Adrenal Gland Physiology & Disorders Flashcards
Where are the adrenal glands located ?
Sit superior and medial to upper pole of kidneys
What are the 2 main anatomical areas of the adrenal glands ?
outer Cortex and a central medulla
What is produced in the cortex of the adrenal gland ?
Cortex has 3 zones:
- Zona Glomerulosa produces - Mineralocorticoids (mainly aldosterone)
- Zona Fasciculata produces - Glucocorticoids (mainly Cortisol)
- Zona Reticularis produces - Sex Steroids + Glucocorticoids (mainly cortisol)
What are the main hormones produced by the adrenal medulla ?
Catecholamines by chromaffin cells :
- Adrenaline
- Noradrenaline
- Dopamine
What are the affects of adrenaline & noradrenaline on the body (hint they bascially function the same way)
- Increase HR & force of heart contractions, increasing blood flow to the muscles and brain
- Relax airway smooth muscles
- Assisting in glucose (sugar) metabolism.
- They also control the squeezing of the blood vessels (vasoconstriction), helping maintain blood pressure and increasing it in response to stress.
- Also often activated in physically and emotionally stressful situations when your body needs additional resources and energy to endure unusual strain.
Describe the hypothalmic, anterior pituitary gland axis in the control of cortisol and androgens
What is the release of aldosterone controlled by ?
Renin-angiotensin system
What are the major actions of glucorticoids on the metabolic system, bones/connective tissues and circulatory/renal system - cortisol in particular ?
Metabolic:
- Carbohydrate: increase blood sugar
- Lipid: increase lipolysis, central redistribution
- Protein: increase proteolysis
Bone/connective tissues:
- Accelerates osteoporosis
- Decreases serum calcium
- Decreases collagen formation
- Decreases wound healing
Circulatory/renal system:
- Increase CO
- Increase BP
- Increase renal blood flow and GFR
What are the 2 main classifications of pathology of the adrenal glands ?
- Hyperfunction or hypofunction
- This can be of either the adrenal cortex or medulla
What may adrenal pathology also be a manfiestation of ?
- Pituitary disease (ACTH secretion from functional pituitary adenoma)
- Shock / DIC
- Various conditions that may damage / destroy adrenal tissue
What are the main hyperfunction adrenocortical (affecting cortex of adrenal gland) problems ?
- Primary hyperaldosteronism
- Hypercortisolism (cushing’s syndrome - covered in other decks)
- Congenital adrenal hyperplasia (CAH)
What are the main underlying causes of adrenocortical hyperfunction
- Hyperplasia
- Adenoma
- Carcinoma
Describe the characteristic features of an adrenocortical adenoma
- Well-circumscribed, encapsulated lesions
- Usually small - upto 2-3cm
- Yellow/yellow-brown surface
- Unilateral
- Less likely to be functional
Describe the characteristic features of an adrenocortical carcinoma
- They are rare
- More likely to be functional than adenomas
- If causing virilisation then likely malignant
- Larger size than andeomas
- Haemorrhage & necrosis seen
What are the 2 types of adrenocortical hyperplasia ?
Congenital adrenal hyperplasia (CAH)
Acquired due to:
- Endogenous ACTH - pituitary adenoma (Cushing’s)
- Ectopic ACTH e.g. SCLC
- Bilateral adrenal enlargement
- Diffuse or nodular adrenal enlargement
What is CAH ?
- It is a group of autosomal recessive disorders where there is a def./lack of the enzyme required for steroid biosynthesis in the adrenal gland
- This results in blood cortisol levels being low & there never being enough to provide neg. feedback to slow/regulate the release of ACTH
- This then results in the adrenal glands being constantly stimulated resulting in hyperplasia of the adrenal gland. This stimulation also results in increased androgen production ==> resulting in virilisation (development of male physical characteristics) in females & precosious puberty in males
What are the enzyme deficiency causes of CAH?
- 21-hydroxylase deficiency (90%)
- 11-beta hydroxylase deficiency (5%)
- 17-hydroxylase deficiency (very rare)
What are the clinical features of CAH?
- Virilisation in females
- Precocious puberty in males
How is CAH diagnosed ?
Blood tests showing high serum 17-hydroxyprogesterone is diagnostic
What is the management of CAH?
- Children tx = hydrocortisone
- Adults tx = prednisolone or dexamethasone
+/- fludrocortisone if needed to control Na & renin levels (if aldosterone levels low)
What is hyperaldosteronism ?
This can be defined as excessive levels of aldosterone which may be either independant of the RAAS (known as primary hyperaldosteronism) or due to high renin levels (known as secondary hyperaldosteronism)
Describe the unlderlying physiology of primary hyperaldosteronism
- Excessive aldosteronism acts at the distal renal tubule
- This results in Na+ retention ==> H20 retention & ==> volume expansion with HTN
- Excretion of K+ also occurs resulting in hypokalaemia
What are the causes of primary hyperaldosteronism ?
- Adrenal adenoma also known as conn’s syndrome - this will unilateral hyperplasia
- Adrenal hyperplasia - this is usually bilateral adrenal hyperplasia (diffuse or nodular)
- Adrenal carcinoma (rare)
- Familial - glucoocrticoid remediable aldosteronism (GRA), characterised by inherited aldosterone producing adenoma or inherited BAH. In this one there is excessive Aldosterone produced in response to normal ACTH
What are the clinical features of primary hyperaldosteronism ?
- Hypertension
- Hypokalaemia - classically causing muscle weakness, also cramps & paraesthesia
- Metabolic alkalosis
- +/- headaches, lethargy, polyuria & normal or increased Na+