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Theme A: Adrenal Structure and Function
Terms in this set (76)
Where do the adrenal glands sit? What shape are they?
One on top of each kidney.
- Right is triangular.
- Left is semicircular.
Generally, what are the 2 divisions of an adrenal gland?
- 90% cortex.
- 10% medulla.
What vessels supply the adrenal glands?
Superior, middle and inferior suprarenal arteries on either side.
- 6 vessels in total.
- Branches of the AA.
What drains the right adrenal gland?
Right suprarenal vein.
- Drains into the IVC.
What drains the left adrenal gland?
Left suprarenal vein.
- Drains into the left renal vein.
- Then drains into the IVC.
What are the 3 zones of the cortex from superficial to deep? What surrounds them by lying over the zona glomerulosa?
1) Zona glomerulosa.
2) Zona fasciculata.
3) Zona reticularis.
What is the function of aldosterone?
- Important in reabsorption of Na+ and H20 from the renal CD.
- Involves secretion of K+ and H+.
- Also BP control (RAAS).
- Controlled by renin.
What is the function of cortisol?
- Carbohydrate metabolism.
- Controlled by HPA axis via ACTH.
What controls the release of sex steroids from the zona reticulata?
Controlled by HPA axis via ACTH.
What does the medulla secrete?
- Fight or flight hormones.
- Controlled by the sympathetic nervous system.
What does each layer of the cortex secrete?
- Zona glomerulosa: mineralocorticoids, aldosterone.
- Zona fasciculata: glucocorticoids, cortisol.
- Zona reticularis: sex steroids, testosterone.
What are the 2 types of corticosteroid? What do they do?
1) Glucocorticoid: i.e. cortisol, control carb/fat/protein metabolism, anti-inflammatory by preventing phospholipid release, decreasing eosinophil action.
2) Mineralocorticoid: i.e. aldosterone, control electrolyte and water levels, mainly by promoting sodium retention in the kidney.
What is an adrenocortical hormone? How are they alike?
Any hormone produced by the cortex of the adrenal gland.
- All steroid hormones.
What is the common molecule of origin of all adrenocortical hormones?
- Becomes aldosterone, cortisol, dihydrotestosterone (DHT) or estradiol via various paths.
What cells regulate aldosterone secretion (and ergo RAAS)?
JG cells sit between the glomerulus and afferent arteriole.
- Detects blood flow (vol + pressure) through the afferent arteriole.
- Macula densa cells in the distal tubule sense Na+ concentration.
The juxtaglomerular apparatus.
What are the 3 components of the JGA?
- Macula densa of the distal convoluted tubule.
- Smooth muscle cells of the afferent arteriole known as juxtaglomerular cells.
- Extraglomerular mesangial cells.
What can directly stimulate the zona glomerulosa to secrete aldosterone?
- Aldosterone involves secretion of K+.
- Bypasses RAAS.
What is hyperaldosteronism?
A state in which there is too much aldosterone being secreted.
- Can be primary or secondary.
- It is a rare form of hypertension (1%).
What can cause primary and secondary hyperaldosteronism?
- Primary: tumour (adenoma), hyperplasia.
- Secondary: dehydration, cardiac failure, cirrhosis.
What is primary hyperaldosteronism also called?
What is the most common cause of primary hyperaldosteronism? What demographics is it more likely to affect?
Aldosterone producing adenoma (primary).
- Females more so than males.
- 30-60 YO.
What are the 3 H's of primay hyperaldosteronism?
- Hypertension (it is a rare form of this).
- Hypernatraemia (the cause of the hypertension).
What is fludrocortisone?
- Used to test for primary hyperaldosteronism, suppression testing.
- Dynamic function testing.
What is Synacthen?
- Used to test for adrenal insufficiency and determine which type.
- If ACTH goes up, primary AI.
- If ACTH goes down, secondary AI.
- Dynamic function testing.
Other then Synacthen testing, how can we distinguish between AI types?
- CT of adrenal glands.
- Mantoux test and CXR for TB.
What investigations could be do for primary hyperaldosteronism?
- Bloods for hypokalaemia and plasma aldosterone/renin ratio.
- Fludrocortisone (synthetic aldosterone) suppression test (the definitive test). Failure of aldosterone to suppress.
- Imaging: US, CT, MRI.
What is dynamic function testing?
- If you suspect adrenal insufficiency, try to stimulate it (Synacthen).
- If you suspect adrenal over functioning (Conn's), try to suppress it (fludrocortisone).
How is primary hyperaldosteronism (Conn's) treated?
