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Adrenal disorders Flashcards

1
Q

the medulla of the adrenal gland is

A

primitive nerve tissue

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2
Q

the cortex of the adrenal gland is

A

endocrine tissue (deep you o the sweeter its gets

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3
Q

Zona glomerulosa

A

Salt and water- mineralocorticoids

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4
Q

Zona fasciculata

A

Sugar -glucocorticoids

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5
Q

Zona reticularis

A

Sex- androgen

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6
Q

Disorders of the adrenal cortex

A

Adrenal insufficiency’s

Cushing’s

Hyperaldosteronism

Congenital adrenal hyperplasia (CAH)

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7
Q

Disorders of the adrenal medulla

A

Pheochromocytoma (dusty coloured cell of a tumour)

Paraganglioma (pheochromocytoma outside the adrenal gland)

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8
Q

Presentation of adrenal medulla disease (noradrenaline/ adrenaline)

A
  • Excessive catecholamine secretion
  • Acute episodes
  • Sweating
  • Palpitations
  • High or low BP
  • Collapse
  • SUDDEN DEATH
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9
Q

Biochemical assessment of adrenal medulla

A
  • 24h urine catecholamines
    • Adrenaline
    • NA
    • Dopamine
    • 3-methoxy-tyramine
  • Usually measure breakdown products of catecholamines- Metanephrines24 h urine metanephrines
    • Metadrenaline
    • Normetadrenaline
  • Plasma metanephrines (more sensitive than 24h urine)
    • Avoid certain foods: coffee, coke, bananas, chocolate, vanilla
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10
Q

Clinical presentation of adrenal cortex disease: Cortisol (lack of glucocorticoid) deficiency

A

weakness, tiredness, weight loss, hypoglycaemia

*Cortisol does the opposite to insulin*

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11
Q

Clinical presentation of adrenal cortex disease: Mineralocorticoid (aldosterone) deficiency

A

– dizziness, hypotension, low Na, high K

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12
Q

Clinical presentation of adrenal cortex disease: Androgen deficiency– e.g. Addisons

A
  • In women- low libido and loss of body hair in women
    • Testosterone only produced in adrenal gland in women
  • In men- no symptoms because produced in testosterone
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13
Q

Clinical presentation of adrenal cortex disease: Cortisol excess

A
  • Weight gain and cushingoid features (cushing’s syndrome)
  • Diabetes
  • Bone weakness
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14
Q

Clinical presentation of adrenal cortex disease: Mineralocorticoid excess (aldosterone)-

A

high BP and low K

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15
Q

Clinical presentation of adrenal cortex disease: androgen excess

A

increased male characteristics in women

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16
Q

ACTH excess from pituitary

A
  • Skin pigmentation due to melanocyte stimulation
  • Pigmentation seen in Addisons and ACTH- driven cushings
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17
Q

Biochemical assessment of adrenal cortex: Suspected adrenal hormone deficiency

A
  • Electrolytes- low Na, high K in aldosterone deficiency
  • 0900 basal cortisol- low when it should be high
  • Stimulation test- inject synthetic ACTH (synacthen)
  • ACTH stimulates cortisol
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18
Q

Biochemical assessment of adrenal cortex :Suspected adrenal hormones excess

A
  • Electrolyte- high BP, low K
  • Midnight cortisol- high, should be low
  • 24h urine cortisol- high
  • Suppression test- failure to suppress
  • Androgens and derivatives – high
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19
Q

Radiological assessment of adrenal disease

CT scan

A
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20
Q

Radiological assessment of adrenal disease

MRI scan

A
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21
Q

Radiological assessment of adrenal disease

functional imaging - MIBG scan

A
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22
Q

Radiological assessment of adrenal disease

functioning imaging - PET scan

A
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23
Q

adrenal cortex disorders are related to which hormones

A

aldosterone, cortisol and androgens

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24
Q

Hperaldosteronisms

A

A condition in which there is excessive production of aldosterone.

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25
Q

Primary hyperaldosteronism:

A

excess aldosterone production due to a defect in the adrenal cortex. Commonoest form of endocrine hypertension.

  1. Bilateral idiopathic adrenal hyperplasia
  2. Or Aldosterone-secreting adenoma (Conns syndrome)
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26
Q

diagnosis of primary hyperaldosteornism

A
  • Hypertension and hyperkalaemia
  • Elevated aldosterone independent of RAAS (suppressed renin)
  • Scan- shows adrenal adenoma or bilateral hyperplasia
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27
Q

Secondary hyperaldosteronism:

