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Endocrine > Adrenal Gland > Flashcards

Adrenal Gland Flashcards

1
Q

What does the zona glomerulosa produce and what is it regulated by?

A 
Produces mineralocorticoids (aldosterone) 
Regulated by potassium
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2
Q

What does the zona fasciculata produce and what is it regulated by?

A

Glucocorticoids (cortisol and corticosterone)

Regulated by ACTH

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3
Q

What does the zona reticularis produce and what is it regulated by?

A 
Adrenal androgens (DHEA, testosterone) 
Regulated by ACTH and other unknown factors
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4
Q

What can be found within the adrenal medulla and what do they produce?

A

Chromaffin cells
Medullary vein
Splanchnic nerve
Produce catecholamines (noradrenaline and adrenaline)

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5
Q

What system regulates the production of aldosterone?

A

Renin-antiogenin system and plasma potassium

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6
Q

What occurs in BP falls?

A

Sensed by kidneys, angiotensionogen is converted to angiotensin 1
This is converted to angiotensin 2 in the lungs by ACE which acts on the adrenal zona golmerulosa to produce aldosterone which acts to retain salt increasing BP

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7
Q

What is the action of angiotensin 2?

A

Direct vasoconstriction

Indirect aldosterone release

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8
Q

What are the 6 classes of steroid receptors?

A 
Mineralocorticoid - aldosterone
Progestin
Oestrogen
Androgen
Vitamin D
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9
Q

What effect does cortisol have on the CNS?

A

Mood liability
Euophoria/psychosis
Decreased libido

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10
Q

What effect does cortisol have on bones/connective tissue?

A

Accelerates osteoporosis

Decreases serum calcium, collagen formation and wound healing

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11
Q

What effect does cortisol have on the immune system?

A

Decreases capillary dilation/permeability

Decreases leucocyte migration, macrophage activation and inflammatory cytokine production

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12
Q

What effect does cortisol have on metabolism?

A

Increases BG
Increases lipolysis
Increases proteolysis

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13
Q

What effect does cortisol have on the circulatory/renal system?

A

Increases cardiac output
Increases BP
Increases renal blood flow and eGFR

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14
Q

What are the 3 main principles of corticosteroid use?

A

Suppress inflammation
Suppress immune system
Replacement treatment

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15
Q

What diseases are corticosteroids particularly useful?

A

Allergic disease: asthma/anaphylaxis
Inflammatory disease: RA, UC, crohns
Malignant: improve appetite, suppress excess hormone production

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16
Q

What are the effects of aldosterone?

A

Sodium/potassium balance: K+/H+ excretion and Na+ reabsorption
BP regulation
Regulation of ECF

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17
Q

What can cause primary adrenal insufficiency?

A

Addison’s disease
Congenital adrenal hyperplasia
Adrenal TB
Adrenal malignancy

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18
Q

What can cause secondary primary adrenal insufficiency?

A

Due to lack of ACTH stimulation
Iatrogenic
Pituitary/hypothalamic disorders

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19
Q

Describe autoimmune polyglandular syndrome type 1 and 2

A

Type 1 = Addisons, hypoparathyroidism, mucosal candidiasis

Type 2 = hypothyroidism, addisons, T1DM

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20
Q

What is waterhouse friderichesen disease?

A

Bilateral haemorrhage into adrenal glands due to sepsis

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21
Q

What are the clinical features of addison disease?

A 
Anorexia, wt loss
Fatigue/lethary
Dizziness/ low BP 
Abdo pain
D+V
Skin pigmentation (buccal mucosa)
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22
Q

What biochem is seen in addison/addisonian crisis?

A

Hyponatraemia
Hyperkalaemia
Hypotension
Hypoglycaemia

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23
Q

What is the short synacthen test?

A

250 micrograms of ACTh and do a cortisol level at 0 and 30 mins
Baseline should be above 250 and after 30 mins should rise to 500
Anything below that is abnormal

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24
Q

What will the ACTH levels be like in addisons?

A

Very high

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25
Q

What will the renin/aldosterone levels be like in addisons?

A

High renin

Reduced aldosterone

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26
Q

What will it suggest is there are high levels of 17-OH progesterone?

A

CAH

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27
Q

What should you do if there is a negative 21-Oh antibody?

A

CT adrenals: infiltrative disease, adrenal haemorrhage, infections, malignant tumours

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28
Q

What is adrenoleukodystrophy?

