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Endocrinology > Adrenal conditions > Flashcards

Adrenal conditions Flashcards

1
Q

What type of hormone is aldosterone?

A

Mineralcorticoid hormone

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2
Q

Where is aldosterone synthesised and secreted from?

A

Zona glomerulosa in the adrenal cortex of the adrenal glands

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3
Q

Describe the function of aldosterone.

A

Aldosterone acts on the distal convoluted tubule and within the nephron to promote sodium reabsorption (hence water reabsorption) and potassium excretion. This therefore increases water retention, increases blood volume and therefore blood pressure.

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4
Q

Which two cells specifically within the distal convoluted tubule does aldosterone act upon?

A

Principal cells and alpha intercalated cells

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5
Q

Which two pumps specifically does aldosterone act upon?

A

Na+/K+ ATPase in principal cells which pumps even more sodium out of the cell back into the blood and retains potassium. This allows more sodium to be reabsorbed into the cell from the tubule, down its concentration gradient.

Stimulates the proton pump ATPase in intercalated cells, which drives more protons to be excreted into the urine. Ion channels on the basal surface drives bicarbonate ions out of the cell into the bloodstream, altering the pH.

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6
Q

Describe the difference between primary and secondary hyperaldosteronism.

A

Primary hyperaldosteronism is caused by a defect with the adrenal cortex itself resulting in the over secretion of aldosterone. Whereas secondary hyperaldosteronism is due to excess aldosterone production as a result to consistent high levels of renin in response to chronic low blood pressure.

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7
Q

Which conditions may induce secondary hyperaldosteronism?

A

Congestive heart failure or cirrhosis

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8
Q

What are the three main causes of primary aldosteronism and briefly describe each one?

A

Idiopathic hyperaldosteronism: where the zona glomerulosa has an increase in aldosterone secreting cells.

Conn’s syndrome: due to an adenoma in the glandular epithelial cells, increasing aldosterone production.

Familial hyperaldosteronism: adrenal cortex secretes aldosterone in response to adrenocorticotropic hormone in addition to renin.

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9
Q

What are some of the clinical manifestations of hyperaldosteronism?

A

Hypokalaemia
Hypernatremia
Hypertension (increased blood volume and hence pressure)
Metabolic alklosis (alkaline pH)

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10
Q

What are some of the symptoms a patient may present with if they have hyperaldosteronism?

A

Symptoms are mainly associated with hypokalaemia such as constipation, weakness, fatigue, heart rhythm changes

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11
Q

How is hyperaldosteronism diagnosed?

A

Usually with a blood test to assess renin and aldosterone levels.

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12
Q

How would you expect blood test results to differ between primary and secondary hyperaldosteronism?

A

In primary hyperaldosteronism, where the defect is in the adrenal cortex you would expect:
Low levels of renin (suppressed due to high blood pressure)
High levels of aldosterone

In secondary hyperaldosteronism, due to consistent high levels of renin you would expect:
High levels of renin
High levels of aldosterone

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13
Q

What is the first line treatment for hyperaldosteronism and what is their mechanism of action?

A

Potassium-sparing diuretic such as Spironolactone which works by competitively binding to aldosterone receptors on both principal and alpha intercalated cells which increases sodium excretion and increase potassium reabsorption.

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14
Q

What are some of the toxic monitoring parameters for the first line treatment of hyperaldosteronism?

A

Should monitor electrolytes, specifically potassium due to risk of hyperkalaemia
Monitor renal function

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15
Q

What other treatments are available for hyperaldosteronism?

A

Managing the underlying cause such as removal of tumour in Conn’s disease or treating heart failure or cirrhosis in secondary hyperaldosteronism.

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16
Q

When is renin secreted in the renin-angiotensin system?

A

When the juxtaglomerular cells in the afferent arteriole of the kidney sense a decrease in blood pressure, renin is secreted.

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17
Q

Describe the conditions required for secondary hyperaldosteronism to occur.

A

Due to abnormally high levels of renin due to when the blood pressure within the kidneys is disproportionate to the blood pressure in the rest of the body.
Caused by either:
Renal artery stenosis
Renal artery obstruction
Heart failure

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18
Q

What is renal artery stenosis?

A

A plaque forms on the renal artery causing it to narrow and hence creating an area of high blood pressure within the artery, decreased blood flow to the kidney and therefore decreased blood pressure within the kidney resulting the activation of the renin angiotensin system.

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19
Q

What are the three ways in which renal artery stenosis can be confirmed?

