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y2 brs (haroop) > Adrenal gland (hyper) > Flashcards

Adrenal gland (hyper) Flashcards

1
Q

What are the clinical features of Cushing’s disease?

A

1) Excess cortisol
2) Centripetal obesity
3) Moon face and buffalo hump
4) Proximal myopathy
5) Hypertension and hypokalaemia
6) Red striae, thin skin, and bruising
7) Osteoporosis and diabetes

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2
Q

What are the main causes of Cushings?

A
  • Overdose of oral corticosteroids
  • Pituitary dependent Cushing’s disease
  • Ectopic ACTH from lung cancer
  • Adrenal adenoma secreting cortisol
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3
Q

What are the investigations that are conducted to determine the cause of Cushing’s syndrome?

A

-24H urine collection for urinary free cortisol
-Blood diurnal cortisol levels
(Cortisol usually highest at 9am and lowest at midnight, if asleep)
-Low dose dexamethasone suppression test

In patient’s with Cushing’s, the cortisol level remains elevated throughout the day

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4
Q

What type of rhythm is exhibited by cortisol secretion?

A

Diurnal rhythm

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5
Q

What is a positive result for a low dose dexamethasone suppression test?

A

There is a failure of cortisol ACTH suppression, therefore morning cortisol remains elevated >50nanomol/L.

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6
Q

What suppressive investigation is done to identify a patient with potential Cushing’s disease?

A

Low dose dexamethasone suppression test.

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7
Q

What pharmacological interventions are implemented for patients with hypersecretion of cortisol from the adrenal cortex?

A

Metryapone

Ketoconazole

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8
Q

Which adrenal cortex structure is affected in a patient with Conn’s syndrome?

A

Tumour of the zona glomerulosa, therefore leading to excess aldosterone

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9
Q

Which enzyme is inhibited by metyrapone?

A

11B-hydroxylase

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10
Q

What is the mechanism of action of metryapone?

A

Inhibition of 11B-Hydroxylase, this arrests steroid synthesis within the zona fasciculata at the 11-deoxycortisol stage

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11
Q

Does 11-deoxycortisol exert negative feedback on the hypothalamus?

A

There is no negative feedback effect on the hypothalamus and pituitary gland.

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12
Q

What are the advantages of using metryapone preoperatively?

A

Improves patient’s symptoms and promotes better post-operative recovery (better wound healing, less infection).

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13
Q

How should cortisol be controlled and regulated in patients taking metryapone?

A

Adjust oral dose according to cortisol level (aim for mean serum cortisol 150-300nmol/L).

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14
Q

What are the side effects of using metryapone on aldosterone synthesis?

A

Deoxycorticosterone accumulates within the zona glomerulosa, exhibiting aldosterone-like (mineralocorticoid) activity, leading to salt retention and hypertension.

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15
Q

What type of effects are exerted by deoxycoticosterone?

A

Mineralocorticoid activity

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16
Q

Where does deoxycorticosterone accumulate in patients taking metryapone?

A

Accumulates in the zona glomerulosa.

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17
Q

What are the unwanted actions of metryapone?

A

Hypertension on long-term administration

Hirsutism (increased adrenal androgen production in women)

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18
Q

What toxic risk is associated with ketoconazole?

A

Hepatotoxicity

Therefore monitor liver function weekly, clinically and biochemically

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19
Q

Which enzyme is inhibited by ketoconazole?

A

17-alpha hydroxylase

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20
Q

What follow up investigations should be conducted in patients prescribed with ketoconazole?

A

Weekly liver function tests due to hepatotoxicity risks (P450 poison)

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21
Q

What is the 1st line of treatment for a patient with an ACTH-secreting pituitary adenoma?

A

Pituitary surgery (transsphenoidal hypophysectomy)

22
Q

What are the surgical interventions for the treatment of Cushing’s?

A

1) Transsphenoidal hypophysectomy
2) Bilateral adrenalectomy
3) Unilateral adrenalectomy for adrenal mass.

23
Q

What is the main cause of Conn’s syndrome?

A

Benign adrenal cortical tumour of the zona glomerulosa

Resulting in an excess production of aldosterone

24
Q

What are the associated clinical features of Conn’s syndrome?

