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Year 2 - Endocrinology > Adrenal Gland And Hormones > Flashcards

Adrenal Gland And Hormones Flashcards

1
Q

What is the difference between primary and secondary insufficiency

A 
Primary - problems with the gland itself 
- Addison's disease
- congenital adrenal hyperplasia (CAH)
- adrenal TB/malignancy 
Secondary - everything else that affects the adrenal gland 
- lack of ACTH stimulation
- iatrogenic (excess exogenous steroid)
- pituitary/hypothalamic disorder
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2
Q

Describe Addison’s disease

A

Autoimmune destruction of the adrenal cortex
- over 90% is destroyed before symptoms are ready
- autoantibodies are found in around 70% of cases
Associated with other autoimmune diseases
- T1DM, autoimmune thyroid diseases, pernicious anaemia

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3
Q

What are the clinical features of Addison’s disease?

A 
Anorexia
Weight loss
Fatigue/lethargy 
Dizziness and low BP
Abdominal pain
Vomiting 
Diarrhoea 
Skin pigmentation
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4
Q

How is primary adrenal insufficiency diagnosed?

A

Biochemistry
- increased potassium and decreased sodium
- hypoglycaemia
Short synACTHen test
Measure ACTH levels
- they should be very high (causes the skin pigmentation)
Renin/aldosterone levels
- renin will be very high and aldosterone will be decreased
Adrenal autoantibodies

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5
Q

What effect does decreased cortisol have on the HPA axis?

A

Lack of cortisol means CRH and ACTH are not inhibited and levels will be very high

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6
Q

Describe the short synACTHen test.

A

Measure plasma cortisol before and 30 mins after an IV ACTH injection
Normal - baseline >250nmol/l, post ACTH >480
Addison’s - baseline will be very low and remain low even after ACTH dosage

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7
Q

What are the actions of cortisol

A 
Promotes lipolysis
Counteracts insulin - decreases peripheral uptake of glucose
Decreased amino acid uptake by muscle
Increased gluconeogensis 
Reduces bone formation 
Slows the immune systems inflammatory response 
Increases appetite 
Maintains BP and CV function
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8
Q

How is primary adrenal insufficiency managed?

A

Hydrocortisone as cortisol replacement
- give IV if very unwell
- 15-30mg tablets daily in divided doses, to try and mimic the diurnal rhythm
Fludrocortisone as aldosterone replacement
- careful monitoring of BP and plasma potassium
Education
- sick day rules - double hydrocortisone dose when very unwell
- can’t suddenly stop
- need to wear identification

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9
Q

Why should you not stop taking fludrocortisone and hydrocortisone?

A

You will suffer from acute adrenal insufficiency, as the body doesn’t have time to produce its own hormones instead.
Causes all the symptoms of adrenal insufficiency, magnified and in a smaller space of time - can result in death in serious cases

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10
Q

What are the most common causes of secondary adrenal insufficiency?

A

Pituitary/hypothalamic diseases
- tumour, surgery or radiotherapy
Exogenous steroid use - most common cause

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11
Q

What does exogenous steroids do to the HPA axis, and give some examples of steroids.

A 
They have a negative effect on CRH and ACTH
Examples 
- high dose prednisolone 
- dexamethasone 
- inhaled corticosteriod
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12
Q

What are the clinical features of secondary adrenal insufficiency?

A

Similar to Addisons, EXCEPT

  • the skin doesn’t darken (ACTH level are not increased)
  • aldosterone levels are normal (production regulated by RAS system)
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13
Q

How is secondary adrenal insufficiency treated?

A

Given hydrocortisone to replace the cortisol loss

Fludorocortisone isn’t needed due to intact aldosterone levels

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14
Q

Briefly describe Cushing’s syndrome.

A

Excess cortisol secretion
High mortality
More common in women (ages 20-40)

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15
Q

Clinical features of cortisol excess.

A 
Easy bruising 
Facial plethora
Striae
Proximal myopathy 
Hypertension 
Thinning of skin
Moon face 
Poor wound healing 
Oestoporosis 
Increases appetite + weight gain
Increased susceptibility to infection
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16
Q

What are the two categories of Cushing’s syndrome?