A
  • excess aldosterone production due to overactivity of the RAAS
  • Renin- producing tumour or renal artery stenosis
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28
Q

signs and symptoms of hyperaldosteronism

A
  • High blood pressure
  • Left ventricular hypertrophy
  • Stroke
  • Hypernatremia
  • Hypokalaemia
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29
Q

treatment of hyperalsteronism

A
  • Dependent on cause
    • Surgical treatment for aldosterone-secreting adenomas or
    • Spironolactone (a mineralocorticoid receptor agonists) can be used for other causes
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30
Q

what is a disorder cause dby excessive exposure to cortisol

A

cushing’s syndrome

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31
Q

causes of cushing’s syndrome can be

A

exogenous or endogenous

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32
Q

exogenous causes of cushing’s syndrome

A

main cause is being prescribed glucocorticoids

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33
Q

endogenous causes of main cause cushing’s syndrome

A
  • Cushing’s disease: benign pituitary adenoma that secretes ACTH
  • Adrenal cushing’s: Adrenal tumour secreting glucocorticoids
  • Non- pituitary-adrenal tumours producing ACTH and/ or CRH (e.g. small cell lung cancer- very rare)
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34
Q

Signs and symptoms of Cushing’s syndrome

A
  • Moon shaped face
  • Buffalo hump
  • Abdominal obesity
  • Striae
  • Acute weight gain
  • Hyperglycaemia – increased gluconeogenesis
  • Hypertension- mineralocorticoid effects of excess cortisol
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35
Q

Non- pituitary-adrenal tumours producing ACTH and/ or CRH

A

e.g. small cell lung cancer- very rare

36
Q

sterid drugs have the same effects as

A

higher levels of cortisol

*steroid dosage should always be decreased gradually and never stopped suddenly*

37
Q

adrenal cushins syndrome

A

ACTH is suppressed- ACTH independent

  • Unlike pituitary and ectopic ACTH
38
Q

symptoms of

Adrenal Cushing’s syndrome

A
  • Androgenic symptoms may be present
    • Hirsutism
    • Acne
    • Greasy skin
  • Virilising features in large tumours
    • Androgenic alopecia
    • Deep voice
    • Clitoromegaly (abnormal enlargement of the clitoris)
39
Q

treatment of adrenal cushing syndrome

A
  • Adrenalectomy- laparoscopic
  • Large tumours need open surgery
40
Q

Androgens are partially regulated by

A

ACTH and CRH.

41
Q

androgens promote

A

Promote axillary and pubic hair growth in both males and females

43
Q

androgens and males

A
  • In prepubescent males dehydroepiandrosterone (DHEA) released from the adrenal glands is converted to testosterone in the testes.
  • After puberty this production is insignificant as the testes themselves release testosterone
44
Q

androgens and females

A
  • Adrenal androgens promote libido and are converted to oestrogen in tissues
  • After menopause this is the only source of oestrogen in the body (not in ovaries)
45
Q

Genital ambiguity in female infants caused by which genetic defect

A

deficiency of the 21-hydroxylase enzyme

46
Q

deficiency of the 21-hydroxylase enzyme results in and can cause what

A

decreased glucocorticoid and mineralocorticoid production

  • Precursor of these hormones- 17a-hydroxypregnenolone is therefore diverted to more androgen synthesis (e.g. testosterone)
  • Can also cause salt wasting crises- high rate of sodium lost
47
Q

ACTH and steroid suppression:

ACTH deficiency

A
  • Occurs in any case of hypopituitarism
  • Similar symptoms to primary adrenal failure
  • No pigmentation as ACTH not raised
  • No hyperkalaemia as no mineralocorticoid deficiency
  • Hyponatraemia due to effect of cortisol on free water excretion
48
Q

ACTH and steroid suppression:

Steroid induced hypoadrenalism

A
  • ACTH suppressed with long-term steroids
  • Abrupt withdrawal can cause hypo-adrenal crisis
  • Important to consider if an unwell patient is on steroids
49
Q

which adrenal disorder is reffered to as Primary adrenal insufficiency

A

Addisons disease

50
Q

Addisons disease

A

hypocortisolism

51
Q

causes of Addisons disease

A
  • Destructive atrophy of the adrenal glands by autoimmune response
  • Fungal infections
  • Adrenal cancer
  • Adrenal haemorrhage
  • TB (in old times- good time lol)
52
Q

Addisons disease signs and symptoms

A
  • Postural hypotension
  • Lethargy
  • Weight loss
  • Anorexia
  • Increased skin pigmentation hypoglycaemia
53
Q

addisons disease and hyperpigmentation

A
  • Decrease in cortisol
  • Reduced negative feedback on the anterior pituitary
  • More POMC produced to synthesis ACTH
  • POMC also produces alpha-MSH
  • Increase in MSH= increase in melanin synthesis- hyperpigmentation
  • ACTH can also activate melanocortin receptors on melanocytes- hyperpigmentation
54
Q

maintenance treatment of Addisons disease

A
  • Lifelong replacement
    • Glucocorticoid: hydrocortisone, prednisolone
    • Mineralocorticoid: fludrocortisone
  • Education
    • Double dose of glucocorticoid at time of illness
    • Emergency HC injection if vomiting
    • Steroid card and bracelet
55
Q

