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year 2 - endocrine > adrenal disease > Flashcards

adrenal disease Flashcards

1
Q

what does the zona glomerulosa produce

A

mineralocorticoids (e.g. aldosterone)

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2
Q

what does the zona fasiculata produce

A

glucocorticoids (cortisol)

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3
Q

what does the zona reticularis produce

A

androgen precursors (e.g. DHEA)

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4
Q

what does the medulla produce

A

catecholamines (e.g. adrenaline, noradrenaline)

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5
Q

what is the zona glomerulosa controlled by

A

renin angiotensin system

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6
Q

what is the zona fasciculata controlled by

A

CRH (hypothalamus) and ACTH (anterior pituitary)

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7
Q

what is the zona reticularis controlled by

A

CRH (hypothalamus) and ACTH (anterior pituitary)

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8
Q

what is the medulla controlled by

A

sympathetic nervous system

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9
Q

what is the effect of the zona glomerulosa

A
  • increased sodium and water reabsorption
  • increased potassium secretion
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10
Q

what is the effect of the zona fasciculata

A
  • increased metabolism
  • increased blood pressure
  • anti-inflammatory effects
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11
Q

what is the effect of the zona reticularis

A

precursors used to produce sex steroids (testosterone)

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12
Q

what is the effect of the medulla

A
  • increased heart rate/contractility
  • increased vasoconstriction
  • bronchodilation
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13
Q

what is primary adrenal insufficiency

A
  • any condition associated with a reduction of steroids (mainly cortisol and aldosterone) due to failure within adrenal glands
  • due to the negative feedback control of cortisol production, reduced levels will be associated with an increase in ACTH (causes increased skin pigmentation)
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14
Q

primary adrenal insufficiency causes

A
  • infection: TB
  • adrenal metastasis: lung, breast, renal, lymphoma
  • autoimmune: Addison’s (most common cause)
  • Waterhouse Friderichsen’s Syndrome (bilateral adrenal haemorrhage due to sepsis)
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15
Q

primary adrenal insufficiency presentation

A
  • myalgia, arthralgia
  • dizziness, weakness
  • depression, psychosis
  • abdominal pain, diarrhoea, vomiting
  • lethargy, weight loss, hypoglycaemia, hypotension
  • hyperpigmentation of skin (esp. palmar creases)
  • vitiligo
  • postural hypotension
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16
Q

primary adrenal insufficiency diagnosis

A
  • bloods: low sodium, high potassium, low glucose
  • diagnostic: short synacthen test
  • give synthetic ACTH: cortisol should increase (normal)
  • measure cortisol before and then 30-60mins after
  • normal results: baseline >170, 30-mins >550
  • Addison’s disease: no significant rise in cortisol
  • chest x-ray
  • CT CA
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17
Q

primary adrenal insufficiency management

A

steroid replacement
- aldosterone deficiency: 50-200mg fludrocortisone
- cortisol deficiency: 15-25mg hydrocortisone (given as divided dose and avoided at night to prevent insomnia)

sick days
- unwell/trauma/surgery: double steroid dose for at least a week
- vomiting: replace oral with IM

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18
Q

Addisonian crisis causes

A

bilateral adrenal haemorrhage, suddenly stopping long-term steroids, illness/trauma/surgery in those with primary adrenal failure

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19
Q

Addisonian crisis presentation

A

shock, weakness, reduced GCS (confusion/coma), hypoglycaemia

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20
Q

Addisonian crisis diagnosis

A

FBC, UEs, glucose, cortisol, ACTH, lactate, cultures

21
Q

Addisonian crisis management

A

ABCDE, fluid resuscitation, IV hydrocortisone (100mg STAT), correct electrolyte imbalances, IV glucose infusion

22
Q

what is bilateral adrenal hyperplasia

A

congenital form of primary adrenal insufficiency

23
Q

bilateral adrenal hyperplasia causes

A

develops due to mutation in 21 alpha hydroxylase enzyme which results in reduced aldosterone, reduced cortisol and increased androgen (due to increased ACTH as result of reduced cortisol)

24
Q

bilateral adrenal hyperplasia presentation in children

A
  • dehydration
  • salt crisis
  • failure to thrive
  • girls: ambiguous genitalia
  • boys: early virilisation, adrenal mass
25
Q

bilateral adrenal hyperplasia presentation in adults

A
  • females: hirsutism, oligomenorrhoea, reduced stature, acne
  • males: acne, short stature, precocious puberty, early virilisation
26
Q

bilateral adrenal hyperplasia diagnosis

A
  • bloods: low sodium, high potassium, low glucose
  • diagnostic: short synacthen test
  • give synthetic ACTH: cortisol should increase (normal)
  • measure cortisol before and then 30-60mins after
  • normal results: baseline >170, 30-mins >550
  • chest x-ray
  • CT CAP
  • auto-antibody screen
  • plasma renin and aldosterone
  • morning ACTH: high
27
Q

