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endocrine > adrenal > Flashcards

adrenal Flashcards

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

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

A

inadequate CRH released by hypothalamus

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

21
Q

adrenal autoantibodies

A

adrenal cortex antibodies

21-hydroxylase autoantibodies

22
Q

sodium and potassium levels in adrenal insufficiency

A

hyponatraemia

hyperkalaemia

23
Q

adrenal insufficiency diagnosis

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

A 
cortisol = low
aldosterone = low
ACTH = high
renin = high
25
Q

management of adrenal insufficiency

A

replacement steroids

  • hydrocortisone = glucocorticoid (replaces cortisol)
  • fludrocortisone = mineralocorticoid (replaces aldosterone)

(fludro in primary only)

26
Q

management of adrenal crisis

A

IV hydrocortisone
IV fluid resus
correct hypoglycaemia
intensive monitoring

27
Q

steriods management

A

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
Q

adrenal crisis (addisonian crisis)

A

medical emergency, immediate treatment, no time for investigations

triggered by -

  • infection
  • trauma
  • rapid withdrawal of steroids from long term users
29
Q

what presentation gives a high clinical suspicion of hyperaldosteronism?

A

most common cause of secondary hypertension

high clinical suspicion = young, resistant hypertension, hypokalaemia

–> also alkalosis

30
Q

aldosterones effects on the kidneys

A

increase sodium reabsorption from distal tubule
increase potassium secretion from distal tubule
increase hydrogen secretion from collecting ducts

31
Q

causes of primary hyperaldosteronism (Conn’s)

A

primay = adrenal glands directly responsible for too much aldosterone

adrenal adenoma secreting alsosterone = commonest
bilateral adrenal hyperplasia
familial hyperaldosteronism
adrenal carcinoma

32
Q

renin levels in primary vs secondary hyperaldosteronism

A

primary (Conns) = low - supressed bt high bp

secondary = high

33
Q

cause of secondary hyperaldosteronism

A

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
Q

hyperaldosteronism investigation

A

renin: aldosterone ratio
- high aldo + low renin = primary (Conns)
- high aldo + high renin = secondary

saline supression test

look for cause

35
Q

hyperaldosteronism / Conns management

A

aldosterone antagonists -

  • eplerenone
  • spironolactone

treat underlying cause -

  • remove adenoma
  • percutaneous renal artery angioplasty
36
Q

congenital adrenal hyperplasia

A

rare conditions associated with enzyme defects in steroid pathway

21alpha hydroxylase deficiency = commonest
autosomal recessive

37
Q

pathophysio of congenital adrenal hyperplasia

A

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
Q

congenital adrenal hyperplasia mild presentation during childhood/post-puberty

A

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
Q

congenital adrenal hyperplasia investigation

A

basal or stimulated 17-OH progesterone

gene analysis

40
Q

congenital adrenal hyperplasia management

A

hydrocortisone - to replace glucocorticoid (cortisol)
fludrocortisone - to replace mineralcorticoid (aldosterone)

surgical correction of genital ambiguity

41
Q

biochemistry results in congenital adrenal hyperplasia

A

hyponatraemia
hyperkalaemia
hypoglycaemia

leads to poor feeding, V+D, arrhythmias shortly after birth if severe

42
Q

Multiple Endocrine Neoplasia (MEN) type I

A

3 P’s
parathyroid
pituitary (eg prolactinoma)
pancreas (eg insulinoma, gastrinoma)

(also adrenal + thyroid)

MEN1 gene

43
Q

most common presentation of MEN I

A

hypercalcaemia
(hyperparathyroidism due to parathyroid hyperplasia)

recurrent peptic ulceration - due to gastrinoma

44
Q

MEN type IIa

A

2 P’s
parathyroid
phaeochromocytoma

RET oncogene

medullary thyroid cancer (70%)

45
Q

MEN type IIb

A

1P = phaeochromocytoma

RET oncogene

medullary thyroid cancer
neuromas (usually between toes)
Marfans body

46
Q

inheritance of MEN

A

autosomal dominant

endocrine (15 decks)

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