Endocrinology Flashcards
Hypothalamus and Pituitary
The hypothalamus releases hormones that stimulate the pituitary gland. The pituitary gland has an anterior and posterior part.
The anterior pituitary gland releases:
Thyroid-stimulating hormone (TSH)
Adrenocorticotropic hormone (ACTH)
Follicle-stimulating hormone (FSH) and luteinising hormone (LH)
Growth hormone (GH)
Prolactin
The posterior pituitary releases:
Oxytocin
Antidiuretic hormone (ADH)
The Thyroid Axis
The hypothalamus releases thyrotropin-releasing hormone (TRH). TRH stimulates the anterior pituitary to release thyroid-stimulating hormone (TSH). TSH stimulates the thyroid gland to release triiodothyronine (T3) and thyroxine (T4).
The hypothalamus and anterior pituitary respond to T3 and T4 by suppressing the release of TRH and TSH, resulting in lower amounts of T3 and T4. The lower T3 and T4 offer less suppression of TRH and TSH, causing more of these hormones to be released, resulting in a rise of T3 and T4. This way, the thyroid hormone level is closely regulated to keep it within normal limits.
When the end hormone (e.g., T3 and T4) suppresses the release of the controlling hormones (e.g., TRH and TSH), this is called negative feedback.
The Adrenal Axis
Cortisol is secreted by the two adrenal glands, which sit above each kidney. The hypothalamus controls the release of cortisol. Cortisol is released in pulses throughout the day and in response to a stressful stimulus. It is a “stress hormone”. It has diurnal variation, meaning it is high and low at different times of the day. Typically cortisol peaks in the early morning, triggering us to wake up and get going, and is at its lowest late in the evening, prompting us to relax and fall asleep.
The hypothalamus releases corticotropin-releasing hormone (CRH). CRH stimulates the anterior pituitary to release adrenocorticotropic hormone (ACTH). ACTH stimulates the adrenal glands to release cortisol.
The adrenal axis is also controlled by negative feedback. Cortisol is sensed by the hypothalamus and anterior pituitary, suppressing the release of CRH and ACTH. This results in lower amounts of cortisol. This way, cortisol is closely regulated to keep it within normal limits.
Actions of cortisol on the body
Increases alertness
Inhibits the immune system
Inhibits bone formation
Raises blood glucose
Increases metabolism
The growth hormone axis
The hypothalamus produces growth hormone-releasing hormone (GHRH). GHRH stimulates the anterior pituitary to release growth hormone (GH). Growth hormone stimulates the release of insulin-like growth factor 1 (IGF-1) from the liver.
Actions of growth hormone on the body
Through this mechanism, growth hormone works directly and indirectly on almost all cells and has many functions. Most importantly, growth hormone:
Stimulates muscle growth
Increases bone density and strength
Stimulates cell regeneration and reproduction
Stimulates growth of internal organs
The parathyroid axis
Parathyroid hormone (PTH) is released from the four parathyroid glands (situated at the four corners of the thyroid gland) in response to a low calcium level in the blood. PTH is also released in response to low magnesium or low phosphate level. The role of PTH is to increase serum calcium concentration.
PTH increases the activity and number of osteoclasts in bone, causing reabsorption of calcium from the bone into the blood, increasing serum calcium concentration.
PTH also stimulates calcium reabsorption in the kidneys, meaning less calcium is excreted in the urine.
PTH also stimulates the kidneys to convert vitamin D3 into calcitriol, the active form of vitamin D. Vitamin D is a hormone that promotes calcium absorption from food in the intestine.
These three effects of PTH (increased calcium absorption from bone, the kidneys and the intestine) all help to increase the serum calcium. When the serum calcium level is high, it suppresses the release of PTH (via negative feedback), helping to reduce the serum calcium level.
The Renin-Angiotensin-Aldosterone System
Renin is an enzyme secreted by the juxtaglomerular cells in the afferent (and some in the efferent) arterioles in the kidney. They sense the blood pressure in these vessels. They secrete more renin in response to low blood pressure and less renin in response to high blood pressure. Renin acts to convert angiotensinogen (released by the liver) into angiotensin I. Angiotensin I converts to angiotensin II in the lungs with the help of an enzyme called angiotensin-converting enzyme (ACE).