- Adrenalectomy. Remove the aldosterone producing adenoma OR the entire gland.
- Mineralocorticoid antagonist if surgery not appropriate. Spironolactone.
What disease involves reduced amounts of aldosterone, cortisol and sex steroids?
- Adrenal glands do not produce enough mineralocorticoids OR glucocorticoids (cortisol) OR androgens.
- Cortex failure.
- Usually due to autoimmune destruction of the adrenal gland (70-90%).
- Can also be due to TB (7-20%), (bilateral adrenal destruction), used to be most common.
What are other causes of Addison's other than autoimmune and TB?
- Infectious diseases i.e. HIV.
- Replacement by metastatic cancer or lymphoma.
- Adrenal haemorrhage or infarction.
What can low levels of glucocorticoid (cortisol) cause?
- Inability to excrete water.
- Inability to metabolise carbs.
Results is hyponatremia and hypoglycaemia respectively.
What are the characteristics of Addison's disease is terms of what you would see upon testing?
- Reduced aldosterone.
- Increased plasma renin and angiotension 2.
- Hyperkalaemia and acidosis (H+).
- Insufficient adrenal androgens (body hair loss in women).
- Insufficient glucocorticoids (hypoglycaemia due to poor carb metabolism).
- Also causes inability to excrete water -> hyponatremia (due to dilution).
What are the 3 H's of Addison's disease? For each what is responsible?
- Hyperkalaemia (aldosterone).
- Hypoglycaemia (GC's).
- Hyponatremia (GC's, dilution of sodium due to inability to excrete water).
What is a key clinical feature of Addison's disease other than the 3 H's?
Hyperpigmentation of skin.
- Usually in skin creases, nipple, and the inside of the cheek.
What causes hyperpigmentation in Addison's? Why?
Overproduction of ACTH due to loss of negative feedback.
- ACTH and MSH (melanocyte-stimulating hormone) share the same precursor (POMC).
- ACTH gets cleaved into a-MSH and MSH, the molecule important in skin pigmentation.
What is POMC?
- Common precursor of ACTH and subsequently MSH.
What does cortisol (glucocorticoid) do? What is the purpose of this?
A catabolic hormone. Preserves glucose, stress hormone ready for fighting etc.
- Stimulates the release of AAs from proteins.
- Stimulates lipolysis to FFA.
- Stimulates gluconeogenesis (FFA and AA to glucose).
- Conserves glucose.
How does cortisol preserve glucose?
- Triggers AA, FFA synthesisand gluconeogenisis to synthesise more glucose.
- Conserves glucose by inhibiting uptake into muscle and fat cells.
Briefly describe the hypothalamic-pituitary-adrenal axis (HPA axis).
- Stressor stimulates hypothalamus to release CRH.
- CRH stimulates the anterior pituitary to release ACTH.
- ACTH stimulates the adrenal cortex to release cortisol.
- Cortisol has a metabolic effect, then acts as a negative feedback loop.
What are the 3 molecules involved in the HPA axis?
- CRH: corticotropin releasing hormone.
- ACTH: adrenocorticotropic hormone.
- Cortisol (CORT).
What 2 parts of the HPA axis does cortisol negatively feedback on?
- Anterior pituitary.
What are the 3 types of adrenal insufficiency?
Primary, secondary, tertiary.
What is the difference between primary, secondary and tertiary adrenal insufficiency?
- Primary AI: pathology is in the adrenal cortex.
- Secondary AI: pathology is in the anterior pituitary.
- Tertiary AI: pathology is in the hypothalamus.
Corresponds to the HPA axis.
What type of adrenal insufficiency is seen in Addison's?
What is the balance of molecules in primary adrenal insufficiency?
- Low cortisol, AC stops producing it.
- This PREVENTS negative feedback so....high CRH and ACTH.
Why is hyperpigmentation only present in primary adrenal insufficiency (Addison's)? Explain the pathophysiology of this.
In primary AI the cortisol negative feedback is lost.
- Overproduction of ACTH from the ant pit occurs (along with CRH).
- ACTH is broken down into a-MSH and MSH.
- Increased MSH causes stimulation of production and release of melanin from melanocytes.
- Darkening occurs.
How do secondary and tertiary adrenal insufficiency differ from primary?
- No hyperpigmentation due to no ACTH hypersecretion.
- Dehydration not present (aldosterone stays same), hypotension less prominent.
What demographics are more likely to get Addison's disease?
- 50% of cases have another endocrine condition, polyendocrinopathy.
- i.e. primary hyperthyroidism.