A

ACTH dependent (secondary)

  • pituitary adenoma (68% - Cushing’s disease)
  • ectopic ACTH (12%)
  • ectopic CRH (
17
Q

How is it established that a patient has cortisol excess?

A

Dexamethasone suppression test - should suppress the cortisol production
24hr urinary free cortisol
Late night salivary cortisol

18
Q

How is the source of the cortisol excess established?

A

The ACTH is measured
- if it can’t be detected, the problem is in the adrenal gland (constantly pumping out cortisol inhibited ) = adrenal CT scan
- if it is normal/high, a CRH stimulation test is performed
CRH stimulation test
- if there is no change in the ACTH levels, it’s ectopic ACTH (as the tissue can still manage any changes in CRH) = CT scan to find
- a large increase means the problem the pituitary, and the remaining healthy tissue is forced to produce more ACTH = pituitary MRI

19
Q

How is Cushing’s disease managed with surgery?

A

Removal of ACTH source
- ectopic
- transsphenoidal pituitary surgery
Laparoscopic adrenalectomy

20
Q

How is Cushing’s managed medically?

A

Methyraprone/ketoconazole
- inhibit cortisol production
Should only be used as short term measure until surgery can be performed

21
Q

Describe iatrogenic Cushing’s syndrome.

A

Commonest cause of cortisol excess
Due to prolonged high dose steroid therapy
- e.g. Asthma, rheumatoid arthritis, IBS and transplants
The body thinks that these steroid are cortisol (because they act like cortisol) and that you have way too much of them = Cushing’s

22
Q

What are the main problems with iatrogenic Cushing’s syndrome?

A

Chronic suppression of pituitary ACTH production and adrenal atrophy - no endogenous cortisol

  • can’t respond to stress
  • need extra doses when I’ll
  • can’t stop suddenly
  • need to gradually withdraw over 4-6 weeks
23
Q

What is essential and secondary hypertension?

A

Essential (90%) - has no known cause
Secondary (10%) - secondary to another disease (e.g. Renal disease, aldosterone excess, drug induced)
- more likely in the young and resistant hypertension

24
Q

Hypertension can result from the adrenal gland, why?

A

Aldosterone is produced in the middle layer of the cortex (is a mineralocorticoid)

25
Q

What is the most common cause of secondary hypertension, and describe it?

A

Primary aldosteronism

  • autonomous production of aldosterone, independent of regulators (angiotensin II, or potassium)
  • due either to single adrenal adenoma or bilateral adrenal nodules
26
Q

What are the clinical features of primary aldosteronism?

A 
Significant hypertension
Low potassium (50%)
Alkalosis 
High aldosterone 
Suppressed renin concentration
27
Q

How do you diagnose primary aldosteronism?

A

Biochemistry - aldosterone, potassium and renin levels
Suppression testing
- not for patients with severe heart failure and uncontrolled hypertension
- IV saline load
- doesn’t lead to aldosterone suppression (like in normal people)
Adrenal CT scan

28
Q

What is the management of primary aldosteronism?

A

Surgical
- unilateral laparoscopic adrenalectomy - only if adrenal adenoma
-cures hypokalaemia and hypertension
Medical
- in bilateral adrenal hyperplasia
- mineralocorticoid antagonists (spironolactone or eplerenone)
- Na reabsorption blockers in the kidney

29
Q

What is phaeochromocytoma?

A

Catecholamine secreting tumour of the adrenal medulla

Very rare 2-8 cases per million people per year

30
Q

What are the clinical symptoms of a phaeochromocytoma?

A 
Hypertension 
Episodes of
- headache 
- palpations
- pallor
- sweating 
Also tremor, anxiety, nausea, vomiting, chest and abdominal pain
31
Q

How is a phaeochromocytoma diagnoses?

A

Measurement of urinary catecholamines

CT scan of the adrenals

32
Q

How is a phaeochromocytoma treated?

A

Adrenalectomy is best

- pre-op treatment is alpha1 and/or beta1 antagonists to block to effects of the catecholamines surge

Year 2 - Endocrinology (14 decks)

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