Angiotensin II acts on blood vessels, causing vasoconstriction. Vasoconstriction increases blood pressure. Angiotensin II also stimulates the release of aldosterone from the adrenal glands, and contributes to cardiac remodelling by promoting hypertrophy of heart muscle cells (myocytes).
Aldosterone is a mineralocorticoid steroid hormone. It acts on the nephrons in the kidneys to:
Increase sodium reabsorption from the distal tubule
Increase potassium secretion from the distal tubule
Increase hydrogen secretion from the collecting ducts
When sodium is reabsorbed in the kidneys, water follows it by osmosis. This leads to increased intravascular volume and, subsequently, blood pressure.
TOM TIP: Understanding the renin-angiotensin-aldosterone system is essential to understanding the mechanism of action of ACE inhibitors and angiotensin II receptor blockers. By blocking the action of angiotensin-converting enzyme or angiotensin II receptors, they reduce the activity of angiotensin II, reducing vasoconstriction, cardiac remodelling and the secretion of aldosterone. Reduced aldosterone leads to reduced sodium reabsorption in the kidneys and less water retention. However, the reduced potassium secretion means these medications can cause hyperkalaemia (raised potassium).
Screening test for thyroid disease
Thyroid-stimulating hormone (TSH) is used as a screening test for thyroid disease. When TSH is abnormal, triiodothyronine (T3) and thyroxine (T4) can be measured to gain more information.
Primary hyperthyroidism
Primary hyperthyroidism is where the thyroid behaves abnormally and produces excessive thyroid hormones. TSH is suppressed by the high T3 and T4, causing a low TSH level.
Secondary hyperthyroidism
Secondary hyperthyroidism is where the pituitary behaves abnormally and produces excessive TSH (e.g., pituitary adenoma), stimulating the thyroid gland to produce excessive thyroid hormones. TSH, T3 and T4 will all be raised.
Primary hypothyroidism
Primary hypothyroidism is where the thyroid behaves abnormally and produces inadequate thyroid hormones. Negative feedback is absent, resulting in increased production of TSH. TSH is raised, and T3 and T4 are low.
Secondary hypothyroidism
Secondary hypothyroidism is where the pituitary behaves abnormally and produces inadequate TSH (e.g., after surgical removal of the pituitary), resulting in under-stimulation of the thyroid gland and insufficient thyroid hormones. TSH, T3 and T4 will all be low.
Thyroid disease antibodies
Anti-thyroid peroxidase (anti-TPO) antibodies are antibodies against the thyroid gland. They are the most relevant thyroid autoantibody in autoimmune thyroid disease. They are usually present in Grave’s disease and Hashimoto’s thyroiditis.
Anti-thyroglobulin (anti-Tg) antibodies are antibodies against thyroglobulin, a protein produced and extensively present in the thyroid gland. They can be present in normal individuals without thyroid pathology. They are usually raised with Grave’s disease, Hashimoto’s thyroiditis and thyroid cancer.
TSH receptor antibodies are autoantibodies that mimic TSH, bind to the TSH receptor and stimulate thyroid hormone release. They cause Grave’s disease and will therefore be present in this condition.
Thyroid imaging
Ultrasound of the thyroid gland helps diagnose thyroid nodules and distinguish between cystic (fluid-filled) and solid nodules. Ultrasound can also be used to guide a biopsy of a thyroid lesion.
Radioisotope scans are used to investigate hyperthyroidism and thyroid cancers. Radioactive iodine is given orally or intravenously and travels to the thyroid, where it is taken up by the thyroid cells. Iodine used by thyroid cells to produce thyroid hormones. The more active the thyroid cells, the faster the radioactive iodine is taken up. A gamma camera detects gamma rays emitted from the radioactive iodine. The more gamma rays emitted from an area, the more radioactive iodine has been taken up. This gives functional information about the thyroid gland:
Diffuse high uptake is found in Grave’s Disease
Focal high uptake is found in toxic multinodular goitre and adenomas
“Cold” areas (abnormally low uptake) can indicate thyroid cancer
Thyrotoxicosis
Thyrotoxicosis refers to the effects of an abnormal and excessive quantity of thyroid hormones in the body.
Subclinical hyperthyroidism
Subclinical hyperthyroidism is where the thyroid hormones (T3 and T4) are normal and thyroid-stimulating hormone (TSH) is suppressed (low). There may be absent or mild symptoms.
Toxic multinodular goitre
Toxic multinodular goitre (also known as Plummer’s disease) is a condition where nodules develop on the thyroid gland, which are unregulated by the thyroid axis and continuously produce excessive thyroid hormones. It is most common in patients over 50 years.
