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Endocrine > Adrenal Disorders > Flashcards

Adrenal Disorders Flashcards

1
Q

What catecholamines are secreted by the the adrenal medulla?

A

Adrenaline

Noradrenaline

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2
Q

What veins and nerves are found in the adrenal medulla?

A

Medullary veins

Splanchnic Nerves

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3
Q

What regulates Aldosterone?

A

Renin-Angiotensin-ALDOSTERONE-System (RAAS)

Plasma Potassium

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4
Q

What are the 6 classes of steroid receptors?

A 
Glucocorticoid
Mineralocorticoid
Progestin
Oestrogen
Androgen
Vitamin D
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5
Q

What action do glucocortiocoids have on the circulatory/ renal systems?

A

Increased:

  • Cardiac output
  • Blood pressure
  • renal blood flow
  • Glomerular Filtration Rate
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6
Q

What effect do glucocorticoids have on the CNS?

A

Mood lability
Euphoria/psychosis
Decreased libido

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7
Q

How do Glucocorticoids affect the bone and connective tissue?

A 
Accelerates osteoporosis
Decreases:
- Serum calcium
- collagen formation
- wound healing
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8
Q

What are the 3 main uses of corticosteroids in practice?

A
  • Suppress inflammation
  • Suppress immune system
  • Replacement treatment
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9
Q

Where are the mineralocorticoid receptors found?

A

Kidneys
Salivary glands
Gut
Sweat glands

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10
Q

What can cause PRIMARY adrenal insufficiency?

A
  • Addison’s disease
  • Congenital Adrenal Hyperplasia (CAH)
  • Adrenal TB/malignancy
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11
Q

What causes secondary adrenal insufficiency?

A
  • lack of ACTH stimulation
  • Iatrogenic (removal of steroid Tx)
  • Pituitary/hypothalamic disorders
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12
Q

What is addison’s disease?

A

Autoimmune destruction of adrenal cortex

Autoantibodies positive in 70%

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13
Q

What percentage of the adrenal cortex is usually destroyed before people experience symptoms in Addison’s disease?

A

> 90%

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14
Q

What other autoimmune diseases are associated with Addison’s disease?

A
  • Type 1 DM
  • autoimmune thyroid disease
  • pernicious anaemia
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15
Q

What features of biochemistry would make you suspicious of adrenal insufficiency?

A

Low Na+
High K+
hypoglycaemia

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16
Q

What treatments are used to manage adrenal insufficiency?

A
  • Hydrocortisone as cortisol replacement

- Fludrocortisone as aldosterone replacement

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17
Q

If people are on treatment for adrenal insufficiency, what should they be educated on?

A
  • ‘sick day rules’ due to needing more steroid when ill
  • Cannot stop medication suddenly
  • Need to wear identification
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18
Q

What hormones are diminished in secondary adrenal insufficiency?

A

CRH and ACTH

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19
Q

Where are striae often seen in Cushing’s syndrome and why?

A
  • Around stomach (due to increased central obesity)

- Inside of proximal thighs

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20
Q

What hormone is found in excess in Conn’s syndrome

A

Aldosterone

21
Q

Describe what is meant by Primary Aldosteronism?

A

Autonomous production of aldosterone independent of its regulators (angiotensin II/potassium)

22
Q

What clinical features normally indicate Primary Aldosteronism?

A
  • Significant hypertension
  • Hypokalaemia (in around 30%)
  • Alkalosis
23
Q

What are the main causes of primary aldosteronism?

A
  • Adrenal adenoma (Conn’s)

- Bilateral adrenal hyperplasia (commonest cause)

24
Q

How is Aldosterone excess confirmed?

A
  • Aldosterone to renin ratio (ARR)
  • Saline suppression test
    (Failure of plasma aldosterone to suppress by > 50% with 2 litres of normal saline)
25
Q

How can the type of primary aldosteronism be confirmed?

A
  • Adrenal CT to demonstrate adenoma

- Adrenal vein sampling to confirm adenoma is true source of aldosterone excess

26
Q

What surgery can be used to treat primary aldosteronism?