A

Doppler ultrasound
CT angiogram
Magnetic resonance angiography

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20
Q

In addition to the renin: aldosterone levels, what other investigations may you make?

A

Electrolyte levels
Blood pressure
Blood gas
CT/MRI
Doppler/MRA

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21
Q

What treatment is usually given for renal artery stenosis?

A

Percutaneous renal artery angioplasty

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22
Q

When should you suspect for hyperaldosteronism?

A

If a patient with hypertension is not responding to usual treatment as hyperaldosteronism is the most common cause of secondary hypertension.

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23
Q

Describe the downstream pathway of cortisol production.

A

Firstly, corticotrophin releasing hormone is secreted from the hypothylamus which then acts on the anterior pituitary stimulating the secretion of of adrenocorticotrophic hormone which acts on the adrenal gland stimulating the production of cortisol.

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24
Q

What are the roles of cortisol in the body?

A

Increases basal mechanisms
Inhibits the immune system
Raises blood glucose
Increases alertness
Inhibits bone formation

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25
Q

What is Cushing’s syndrome?

A

Clinical features of having excess cortisol in the body

26
Q

What are some of the clinical manifestations of Cushing’s syndrome?

A

More prone to infection
Osteoporosis
Type 2 diabetes
Hypertension
Hiruitism
Psychosis
Depression

27
Q

What are some of the symptoms of Cushing’s syndrome?

A

Thin arms and legs
Red puffy face or moon face
Increased fat on the stomach and chest
Bruising more easily
Purple stretch marks
Women experience irregular or complete loss of periods
Reduced sex drive

28
Q

Explain the four causes of Cushing’s syndrome?

A

Long-term use of exogenous steroids
Adrenal Cushings - adrenal adenoma produces excess cortisol
Cushings disease - when a pituitary adenoma secretes more ACTH which further stimulates the adrenal gland to produce cortisol
Paraneoplastic Cushings - cancer produces excess etopic ACTH (normally from small cell lung cancer) stimulating excessive cortisol secretion

29
Q

What is one of the diagnostic tests used to detect Cushing’s syndrome?

A

The dexamethasone suppression test

30
Q

Describe the process of the dexamethasone suppression test.

A

Patient is given it at 10pm at night and then at 9am the following morning the patient’s levels of cortisol and ACTH is measured.

The test is usually done in two steps:
The first step is a having a 1mg Dexamethasone tablet (this is used to assess the normal function of the adrenal cortex or confirm whether they indeed have Cushing’s syndrome.

The following test requires the patient to have 8mg dexamethasone (this is to understand the possible cause of cortisol hyper secretion).

31
Q

Describe the rationale of the 1mg dexamethasone suppression test.

A

Dexamethasone acts on both the hypothylamus and pituitary gland to suppress secretion of CRH and ACTH, causing a drop in cortisol levels (patient without Cushing’s).

A patient with Cushing’s, cortisol secretion is so high so 1mg dexamethasone fails to inhibit cortisol secretion and it remains high.

32
Q

If the 1mg Dexamethasone test is positive then what happens?

A

The patient would then have the 8mg dexamethasone suppression test.

33
Q

How would results differ for each of the causes of the 8mg Dexamethasone suppression test?

A

Cushing’s disease (pituitary adenoma) - Dexamethasone will suppress and target the pituitary resulting in low ACTH and low cortisol.

Adrenal Cushing’s- cortisol remains high/ normal but ACTH is low.

Paraneoplastic Cushings- cortisol remains high/normal but ACTH is high (suggesting adenoma is not in the pituitary but elsewhere for example small cell lung cancer).

34
Q

What is some of the treatment available for Cushing’s syndrome?

A

Surgery/ radiotherapy to remove the tumour
Corticosteroid inhibitors

35
Q

How does Metyrapone work?

A

It is a competitive inhibitor of 11β-hydroxylation in the adrenal cortex

36
Q

How does ketoconazole work?

A

It inhibits the activity of 17α-hydroxylase, 11-hydroxylation steps and at
higher doses the cholesterol side-chain cleavage enzyme. It also inhibits the activity of adrenal C17-20 lyase enzymes resulting in androgen synthesis inhibition.

37
Q

How does trilostane work?

A

Blocks 3 beta-dehydrogenase preventing
pregenenelone conversion to progesterone

38
Q

How does Aminoglutethimide work?

A

It prevents the initial step of cholesterol to pregenenelone

39
Q

How does Mitotane work?