Hyperthyroidism and exophthalmos
Exophthalmos (also known as proptosis) describes the bulging of the eyes caused by Graves’ disease. Inflammation, swelling and hypertrophy of the tissue behind the eyeballs force them forward, causing them to bulge out of the sockets.
Pretibial myxoedema
Pretibial myxoedema is a skin condition caused by deposits of glycosaminoglycans under the skin on the anterior aspect of the leg (the pre-tibial area). It gives the skin a discoloured, waxy, oedematous appearance over this area. It is specific to Grave’s disease and is a reaction to TSH receptor antibodies.
Goitre
Goitre refers to the neck lump caused by swelling of the thyroid gland.
Causes of hyperthyroidism
G – Graves’ disease
I – Inflammation (thyroiditis)
S – Solitary toxic thyroid nodule
T – Toxic multinodular goitre
Thyroiditis (thyroid gland inflammation) often causes an initial period of hyperthyroidism, followed by under-activity of the thyroid gland (hypothyroidism). The causes of thyroiditis include:
De Quervain’s thyroiditis
Hashimoto’s thyroiditis
Postpartum thyroiditis
Drug-induced thyroiditis
Presentation of hyperthyroidism
Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Insomnia
Frequent loose stools
Sexual dysfunction
Brisk reflexes on examination
Presentation of Graves’ disease
Graves’ disease has specific features relating to the presence of TSH receptor antibodies:
Diffuse goitre (without nodules)
Graves’ eye disease, including exophthalmos
Pretibial myxoedema
Thyroid acropachy (hand swelling and finger clubbing)
Solitary Toxic Thyroid Nodule
A solitary toxic thyroid nodule is where a single abnormal thyroid nodule acts alone to release excessive thyroid hormone. The nodules are usually benign adenomas. Treatment involves surgical removal of the nodule.
De Quervain’s Thyroiditis
De Quervain’s thyroiditis, also known as subacute thyroiditis, is a condition causing temporary inflammation of the thyroid gland. There are three phases:
Thyrotoxicosis
Hypothyroidism
Return to normal
The initial thyrotoxic phase involves:
Excessive thyroid hormones
Thyroid swelling and tenderness
Flu-like illness (fever, aches and fatigue)
Raised inflammatory markers (CRP and ESR)
Treatment of De Quervain’s Thyroiditis
It is a self-limiting condition, and supportive treatment is usually all that is necessary. This may involve:
NSAIDs for symptoms of pain and inflammation
Beta blockers for the symptoms of hyperthyroidism
Levothyroxine for the symptoms of hypothyroidism
A small number (under 10%) remain hypothyroid long-term.
Thyroid storm
Thyroid storm is a rare presentation of hyperthyroidism. It is also known as thyrotoxic crisis. It is a rare and more severe presentation of hyperthyroidism with fever, tachycardia and delirium. It can be life-threatening and requires admission for monitoring. It is treated the same way as any other presentation of thyrotoxicosis, although they may need additional supportive care with fluid resuscitation, anti-arrhythmic medication and beta blockers.
Managing hyperthyroidism
A specialist endocrinologist guides the treatment of hyperthyroidism.
Carbimazole is the first-line anti-thyroid drug, usually taken for 12 to 18 months. Once the patient has normal thyroid hormone levels (usually within 4-8 weeks), they continue on maintenance carbimazole and either:
The carbimazole dose is titrated to maintain normal levels (known as titration-block)
A higher dose blocks all production, and levothyroxine is added and titrated to effect (known as block and replace)
TOM TIP: The MHRA issued a warning in 2019 about the risk of acute pancreatitis in patients taking carbimazole. In your exams, look out for a patient on carbimazole presenting with symptoms of pancreatitis (e.g., severe epigastric pain radiating to the back).
Propylthiouracil is the second-line anti-thyroid drug. It is used in a similar way to carbimazole. There is a small risk of severe liver reactions, including death, which is why carbimazole is preferred.
TOM TIP: Both carbimazole and propylthiouracil can cause agranulocytosis, with a dangerously low white blood cell counts. Agranulocytosis makes patients vulnerable to severe infections. A sore throat is a key presenting feature of agranulocytosis. In your exams, if you see a patient with a sore throat on carbimazole or propylthiouracil, the cause is likely agranulocytosis. They need an urgent full blood count and aggressive treatment of any infections.