A
  • Unilateral laparoscopic adrenalectomy

Only if adrenal adenoma confirmed by vein sampling

27
Q

What type of treatment can be used in bilateral adrenal hyperplasia?

A

Use Mineralocorticoid Receptor antagonists (spironolactone or eplerenone)

28
Q

Aldosterone excess is a common cause of secondary hypertension. TRUE/FALSE?

29
Q

What enzyme is deficient in Congenital Adrenal Hyperplasia

A

21α hydroxylase

30
Q

Is Congenital Adrenal Hyperplasia Autosomal Dominant or Recessive?

A

Autosomal Recessive

31
Q

What marker is tested for in the suspicion of Congenital Adrenal Hyperplasia

A

17-OH Progesterone

32
Q

How does Congenital Adrenal Hyperplasia classically present in males?

A
  • Adrenal insufficiency
  • Often around two to three weeks
  • Poor weight gain
  • Biochemical pattern (Low Na, High K, Hypoglycaemic)
33
Q

How does Congenital Adrenal Hyperplasia classically present in females?

A

Genital ambiguity

34
Q

Describe a “non-classical” presentation of Congenital Adrenal Hyperplasia

A 
Hirsutism
Acne
Oligomenorrhoea
Precocious puberty
Infertility or sub-fertility
35
Q

How are children with CAH usually treated?

A
  • Glucorticoid replacement
  • Mineralocorticoid replacement ONLY SOME
  • Surgical correction
    => Achieve maximal growth potential
36
Q

If CAH is not noticed until adulthood, how is it treated at this stage?

A
  • Control androgen excess
  • Restore fertility
  • Avoid steroid over-replacement
37
Q

How does Phaeochromocytoma usually present?

A
  • Labile hypertension
  • Postural hypotension
  • Paroxysmal sweating/headache/pallor/tachycardia
  • *sometimes presents with none of these**
38
Q

What colour are phaechromocytomas and why?

A

Chromaffin cells reduce chrome salts to metal chromium

=>resulting in a brown colour reaction

39
Q

In what section of the adrenal gland is a phaechromocytoma found?

40
Q

Why does compression of a phaechromocytoma cause an increase in blood pressure?

A

Squeezes out noradrenaline and adrenaline

=> sympathetic drive increases BP

41
Q

What complications of phaeochromocytoma can appear to present as stand alone illness?

A 
Left ventricular failure
Myocardial necrosis
Stroke
Shock
Paralytic ileus of bowel
42
Q

What biochemical abnormalities are often seen in Phaechromocytoma?

A
  • Hyperglycaemia – adrenaline secreting tumours
  • low K+ level
  • raised Hb conc.
  • Mild hypercalcaemia
  • Lactic acidosis – in absence of shock
43
Q

What patients should be investigated on suspicion of phaeochromocytoma?

A
  • Family members with syndromes
  • Resistant hypertension
  • The young [<50] with hypertension
  • Classical symptoms
  • Consider with hypertension and hyperglycaemia
44
Q

How is an excess in catecholamines in phaeochromocytoma confirmed?

A

Urine – 2x24hour catecholamines or metanephrins

45
Q

What imaging modalities can be used to identify the source of catecholamine excess?

A 
MRI Scan (Abdomen/Whole body)
MIBG – meta-iodobenzylguanidine
PET Scan
46
Q

What medical treatments are used in phaeochromocytoma?

A
  • Phenoxybenzamine (α-blocker)
  • Propranolol, atenolol or metoprolol (β-blocker)

A before B

47
Q

What surgical treatment can be used in phaechromocytoma?

A

Laparoscopic surgery
Attempt full excision
**chemotherapy can also be used if malignant
=> Radio-labelled MIBG

48
Q

Phaeochromocytoma is linked to what genetic conditions?

A
  • Multiple Endocrine Neoplasia 2 (MEN2)
  • Von-Hippel-Lindau syndrome
  • Succinate dehydrogenase mutations (SDH)
  • Neurofibromatosis
  • Tuberose sclerosis

Endocrine (24 decks)

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