A

X-linked - breakdown of myelin which is the fatty covering of nerve cells, causes progressive dysfunction of the adrenal gland

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29
Q

Why is ACTH increased in addison’s if there is not cortisol?

A

Failure in the negative feedback loop- cortisol acts to suppress the hypothalamic (CRH) and anterior pituitary and therefore when there is no cortisol the levels of CRH and ACTH increase

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30
Q

How is an addisonian crisis managed?

A

IV hydrocortisone - 100mg IV/IM then 50mg every 6hr until well
0.9% saline - due to salt loss
Fludrocortisone for lack of mineralocoritoids

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31
Q

How is addison disease managed?

A

Give hydrocortisone to mimic physiological steroids - diurnal variation
Fludrocortisone - need to monitor BP and K

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32
Q

What are the sick rules in addison’s disease?

A

Double hydrocortisone for intercurrent illness until recovery - if unable to tolerate medication due to gastroenteritis need IM or SC hydrocortisone
Major surgery - 100mg IV pre op then continous infusion of 200mg/24hr

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33
Q

What can cause secondary adrenal insufficiency (lack of CRH/ACTH)?

A

Pituitary/hypothalamic disease tumours

Exogenous steroid use

34
Q

What are the clinical features of secondary adrenal insufficiency?

A

Similar to addisons EXCEPT:
skin pale
Aldosterone production intact
Treat with hydrocortisone replacement

35
Q

What are the clinical features of cortisol excess?

A 
Easy bruising
Facial plethora
Striae
Proximal myopathy
Mental health: anxiety, fear, depression 
Interscapular fat pad
Poor wound healing
Central obesity
Moon face
Osteoporosis
Increased appetitie
T2DM
36
Q

What is a common presentation of cushing’s?`

A

17 year old girl with a 3 year history of central weight gain, acne, amenorrhoea, hypertension, severe osteoporosis, proximal muscle weakness

37
Q

What causes ACTH dependent cushing’s?

A

Pituitary adenoma - cushing’s disease
Ectopic ACTH
Ectopic CRH

38
Q

What causes ACTH independent cushing’s syndrome?

A

Adrenal adenoma
Adrenal carcinoma
Nodular hyperplasia

39
Q

What tumours commonly produce ACTH?

A 
Small cell lung carcinoma
Bronchial carcinoid tumour
Thymic carcinoid
Pancreatic islet cell tumour
Pheochromocytoma
Medullary carcinoma
40
Q

How is cushing’s diagnosed?

A

Establish cortisol excess: overnight dexamethasone suppression test
24 urinary free cortisol
Late nigh salivary cortisol

41
Q

What occurs in the low dose dexamethasone suppression test?

A

0.5mg every 6hrs for 48hrs - 2mg overall

If dexamethasone suppresses cortisol levels then you don’t have cushing’s

42
Q

What is the commonest cause of cushing’s syndrome?

A

Prolonged high dose steroid therapy - asthma, RA, IBD, transplants
Chronic suppression of pituitary ACTH production and adrenal atrophy

43
Q

What are the implications of long term steroid use?

A

Unable to respond to stress
Need extra doses when ill/surgical procedure
Cannot stop suddenly
Gradual withdrawal of steroid therapy if >4-6 weeks

44
Q

What are the endocrine causes of hypertension?

A

Conn’s syndrome
Pheochromocytoma
Cushing’s
Acromegaly

45
Q

What does hypertension, hypokalemia and alkalosis suggest?

A

Primary aldosteronism

46
Q

What is primary aldosteronism?

A

Autonomous production of aldosterone independent of its regulators (angiotensin 2/potassium)

47
Q

What is conn’s syndrome?

A

Aldosterone adenoma in the adrenal cortex

48
Q

What occurs are the apical membrane?

A

Retention of sodium and excreting potassium

49
Q

How does spironolactone work?

A

mineralocorticoid receptor antagonists - can cause hyperkalaemia

50
Q

What are the CV actions of aldosterone?

A 
Increases symp flow
Increased cardiac collagen
Altered endothelial function 
BP 
Sodium retention 
LVH
Increased production of free radicals
51
Q

What can cause primary aldosteronism?

A

Conn’s syndrome
Bilateral adrenal hyperplasia
Genetic mutations
Unilateral hyperplasia

52
Q

What is step 1 in the diagnosis of primary aldosteronism?

A

Measure plasma aldosterone and renin and express as ratio
If raised, then investigate further with saline suppression test
Failure of plasma aldosterone to suppress by more than 50% with 2 litres of normal saline confirms PA

53
Q

What is step 2 in the diagnosis of primary aldosteronism?