Radioactive iodine treatment involves drinking a single dose of radioactive iodine. The thyroid gland takes this up, and the emitted radiation destroys a proportion of the thyroid cells. The reduction in the number of cells results in a decrease in thyroid hormone production. Remission can take 6 months, after which the thyroid is often underactive, requiring long-term levothyroxine. Treatment with radioactive iodine involves strict rules:
Women must not be pregnant or breastfeeding and must not get pregnant within 6 months of treatment
Men must not father children within 4 months of treatment
Limit contact with people after the dose, particularly children and pregnant women
Beta blockers are used to block the adrenalin-related symptoms of hyperthyroidism. Propranolol is the usual choice, as it non-selectively blocks adrenergic activity (as opposed to something like bisoprolol, which is more selective). Beta blockers do not treat the underlying problem but control the symptoms, while definitive treatment takes time. They are particularly useful in patients with thyroid storm.
Surgery is a definitive option. Removing the whole thyroid gland (thyroidectomy), or the toxic nodules, effectively stops the excess thyroid hormone production. Patients will be hypothyroid after a thyroidectomy, requiring life-long levothyroxine.
Causes of primary hypothyroidism
Hashimoto’s thyroiditis is the most common cause of hypothyroidism in the developed world. It is an autoimmune condition causing inflammation of the thyroid gland. It is associated with anti-thyroid peroxidase (anti-TPO) antibodies and anti-thyroglobulin (anti-Tg) antibodies.
Iodine deficiency is the most common cause of hypothyroidism in the developing world. In the UK, iodine is particularly found in dairy products and may be added to non-dairy milk alternatives (e.g., soya milk).
Treatments for hyperthyroidism have the potential to cause hypothyroidism:
Carbimazole
Propylthiouracil
Radioactive iodine
Thyroid surgery
Lithium inhibits the production of thyroid hormones in the thyroid gland and can cause a goitre and hypothyroidism.
Amiodarone interferes with thyroid hormone production and metabolism, usually causing hypothyroidism but can also cause thyrotoxicosis.
Causes of secondary hypothyroidism
Secondary hypothyroidism is often associated with a lack of other pituitary hormones, such as ACTH, referred to as hypopituitarism. This is rarer than primary hypothyroidism, and may be caused by:
Tumours (e.g., pituitary adenomas)
Surgery to the pituitary
Radiotherapy
Sheehan’s syndrome (where major post-partum haemorrhage causes avascular necrosis of the pituitary gland)
Trauma
Presentation of hypothyroidism
Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention (including oedema, pleural effusions and ascites)
Heavy or irregular periods
Constipation
Iodine deficiency causes a goitre.
Hashimoto’s thyroiditis can initially cause a goitre, after which there is atrophy (wasting) of the thyroid gland.
Managing hypothyroidism
Oral levothyroxine is the mainstay of treatment of hypothyroidism. Levothyroxine is a synthetic version of T4 and metabolises to T3 in the body.
The dose is titrated based on the TSH level, initially every 4 weeks.
TSH Result
Levothyroxine Dose
Action
High
Too low
Increase the dose
Low
Too high
Reduce the dose
Liothyronine sodium is a synthetic version of T3 and is very rarely used under specialist care where levothyroxine is not tolerated.
Cushing’s syndrome
Cushing’s syndrome refers to the features of prolonged high levels of glucocorticoids in the body.
There are two groups of corticosteroid hormones:
Glucocorticoids (e.g., cortisol)
Mineralocorticoids (e.g., aldosterone)
The prolonged use of exogenous corticosteroids, such as prednisolone or dexamethasone, often causes Cushing’s syndrome. Exogenous refers to when it originates (-genous) is outside (exo-) the body.
Cushing’s disease
Cushing’s disease refers to a pituitary adenoma secreting excessive adrenocorticotropic hormone (ACTH), stimulating excessive cortisol release from the adrenal glands. This is not the only cause of Cushing’s syndrome.