Addisonian crisis

A

Life threatening emergency due to adrenal insufficiency

56
Q

causes of addisonian crisis

A
  • Abrupt steroid drug withdrawal
  • Severe stress
  • Salt depravation
  • Infection
  • Trauma
  • Cold exposure
  • Over exertion
57
Q

addisonian crisis signs and symptoms

A

Collapse

Nausea

Vomiting

Pyrexia

Hypotension

Vascular collapse

58
Q

addisonian crisis treatment

A

fluid replacement and cortisol

59
Q

Diagnosis of suspected adrenocortical disease

A
  • Measurement of cortisol and ACTH
  • Measurement of 24hr urinary excretion of cortisol and its breakdown products
  • Dynamic function tests
60
Q

dynamic functions test for adrenocortical disease

A

Dexamethasone suppression test

and

ACTH stimulation test

61
Q

Dexamethasone suppression test

A

Suppression of plasma cortisol by >50% is characteristic of Cushing’s disease, but suppression doesn’t normally occur in adrenal tumour or ectopic ACTH production

62
Q

ACTH stimulation test

A

Admission of Synacthen would normally increase plasma cortisol, and a normal response to this usually excludes Addison’s disease

63
Q

Congenital adrenal hyperplasia (CAH)

A

is a group of rare inherited autosomal recessive disorders characterized by a deficiency of one of the enzymes needed to make specific hormones.

64
Q

CAH effects which organs

A

adrenal glands located at the top of each kidney

65
Q

Normally, the adrenal glands are responsible for producing three different hormones:

A
  1. corticosteroids, which gauge the body’s response to illness or injury;
  2. mineralocorticoids, which regulate salt and water levels; and
  3. androgens, which are male sex hormones.
66
Q

In CAH an enzyme deficiency will make the body unable to produce one or more of these hormones, which in turn will result in

A

the overproduction of another type of hormone precursor in order to compensate for the loss.

67
Q

The most common cause of CAH is

A

the absence of the enzyme 21-hydroxylase.

68
Q

Congenital adrenal hyperplasia (CAH) can cause

A

adrenal crisis and ambiguous genitalia

  • Block in adrenal cortex pathway
  • Presentation depends on enzyme defect
  • Lack of enzyme leads to:
    • Low cortisol and aldosterone
    • High male hormones (androgens)
70
Q

signs of Congenital adrenal hyperplasia (CAH)

A
  • Hypotension
  • Hyponatraemia
  • Hyperkalaemia
  • Hypoglycaemia
  • Virilisation – development of male body parts
71
Q

treatment of CAH

A
  • Treat adrenal crisis
  • Determine sex of baby
  • Longer term GC and MC
  • Corrective surgery
72
Q

Disorders of adrenal medulla

A
  • Phaeochromocytoma and paraganglioma
73
Q
  • Phaeochromocytoma and paraganglioma is
A

Genetic disorder

  • Familial causes
    • Multiple endocrine neoplasia type 2- MEN_2
    • Von Hippel- Lindau- VHL
    • Neurofibromatosis type 1- NF1
  • Associated disease
  • MEN-2= medullary thyroid cancer and hyperparathyroidism
  • VHL= renal cancer, angiomas
74
Q

symptoms of

Phaeochromocytoma and paraganglioma (think high A/NA)

A
  • Acute episodes
  • Sweating
  • Panic attacks
  • Palpitations
  • High or low BP
  • Collapse
75
Q

Phaeochromocytoma

A

Tumour of adrenal medulla

76
Q

Paraganglioma

A

Extra-adrenal tumour- chromaffin tissue origin

77
Q

Phaeochromocytoma and paraganglioma : acute crisis

A

Hypertensive crisis

Encephalopathy

Hyperglycaemia

Cardiac arrhythmias

Sudden death

78
Q

Phaeochromocytoma and paraganglioma : investigatiosn

A
  • 24h urine metanephrines
  • 2-3 x collections needed
  • Plasma metanephrine
  • Neuro-endocrine marker: Chromogranin A
79
Q

radiological investigations of Phaeochromocytoma and paraganglioma

80
Q

Management of Phaeochromocytoma and paraganglioma

A
  • α-blockade phenoxybenzamine
  • β-blockade bisoprolol
  • surgical excision
81
Q

alpha blockade- phenoxybenzamine

A

always do an alpha-block before b-block

82
Q

why always do an always do an alpha-block before b-block

A

Unopposed alpha stimulation can cause hypertensive crisis

83
Q

surgical excision of phaeochromocytoma and paraganglioma

A
  • Perioperative management
    • Specialist anaesthetic team
    • Risk of crisis during operation
    • Maximal vasodilaton and filling with IV fluids
84
Q

Pheochromocytoma secretes

A

catelcholamine s(mainly NA)

stains dark with chromium salts

85
Q

Signs and symptoms of Pheochromocytoma

A
  • Severe hypertension
  • Headaches
  • Palpitation
  • Diaphoresis
  • Anxiety
  • Weight loss
  • Elevated blood glucose
86
Q

Paraganglioma

A

Extra-adrenal tumour (chromaffin tissue origin)

87
Q

spiralactone

A

diuretic to reduce bp

e.g. heart failure

Endocrinology (12 decks)

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