism. A long-term endocrine disorder in which the adrenal glands do not produce enough steroid hormones.


What are some of the clinical features of addisons disease?

- weakness,fatigue,anorexia,weight loss
-gastrointestinal disturbances
-salt craving
-postural symptoms


What is the treatment for Addinson's disease

Replacement therapy with fludrocortisone


What in general do hormones do?

stimulate cell function
inhibit cell function
stimulate/inhibit cell growth or differentiation
maintain physiological state


Describe the endocrine hierarchy

1.) Hypothalamic hormone
2.)Pituitary hormone
3.) Target hormone
4.) End organ effects


Describe the thyroid axis.

1.) hypothalamus,releasing factor: TRH= thyrotropin releasing hormone
2.) Pituitary,trophic hormone: TSH= thyroid stimulating hormone
3.) Target organ-thyroid: T4 (thyroxine) and
T3( triodothyronine)
4.) End organ(s): Basal metabolic rate, pulse


Which thyroid hormone is the active hormone?

T4 is converted to T3 by deiodinaton which acts on the end organ as T3 is more active and has a longer half life.


Describe the different classes of hypothyroidism deficiency.

-Primary: thyroid deficiency, so the end organ receives less hormone. The hypothalamus and pituitary are still working fine.
-Secondary:pituitary deficiency: so less stimulation of the thyroid (TSH) but TRH levels remain high
-Tertiary: hypothalamic deficiency: so less stimulation of the pituitary (by TRH), so less TSH released. This is RARE,


Describe the sella turcica.

A 'pocket' within the sphenoid bone. This pocket is called pituitary fossa and is a bony cavity.


What hormones does the posterior pituitary make?

Oxytocin and ADH