Features of Cushing’s Syndrome
Features on inspection (round in the middle with thin limbs):
Round face (known as a “moon face”)
Central obesity
Abdominal striae (stretch marks)
Enlarged fat pad on the upper back (known as a “buffalo hump”)
Proximal limb muscle wasting (with difficulty standing from a sitting position without using their arms)
Male pattern facial hair in women (hirsutism)
Easy bruising and poor skin healing
Hyperpigmentation of the skin in patients with Cushing’s disease (due to high ACTH levels)
Metabolic effects:
Hypertension
Cardiac hypertrophy
Type 2 diabetes
Dyslipidaemia (raised cholesterol and triglycerides)
Osteoporosis
Mental health effects:
Anxiety
Depression
Insomnia
Rarely psychosis
Causes of Cushing’s Syndrome
You can remember the causes of Cushing’s syndrome with the “CAPE” mnemonic:
C – Cushing’s disease (a pituitary adenoma releasing excessive ACTH)
A – Adrenal adenoma (an adrenal tumour secreting excess cortisol)
P – Paraneoplastic syndrome
E – Exogenous steroids (patients taking long-term corticosteroids)
Paraneoplastic Cushing’s syndrome occurs when ACTH is released from a tumour somewhere other than the pituitary gland. ACTH from somewhere other than the pituitary gland is called ectopic ACTH. Small cell lung cancer is the most common. Ectopic ACTH stimulates excessive cortisol release from the adrenal glands.
TOM TIP: A high level of ACTH causes skin pigmentation by stimulating melanocytes in the skin to produce melanin, similar to melanocyte-stimulating hormone. This is an important sign of Cushing’s disease (where excess ACTH comes from a pituitary adenoma) and also primary adrenal insufficiency (where there is inadequate cortisol from the adrenals with a lack of negative feedback to the pituitary). In a patient with Cushing’s syndrome, the pigmentation allows you to determine the cause as excess ACTH, either from Cushing’s disease or ectopic ACTH. This sign is absent in an adrenal adenoma or exogenous steroids.
Dexamethasone suppression tests
The dexamethasone suppression tests are used to diagnose Cushing’s syndrome caused by a problem inside the body. There is no point in using them to diagnose Cushing’s syndrome caused by exogenous steroids.
A normal response to dexamethasone is suppressed cortisol due to negative feedback. Dexamethasone causes negative feedback on the hypothalamus, reducing the corticotropin-releasing hormone (CRH) output. It causes negative feedback on the pituitary, reducing the ACTH output. The lower CRH and ACTH levels result in a low cortisol output by the adrenal glands. A lack of cortisol suppression in response to dexamethasone suggests Cushing’s syndrome.
There are three types of dexamethasone suppression test:
Low-dose overnight test (used as a screening test to exclude Cushing’s syndrome)
Low-dose 48-hour test (used in suspected Cushing’s syndrome)
High-dose 48-hour test (used to determine the cause in patients with confirmed Cushing’s syndrome)
Low-dose overnight dexamethasone test
For the low-dose overnight test, dexamethasone (1mg) is given at night (usually 10 or 11 pm), and the cortisol is checked at 9 am the following morning. A normal result is that the cortisol level is suppressed. Failure of the dexamethasone to suppress the morning cortisol could indicate Cushing’s syndrome, and further assessment is required.
Low-dose 48-hour dexamethasone test
For the low-dose 48-hour test, dexamethasone (0.5mg) is taken every 6 hours for 8 doses, starting at 9 am on the first day. Cortisol is checked at 9 am on day 1 (before the first dose) and 9 am on day 3 (after the last dose). A normal result is that the cortisol level on day 3 is suppressed. Failure of the dexamethasone to suppress the day 3 cortisol could indicate Cushing’s syndrome, and further assessment is required.
High-dose 48-hour dexamethasone test
The high-dose 48-hour test is carried out the same way as the low-dose test, other than using 2mg per dose (rather than 0.5mg). This higher dose is enough to suppress the cortisol in Cushing’s syndrome caused by a pituitary adenoma (Cushing’s disease), but not when it is caused by an adrenal adenoma or ectopic ACTH.
Adrenocorticotropic hormone (ACTH) can be measured directly. ACTH is suppressed due to negative feedback on the pituitary when excess cortisol comes from an adrenal tumour (or endogenous steroids). It is high when produced by a pituitary tumour or ectopic ACTH (e.g., small cell lung cancer).
Summary of dexamethasone suppression tests
Low Dose Test (Cortisol Result)
High Dose Test (Cortisol Result)
ACTH
Normal
Low
Low
Normal
Adrenal Adenoma
Not Suppressed
Not Suppressed
Low
Pituitary Adenoma
Not Suppressed
Low
High
Ectopic ACTH
Not Suppressed
Not Suppressed
High
Investigating Cushing’s Syndrome
A 24-hour urinary free cortisol is an alternative to the dexamethasone suppression test. However, it is cumbersome to carry out and does not indicate the underlying cause.