A

It inhibits glucocorticoid synthesis by an unknown direct effect on the adrenal gland

40
Q

How does Carbenexone work?

A

It inhibits hydrocortisone conversion to cortisone

41
Q

What are some of the patient demographics of Addison’s disease?

A

More common in females than males and the age of diagnosis is usually between the ages of 30-50.
9000 people in the UK have Addison’s disease and there are 300 new cases each year.

42
Q

What is Addison’s disease?

A

Caused by adrenal insufficiency and failure to produce sufficient cortisol and sometimes aldosterone.

43
Q

What are some of the causes of Addison’s disease?

A

Often caused by autoimmune conditions such as:
Type 1 diabetes , Vitilgo , Hypothyroidism
Tuberculosis
Hemorrhage
Cancer
Amyloidosis
Surgically removing both adrenal glands

44
Q

What are some of the clinical presentations of Addison’s disease?

A

Hyperpigmentation
Low blood pressure
Weakness
Weight loss
Nausea
Vomitting
Diarrhea
Constipation
Abdominal pain
Vitiligo

45
Q

When can an Addison’s crisis occur?

A

When you have untreated Addison’s disease and when there is stress on the body such as times of infection, injury or illness when the body would normally produce more cortisol.

46
Q

What are some of the symptoms of Addison’s crisis?

A

Hypoglycaemia
Convulsions
Fever
Severe vomiting and diarrhea
Hyponatremia
Syncope

47
Q

What is used for the treatment of Addison’s crisis?

A

100mg IV hydrocortisone every 6-8 hours
IV fluid resuscitation
Intensive monitoring

48
Q

Which medication would you expect a patient with Addison’s disease to be taking?

A

Hydrocortisone (replace cortisol)- 20mg-30mg to be taken daily in divided doses to mimic the body’s natural production of cortisol (10mg in the morning, 5mg at lunch, 5mg at dinner)

Fludrocortisone (replace aldosterone) - 50-300mcg daily

49
Q

Where are the two adrenal glands located in the body?

A

They sit on top of each kidney

50
Q

Describe each of the layers of the adrenal glands and the hormones that are produced there.

A

Outermost layer of the adrenal cortex is known as the Zona glomerulosa- secretes aldosterone.
Next inner layer is the Zona fasciculata and secretes cortisol and other corticosteroids
Innermost layer is the Zona reticularis and it produces androgens.

Epinephrine and Norephrine is produced from the medulla.

51
Q

What are the three distinct steroids classes and examples of each?

A

Glucocorticoids - cortisol
Mineralcorticoids - aldosterone
Sex hormones - DHEA

52
Q

What are steroids synthesised from?

A

Cholestrol

53
Q

What are the two mechanisms of how aldosterone secretion is stimulated?

A

Activated by renin (renin-angiotensin system)
Rise in plasma potassium levels

54
Q

Describe cortisol’s role in metabolism?

A

Tries to increase blood glucose levels at expense of protein and fat stores
Stimulates hepatic gluconeogenesis
Inhibits glucose uptake by several tissues
Stimulates protein breakdown in several tissues, especially muscle
Stimulates lipolysis in adipose tissue to provide alternative source of free fatty acids to tissues rather than using up glucose

55
Q

Aside of metabolism what are some of the other roles of cortisol in the body?

A

Need enough cortisol to produce catecholamines which are then required for induced vasoconstriction
Cortisol provides an immediate source of energy in flight/fight situations
Anti-inflammatory effects as it suppresses key cytokines, neutrophil recruitment, fibroblast proliferation.

56
Q

When is the ideal time of day for a surgery?

A

In the morning, as cortisol levels are raised and therefore it help the body respond better to stress.
Cortisol levels are lower at night.

57
Q

Give examples of stresses that will increase cortisol levels?

A

Anxiety
Trauma
Injury
Illness
Infection
Heat
Cold
Pain
Intensive exercises
Surgery

58
Q

What does cortisol do in times of stress?

A

Stimulates protein catabolism
Stimulates gluconeogenesis by liver
Inhibits glucose uptake by tissues, not brain
Stimulates lipolysis to free fatty acids
Inhibits inflammation and specific immune responses
Inhibits non-essential functions eg reproduction, growth etc)

59
Q

What are some examples of glucocorticoids used as medicines?

A

Prednisolone
Dexamethasone
Prednisone
Beclometasone
Betamethasone
Hydrocortisone
Budesonide

60
Q

What are some examples of mineralcorticoids used as medicines?

A

Fludrocortisone

Endocrinology (13 decks)

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