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adrenal Flashcards

(46 cards)

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1
Q

adrenal medullary tumours

A

phaeochromocytoma

neuroblastoma - kids

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2
Q

phaeochromocytoma

A

a tumour of the chromaffin cells that secretes unregulated + excessive amounts of catecholaine (adrenaline)

rare asf

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3
Q

incidence of phaeochromocytoma

A

10% rule

  • bilateral
  • cancerous
  • outside adrenal gland = paragangliomas
  • assoc. with hyperglycaemia
  • kids

25% are familial + assoc. with MEN2

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4
Q

phaeochromocytoma pathophysio

A

adrenaline is secreted by chromaffin cells in the adrenal medulla

in phaeochromocytoma, adrenaline is secreted in burts giving periods of worse symptoms folled by more settled periods

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5
Q

phaeochromocytoma classic triad

A

hypertension
headache
sweating

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6
Q

phaeochromocytoma presentation

A 
paroxysmal signs + symptoms - fight or flight
anxiety, sweating
headache
hypertension
postural hypotension
palpitations, tachycardia

paroxysmal atrial fibrillation
adipose tissue turns brown

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7
Q

diagnosis of phaeochromocytoma

A

24hr catecholimes
plasma free metaphrines

MRI, PET

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8
Q

patients with a high clinical suspicion of phaeochromocytoma

A

young with resistant hypertension + hyperglycaemia

also fam members with it

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9
Q

why can 24hr catecholamines be an unreliable test?

A

catecholamines rise in heart failure

secretion of catecholamines in phaeochromocytoma is episodic so results may be normal

malignant + extra-adrenal tumours less efficient at catecholamine synthesis

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10
Q

management of phaeochromocytoma

A

alpha blockers - phenoxybenzamine
beta blocker once established on alpha blockers (propranolo, atenolol)

adrenalectomy = definitive, symptoms must be medically controlled prior to surgery

fam tracing

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11
Q

signs of complication in phaeochromocytoma

A 
left ventricular failure
myocardial necrosis
stroke
shock
paralytic ileus of bowel
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12
Q

syndromes associated with phaeochromocytoma

A 
MEN2
Von-Hippel-Lindau syndrome
succinate dehyrogenase mutations
neurofibromatosis
tuberose sclerosis
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13
Q

effects of cortocosteroids on bone

A

direct

  • reduction of osteoblast activity + lifespan
  • suppression of replication of osteoblast precursors
  • reduction in calcium absorption

indirect
- inhibition of gonadal + adrenal steroid production

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14
Q

what is addisons?

A

primary adrenal insufficiency

where adrenal glands do not produce enough steroid hormones esp cortisol + aldosterone

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15
Q

causes of addisons

A

(primary adrenal insufficiency)

autoimmune = commenest
infections - TB, fungal, HIV
metastatic malignancy

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16
Q

adrenal insufficiency presentation

A

fatigue, nausea
cramps, abdo pain
reduced libido
postural hypotension

bronze hyperpigmentation with increased ACTH

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17
Q

pigmentation of skin in primary vs secondary adrenal insufficiency

A

(ACTH is secreted with MSH which stimulates maleanocytes to produce melanin)

primary (addisons) - bronze hyperpigmentation

secondary - pale skin (no increase in ACTH)

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18
Q

secondary adrenal insufficiency

A

inadequate ACTH stimulating the adrenal glands = low cortisol released

caused by damage to pituitary

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19
Q

causes of secondary adrenal insufficiency

Study These Flashcards
A 
caused by loss or damage to pituitary via - 
congenital underdevelopment (hypoplasia)
surgery
exogenous steroids
infection
loss of blood flow
radiotherapy
20
Q

cause of tertiary adrenal insufficiency

Study These Flashcards
A

inadequate CRH released by hypothalamus

caused by patients on long term steroids (>3weeks) - supresses hypothalamus

21
Q

adrenal autoantibodies

Study These Flashcards
A

adrenal cortex antibodies

21-hydroxylase autoantibodies

22
Q

sodium and potassium levels in adrenal insufficiency

Study These Flashcards
A

hyponatraemia

hyperkalaemia

23
Q

adrenal insufficiency diagnosis

Study These Flashcards
A

short synacthen test (ACTH)

cortisol level should double in response to aynacthen, if less = positive
–> do serial levels, 0, 30 and 60mins