Other investigations:
Full blood count may show a high white blood cell count
U&Es may show low potassium if an adrenal adenoma is also secreting aldosterone
MRI brain for a pituitary adenoma
CT chest for small cell lung cancer
CT abdomen for adrenal tumours
Treating Cushing’s Syndrome
The primary treatment is to remove the underlying cause:
Trans-sphenoidal (through the nose) removal of pituitary adenoma
Surgical removal of adrenal tumour
Surgical removal of the tumour producing ectopic ACTH (e.g., small cell lung cancer), if possible
Where surgical removal of the cause is not possible, another option is to surgically remove both adrenal glands (adrenalectomy) and give the patient life-long steroid replacement therapy.
Nelson’s syndrome involves the development of an ACTH-producing pituitary tumour after the surgical removal of both adrenal glands due to a lack of cortisol and negative feedback. It causes skin pigmentation (high ACTH), bitemporal hemianopia and a lack of other pituitary hormones.
Metyrapone reduces the production of cortisol in the adrenals and is occasionally used in treating of Cushing’s.
Hyperaldosteronism definition
Hyperaldosteronism refers to high levels of aldosterone. Conn’s syndrome refers to an adrenal adenoma producing too much aldosterone.
Hyperaldosteronism may be present in 5-10% of patients with hypertension. Hypertension is the key presenting feature, and many patients are otherwise asymptomatic. It may cause non-specific symptoms such as headaches, muscle weakness and fatigue.
Causes of primary hyperaldosteronism
Primary hyperaldosteronism is when the adrenal glands are directly responsible for producing too much aldosterone. Serum renin will be low as the high blood pressure suppresses it.
The adrenals may produce too much aldosterone for several possible reasons:
Bilateral adrenal hyperplasia (most common)
An adrenal adenoma secreting aldosterone (known as Conn’s syndrome)
Familial hyperaldosteronism (rare)
Causes of secondary hyperaldosteronism
Secondary hyperaldosteronism is caused by excessive renin stimulating the release of excessive aldosterone.
Excessive renin is released due to disproportionately lower blood pressure in the kidneys, usually due to:
Renal artery stenosis
Heart failure
Liver cirrhosis and ascites
Renal artery stenosis refers to a narrowing of the artery supplying the kidney, usually due to atherosclerosis, similar to the narrowing of the coronary arteries in angina. Renal artery stenosis can be confirmed with:
Doppler ultrasound
CT angiogram
Magnetic resonance angiography (MRA)
Investigating hyperaldosteronism
The aldosterone-to-renin ratio (ARR) is used as a screening test:
High aldosterone and low renin indicate primary hyperaldosteronism
High aldosterone and high renin indicate secondary hyperaldosteronism
Other investigations that relate to the effects of aldosterone include:
Raised blood pressure (hypertension)
Low potassium (hypokalaemia)
Blood gas analysis (alkalosis)
Investigations for the underlying cause include:
CT or MRI to look for an adrenal tumour or adrenal hyperplasia
Renal artery imaging for renal artery stenosis (Doppler, CT angiogram or MR angiography)
Adrenal vein sampling of blood from both adrenal veins to locate which gland is producing more aldosterone
Managing hyperaldosteronism
Medical management is with aldosterone antagonists:
Eplerenone
Spironolactone
Treating the underlying cause involves:
Surgical removal of the adrenal adenoma
Percutaneous renal artery angioplasty via the femoral artery to treat renal artery stenosis
TOM TIP: Hyperaldosteronism is worth remembering as the most common cause of secondary hypertension. Consider testing for hyperaldosteronism in patients with hypertension, who are younger, fail to respond to treatment or have a low potassium. Be aware that potassium levels may be normal in hyperaldosteronism.
Adrenal insufficiency definition
Adrenal insufficiency is where the adrenal glands do not produce enough steroid hormones, particularly cortisol and aldosterone. Steroids are essential for life. Therefore, the condition is life-threatening unless the hormones are replaced.
Addison’s disease
Addison’s disease refers specifically to when the adrenal glands have been damaged, resulting in reduced cortisol and aldosterone secretion. This is called primary adrenal insufficiency. The most common cause is autoimmune.