A

Adrenal CT to demonstrate adenoma

Adrenal vein sampling to confirm adrenoa is true source of aldosterone excess

54
Q

At a cellular level, what causes conns?

A

Mutation in the potassium channel of adrenocorticoid cells

55
Q

How is PA treated?

A

Surgical onlyif adrenal adenoma and excess confirmed in adrenal vein sampling
Medical in bilateral adrenal hyperplasia
Use MR antagonists - spirnoloacton

56
Q

What will surgery cure in PA?

A

Hypokalaemia

Hypertension in 30-70% of cases

57
Q

What is CAH?

A

Disorder resulting in malfunction in steroid production due to mutations int he enzyme 21-alpha hydroxylase
Very high levels of testosterone

58
Q

What is the mode of inheritance of CAH?

A

Autosomal recessive inheritance in consanguineous parents

Can be sporadic

59
Q

What are the classical symptoms of CAH?

A

Salt-wasting
Hypotension
Adrenal crisis
Simple virilising of females

60
Q

How is CAH diagnosed?

A

Basal 17-OH progesterone levels

61
Q

How will CAH present in males?

A

Adrenal insufficiency within first 2/3 weeks
Poor weight gain
Biochemical pattern of addisons
Percocious puberty

62
Q

How will CAH present in females?

A

Genital ambiguity
Hirsutism
Acne
Oligomenorrhea

63
Q

How is CAH treated in children?

A

Glucocorticoid replacement
Surgical correction
Achieve maximal growth potential

64
Q

How is CAH treated in adults?

A

Control androgen excess
Restore fertility
Avoid steroid over-replacement

65
Q

What are the precursors of adrenaline and noradrenaline?

A

Tyrosine to L-dope to dopamine which converts to noradrenaline which then converts to adrenaline

66
Q

What is a paraganglioma?

A

Extra-adrenal pheochromocytoma that can occur anywhere in the symp chain

67
Q

What is a MIBG scan?

A

Scan that shows the ability of a phaeo to take up a radio-isotope linked to the MIBG tracer

68
Q

What cells does the phaeo originate from?

A

Neuroendocrine tumour of the medulla originating from the chromaffin cells

69
Q

What are clinical clues to phaeochromocytoma?

A 
Labile hypertension (see-sawing hypertension) 
Postural hypotension 
Paroxysmal sweating
Headache
Pallor
Tachycardia
70
Q

What is the rule of 10s in a phaeo?

A 
10% malignant
10% bilateral
10% extra-adrenal
10% familial
10% associated with hyperglycaemia
10% children
71
Q

What colour will a phaeo turn the adrenal gland?

A

Reduces chrome salts to metal chromium resulting in a brown colour reaction

72
Q

What is included in the differential of a phaeo?

A 
Angina
Anxiety
Carcinoid
Thyrotoxicosis
Insulinoma
Menopause
Arrhythmia e.g. SVT
Migraine
Drug toxicity
Alcohol withdrawal
Pregnancy
Hypoglycaemia
73
Q

What is the classic symptoms in a phaeo?

A 
Hypertension 
Headache
Sweating 
Palipatations
Breathlessness
Constipation 
Wt loss
Anxiety/fear
FHx
74
Q

What are signs of complications in a phaeo?

A 
LVF
Myocardial necrosis
Stroke
Shock
Paralytic ileus of bowel
75
Q

What biochemical abnormalities are present in a phaeo?

A 
Hyperglycaemia
Hypokalaemia
High haematocrit
Mild hypercalcaemia
Lactic acidosi
76
Q

Who should be investigated for a phaeo?

A 
Family members with syndromes
Resistant hypertension 
Young (under 50) with hypertension 
Classical symptoms
Consider with hypertension and hyperglycaemia
77
Q

How are catecholamines excess confirmed?

A

Urine - 2x24h4 catecholamines

Plasma - ideally at time of symptoms

78
Q

How is a phaeochromocytoma diagnosed?

A

MRI scan: abdomen, whole body
MIBG
PET scan

79
Q

How is a phaeo treated?

A 
Always A before B 
Alpha blockage
Beta blocker
Fluid/ blood replacement
Careful anaesthetic assessment
Surgery 
Chemo is malignant
80
Q

What clinical syndromes is a pheochromocytoma associated with?

A 
MEN2
VHL
SDH - B and D 
Neurofibromatosis
Tuberous sclerosis

Endocrine (35 decks)

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