bilateral adrenal hyperplasia management

A
  • steroid replacement (fludrocortisone and hydrocortisone)
  • female children: karyotyping and gender assignment
28
Q

what is secondary adrenal insufficiency

A

failure to produce adequate steroids as a result of ACTH deficiency

29
Q

secondary adrenal insufficiency causes

A
  • pituitary disease
  • long term, excessive steroid use (develops due to high levels of synthetic steroid dampening down steroid axis)
  • only corticosteroid production is reduced, mineralocorticoid production is maintained (meaning low cortisol and normal aldosterone)
  • insufficiency will only become apparent following withdrawal from steroids
30
Q

secondary adrenal insufficiency presentation

A
  • myalgia, arthralgia
  • dizziness, weakness
  • depression, psychosis
  • abdominal pain, diarrhoea, vomiting
  • lethargy, weight loss, hypoglycaemia, hypotension
  • vitiligo
  • postural hypotension
31
Q

secondary adrenal insufficiency diagnosis

A
  • short synacthen test
  • morning ACTH is low
32
Q

secondary adrenal hyperplasia management

A

oral hydrocortisone

33
Q

what is primary hyperaldosteronism

A

excessive amounts of aldosterone independent of functions of RAAS

34
Q

primary hyperaldosteronism causes

A
  • idiopathic bilateral adrenal hyperplasia (most common)
  • conn’s syndrome (aldosterone secreting adrenal adenoma)
35
Q

primary hyperaldosteronism presentation

A
  • polyuria
  • polydipsia
  • headaches
  • weakness, cramps, paraesthesia, muscle spasms
  • hypertension that is young onset and treatment resistant
36
Q

primary hyperaldosteronism diagnosis

A
  • bloods: high sodium, low potassium
  • first line: plasma renin and aldosterone
  • diagnostic
  • plasma aldosterone: renin ratio > 750
  • saline suppression test (failure to suppress aldosterone production by 50 following consumption of water)
  • CT abdomen to identify adenoma (incidentaloma -> adrenal mass identified on CT with no clinical findings)
37
Q

primary hyperaldosteronism management

A
  • medical: aldosterone antagonist (spironolactone)
  • surgical: removal of adenoma in conn’s
38
Q

what is Cushing’s syndrome

A

umbrella term that describes symptoms caused by cortisol excess

39
Q

what is Cushing’s disease

A

Cushing’s syndrome caused by caused by ACTH secreting pituitary tumour

40
Q

Cushing’s syndrome endogenous causes

A
  • ACTH dependent: pituitary adenoma, ectopic secretion (small cell lung cancer)
  • ACTH independent: benign adrenal adenoma, malignant adrenal carcinoma
41
Q

Cushing’s syndrome exogenous causes

A

prolonged steroid use

42
Q

Cushing’s syndrome presentation

A
  • central obesity, with striae
  • moon face with facial plethora
  • proximal muscle wasting (thin arms and legs, proximal myopathy so find standing up difficult)
  • skin: loss of scalp hair, skin thinning, easy bruising, frontal male pattern baldness
  • psychiatric: euphoria, depression, psychosis
  • virilisation and hirsutism
  • oligomenorrhoea or amenorrhoea
  • medical conditions: hypertension, osteoporosis, hyperglycaemia, susceptibility to infection, poor wound healing, oligomenorrhoea, amenorrhoea
  • ‘lemon on a stick’
  • more prone to diabetes because cortisol is insulin antagonist
  • skin is paper thin
43
Q

Cushing’s syndrome diagnosis

A
  • blood glucose: hyperglycaemia
  • 24 hour urinary cortisol increased
  • screening: overnight dexamethasone suppression test
  • CT/MRI head
  • CT CAP
  • plasma ACTH
  • hypokalaemic metabolic alkalosis
44
Q

Cushing’s syndrome management

A
  • iatrogenic: stop steroid
  • pituitary or adrenal adenoma: surgical excision
  • ectopic secretion: depends on site/extent of primary
  • adrenal enzyme inhibitors
  • metyrapone
  • ketoconazole
45
Q

what is a phaeochromocytoma

A

catecholamine producing tumours of the adrenal medulla, which predominately produce noradrenaline

46
Q

phaeochromocytoma presentation

A
  • headache
  • palpitations
  • sweating
  • hypertension
  • feeling of utter terror intermittently
  • facial flushing
  • shortness of breath
  • chest tightness
  • abdominal pain
47
Q

phaeochromocytoma diagnosis

A
  • 24 hour urinary collection of metanephrines
  • MIBG scan (uses chromaffin seeking isotope)
48
Q

phaeochromocytoma management

A
  • surgical excision of tumour
  • before surgery is carried out, blood pressure needs to be protected by alpha blockage (phenoxybenzamine) followed by beta blockage (atenolol)

year 2 - endocrine (6 decks)

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