A

Hypertension
Hypokalaemia
Hypernatremia

25
Q

What type of hyperaldosteronism is Conn’s syndrome?

A

Priamry hyperaldosteronism

26
Q

What impact does Conn’s syndrome have on the Renin-angiotensin system?

A

RAAS should be suppressed (exclude secondary hyperaldosteronism)

27
Q

What two main drugs are prescribed in patients with Conn’s syndrome?

A

Spironolactone

Epleronone

28
Q

What is the mechanism of action of spironolactone?

A

Converted to several active metabolites, including canrenone, a competitive antagonist of mineralocorticoid receptors (MR)

  • Blocks sodium reabsorption and potassium excretion in the kidney tubules (potassium sparing diuretic)
  • antihypertensive
29
Q

Which metabolite is formed through the conversion of spironolactone?

A

Canrenone

30
Q

Which receptors are antagonised by spironolactone metabolites?

A

Mineralocorticoid receptors

31
Q

Describe the pharmacokinetics of spironolactone?

A

Orally active

Highly protein bound and metabolised in the liver.

32
Q

What are the unwanted actions of spironolactone?

A

Menstrual irregularities (+progesterone receptor)

Gynaecomastia (inhibits androgen receptors)

33
Q

What type of antagonist is epleronone?

A

A mineralocorticoid receptor antagonist

34
Q

Which conn’s syndrome drug is better tolerated?

A

Epleronone

35
Q

Why is epleronone better tolerated than spironolactone?

A

Less binding to androgen and progesterone receptors compared to spironolactone

36
Q

What is a phaechromocytoma?

A

Tumours of the adrenal medulla which secrete catecholamines

37
Q

How are catecholamines secreted from the adrenal medulla?

A

Secreted in response to sympathetic stimulation

38
Q

What type of receptors does cortisol bind onto?

A

Mineralocorticoid and glucocorticoid receptors

39
Q

Which enzyme is secreted by the kidney to convert bioactive cortisol to cortisone?

A

11B-hydroxysteroid dehydrogenase 2

40
Q

What is the purpose of 11b-hydroxysteroid dehydrogenase 2?

A

Converts bioactive cortisol to cortisone, constantly removing cortisol to reduce interference with mineralocorticoid receptors

41
Q

What are the catecholamine producing cells of the adrenal medulla?

A

Chromaffin cells

42
Q

What are the potential risks with a phaeochromocytoma?

A

Elevations in adrenaline typically manifest as severe hypertension causing potential myocardial infarctions or strokes, as well as ventricular fibrillation within patients becoming a medical emergency.

43
Q

How are catecholamines released from the adrenal medulla in patients with a phaeocromocytoma?

A

Released upon sympathetic activation leading to an adrenaline storm.

44
Q

Which hormone can be measured in urine and blood as a marker for phaeochromocytoma associated release of adrenaline?

A

metanephrine (has a long half life)

45
Q

What is the classic triad of symptoms for patients with a phaeocromocytoma?

A

Palpitations
Headaches
Diaphoresis (excessive sweating)

46
Q

What is the main clinical feature of a phaeochromocytoma?

A

Sustained or paroxysmal hypertension
Cases of hypertension may proceed after abdominal pain episodically, in comparison to Conn’s syndrome (smooth secretion of aldosterone)

47
Q

What are the associated risks with a phaeochromocytoma?

A

Family history of endocrine disorders

MEN, Von-Hippel-Lindau syndrome, germline mutations in the succinate dehydrogenase

48
Q

What is the first line of treatment of a phaeochromocytoma?

A

Anti-hypertensive agents: phentolamine IV and sodium nitroprusside

49
Q

What are the precautions required for patients with a phaeochromocytoma surgical excision?

A

Careful preparation as anaesthetic can precipitate a hypertensive crisis

50
Q

Why is an alpha-blockade administered in the management of a phaeochromocytoma?

A

Inhibition of alpha-receptors minimises the impact of vasoconstriction induced by noradrenaline/adrenaline, therefore reducing blood pressure.

-IV fluids to compensate for potential hypotensive crisis

51
Q

Why is a beta-blockade administered in the management of a phaeochromocytoma?

A

Administer atenolol/metoprolol/propanolol to prevent tachycardia and arrhythmia.

y2 brs (haroop) (62 decks)

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