24
Q

hormone levels in addisons

Study These Flashcards
A 
cortisol = low
aldosterone = low

ACTH = high
renin = high
25
management of adrenal insufficiency
replacement steroids - hydrocortisone = glucocorticoid (replaces cortisol) - fludrocortisone = mineralocorticoid (replaces aldosterone) (fludro in primary only)
26
management of adrenal crisis
IV hydrocortisone IV fluid resus correct hypoglycaemia intensive monitoring
27
steriods management
steroid ID educate - dont stop suddenly sick day rules- - increase dose when acute ill - blood sugar monitored - eat regular carbs - D+V - IM or admission for IV
28
adrenal crisis (addisonian crisis)
medical emergency, immediate treatment, no time for investigations triggered by - - infection - trauma - rapid withdrawal of steroids from long term users
29
what presentation gives a high clinical suspicion of hyperaldosteronism?
most common cause of secondary hypertension high clinical suspicion = young, resistant hypertension, hypokalaemia --> also alkalosis
30
aldosterones effects on the kidneys
increase sodium reabsorption from distal tubule increase potassium secretion from distal tubule increase hydrogen secretion from collecting ducts
31
causes of primary hyperaldosteronism (Conn's)
primay = adrenal glands directly responsible for too much aldosterone adrenal adenoma secreting alsosterone = commonest bilateral adrenal hyperplasia familial hyperaldosteronism adrenal carcinoma
32
renin levels in primary vs secondary hyperaldosteronism
primary (Conns) = low - supressed bt high bp secondary = high
33
cause of secondary hyperaldosteronism
excessive renin stimulationg adrenal to produce more aldosterone cause = bp in kidney disproportionately lower than bp in rest of body, due to - - renal artery stenosis - atherosclerosis - renal artery obstruction - heartfailure
34
hyperaldosteronism investigation
renin: aldosterone ratio - high aldo + low renin = primary (Conns) - high aldo + high renin = secondary saline supression test look for cause
35
hyperaldosteronism / Conns management
aldosterone antagonists - - eplerenone - spironolactone treat underlying cause - - remove adenoma - percutaneous renal artery angioplasty
36
congenital adrenal hyperplasia
rare conditions associated with enzyme defects in steroid pathway 21alpha hydroxylase deficiency = commonest autosomal recessive
37
pathophysio of congenital adrenal hyperplasia
21-hydroxylase is responsible for converting progesterone into aldosterone + cortisol, it is also used to create testosterone (*this conversion does NOT rely on 21-hydroxylase enzyme*) deficiency of 21-hydroxylase means that there is extra progesterone that cannot be converted to aldo or cortisol so is vonverted to testoterone
38
congenital adrenal hyperplasia mild presentation during childhood/post-puberty
tall for their age deep voice early puberty skin hyperpigmentation - low cortisol causes increased ACTH girls - absent periods, facial hair, genital ambiguity, big clit boys - large penis, small testes
39
congenital adrenal hyperplasia investigation
basal or stimulated 17-OH progesterone | gene analysis
40
congenital adrenal hyperplasia management
hydrocortisone - to replace glucocorticoid (cortisol) fludrocortisone - to replace mineralcorticoid (aldosterone) surgical correction of genital ambiguity
41
biochemistry results in congenital adrenal hyperplasia
hyponatraemia hyperkalaemia hypoglycaemia leads to poor feeding, V+D, arrhythmias shortly after birth if severe
42
Multiple Endocrine Neoplasia (MEN) type I
3 P's parathyroid pituitary (eg prolactinoma) pancreas (eg insulinoma, gastrinoma) (also adrenal + thyroid) MEN1 gene
43
most common presentation of MEN I
hypercalcaemia (hyperparathyroidism due to parathyroid hyperplasia) recurrent peptic ulceration - due to gastrinoma
44
MEN type IIa
2 P's parathyroid phaeochromocytoma RET oncogene medullary thyroid cancer (70%)
45
MEN type IIb
1P = phaeochromocytoma RET oncogene medullary thyroid cancer neuromas (usually between toes) Marfans body
46
inheritance of MEN
autosomal dominant

endocrine (15 decks)

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