- Younger men (0-20), older women (40+), equal between.
Why is Addison's difficult to diagnose?
Symptoms may be insidious until presenting with a crisis.
- Very generalised.
What are the symptoms (not signs) of Addison's?
- Chronic malaise.
- Generalised weakness.
- Weight loss.
- Lassitude (mental weariness).
What are the signs of Addison's?
- GI complaints.
How would adrenal insufficiency such as Addison's be treated?
- Glucocorticoids: hydrocortisone or prednisolone.
- Mineralocorticoids: fludrocortisone.
What is an adrenal crisis?
Acute onset of severe symptoms.
- Hypotensive shock.
- Precipitated by serious infection or stress.
Patients carry cards/markers to let paramedics know they have Addison's.
- Glucocorticoids and fludrocortisone given.
How are mineralocorticoids affected by primary adrenal insufficiency?
- Primary: effected (aldosterone drops).
- Secondary/tertiary: not effected.
What are Cushing's disease and Cushing's syndrome?
- Disease: ACTH producing pituitary adenoma causing hypercortisolaemia. High ACTH and cortisol. CRH low.
- Syndrome: resulting from ANY cause of hypercortisolism.
What are the 2 types of Cushing's syndrome?
1) ACTH dependent (pituitary adenoma),same as disease? ACTH high due to AP tumour. Cortisol also high. CRH low.
2) ACTH independent, majority caused by exogenous steroids or adrenal adeomas/carcinomas. ACTH low due to cortisol production. CRH low.
What determines the signs of Cushing's?
- Severity and duration of steroid production.
- Presence of androgen production.
What are the most important signs and symptoms of Cushing's?
- Central obesity.
- Easy bruising.
- Weight gain.
- Moon face.
- Buffalo hump.
How is Cushing's investigated?
- 24 hour urine cortisol, 2-3x normal level.
- ACTH level measured.
- Midnight cortisol test.
What is the diurnal variation of cortisol?
High at 9am, low at midnight.
- Midnight cortisol -> Cushing's.
- MRI imaging of pituitary.
How do we test for Cushing's using dynamic function testing?
Dexamethasone suppression test. Same as Synacthen.
- We suspect high cortisol.
- Absence of suppression means Cushing's.
What is the main source of testosterone in both sexes?
- Men = testes.
- Women = adrenal cortex (ZR).
What do androgens (DHT etc) do?
- Stimulate cell growth.
- Enhance muscle mass.
- Aid in development of secondary sexual characteristics.
What happens with adrenal androgen excess in men?
Little effect. Not main source.
- Inhibition of gonadotropin secretion. Testicles shrink, reduces spermatogenisis.
What happens with adrenal androgen excess in women?
- Facial hair growth (hirsutism).
- Male pattern baldness.
- Menstrual irregularities.
What is the adrenal medulla derived from?
The embryonic neural crest.
What does the adrenal medulla do?
Principle site of conversion of tyrosine to catecholamines.
- Adrenaline (80%) and noradrenaline (20%).
- Release in response to immediate danger.
- Composed mainly of hormone-producing chromaffin cells.
What to catecholamines do?
- HR up.
- BV constriction.
- Bronchiole dilatation.
- Increased metabolism.
- Fight or flight.
- Doubles when one stands up from lying to increase BP and prevent vasovagal syncope.
- Catebolic (glycogenolysis, lypolysis).
Why is the adrenal medulla not essential for life?
Majority of noradrenaline produced by postganglionic sympathetic neurons.
- Most actions of adrenaline mediated by noradrenaline.
What is pheochromocytoma (PCC)?
An increased state of catecholamines.
- Paroxsymal and spontaneous attacks.
- Precipitated by B-blockers, anaesthesia, strenuous exercise, increasing abdo-pressure.
- A rare form of hypertension.
What causes pheochromocytoma?
A neuroendocrine tumor of the medulla of the adrenal glands (originating in the chromaffin cells(.
What are the 5 P's of pheochromocytoma from most common to least?
- Pressure (hypertension).
- Pain (headache).
What is the classic triad of pheochromocytoma?
- Pain, perspiration and pallor.
- Lack of all 3 excludes diagnosis.
What are the investigations for pheochromocytoma?
- 24 hour urinary catecholamines.
- 24 hour urinary metanephrines.
- CT scan and MRI for localisation.
How is pheochromocytoma managed?
- Preoperative management with alpha and beta blockade.
- Salt and fluid replacement given.
- Adrenal gland removed.
What are metanephrines?
Metabolites of catecholamines.
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