enocrinolology 2 Flashcards
discuss addisons disease
primary adrenal insufficiency–> low cortisol + aldosterone
Autoimmune destruction of adrenal cortex OR steroid withdrawal
specifically a reaction of 21-hydroxylase which is used to make aldosterone and corsitol.
this means there is a greater stockpiles for the sex hormines and more is made.
more common in women 30-50
1 in 100000
signs and symptoms of addisons
fatigue, weakness, anorexia, weight loss, hairloss (sex hormone), postural hypotension, hyperkalaemia, salt craving, hyperpigmentation in skin- excess ACTH stims melanocite receptors.
in a chrisis- severe hypotension, dehydration. hypovolaemic shock, fever, vom.
Ix of addisons
U+E- low Na, K high, Ca2+ will be high.
glucose can be low or normal
ACTH stimulation test (synacthen test)
give dose of synachten (250mg) - aiming to stimulate cortisol production
measure at 0 and 30 mins post administration- if a rise of more than 200 or above 550 then it is a normal response.
to chec for pituitary causes (if the adrenals have shrunk)
give a big IM shot- long lasting effects- no change in levels after 1 hour, but 24 hours there will be a response.
OR insulin test
make pt hypoglycaemic - see if there is a rise in cortisol and acth.
Rx of addisons
if hypoadrenalism is suspected + pt is hypotensive give:
100mg IV hydrocortisone + saline without confirmation of disease.
give more 0.9 saline + 6 hourly infusion of 100mg hydrocortisone untill stable.
then oral doses of hydrocortisone (not at night)
fludrocortisone- replaces aldosterone.
discuss addisonian crisis
constallation of symptoms that indicate severe adrenal insufficiency
can be triggered by infection trauma etc- in someone with addisons
medical emergency and life threatening
sudden pain in legs back abdomen
vom and diarrhoea- resulting in dehydration
Hypotenion + sycope + hyponatremia + hyperkalaemia
Rx:
IV glucocorticoids, + loads of saline + glucose
discuss cushings syndrome
excess glucocorticoid (cortisol)
(HPA hypothalamus –> CRH –> ACTH– > cortisol.)
causes: exogenous administration of glucocorticoids - adrenals atrophy
cushings disease- pituitary adenoma prod excess acth- adrenals hyperplase.
can also get specific tumors in the fasiculata, or small cell bronchial cancer producing ACTH.
risk factors for cushings + signs and symptoms
diabetes
obesity
female
25-40
S+S
central weight gain, depression, insomnia
poor libido, amenorrhoea/ oligomenorrhoea
prox myopathy
teeny legs and arms
hair loss, thin skin
moon face
hypertension (salt retention) - cortisol is a weak mineralocorticoid
osteoperosis
investigations of cushing disease
urinary freee cortisol over 24 hours- look at diurnal rythm
is it truly raised (it is if mroe than 280)
overnight low dose dex suppression test–>
measure cortisol at 8am
give 1gm dex at 11pm
measure at 8
if drops to less than 50 –> normal
if not then cushings is diagnosed
to differentiate cause- give high dose dex- 2mg every 6 hrs for 48 hrs.
if lowers to less than 50% of baseline –> cushings
if not lower- then ectopic acth prod.
how to manage cushings
11 beta hydrolase blocker (metyrapone or ketoconazole) – an enzyme needed to produce cortisol.
Surgery + radiotherapy to pituitary tumor if cancerous.
what is conns syndrome
changed to primary hyperaldosteronism
excessive secretion of alosterone- increaced NA + water reabsorbtion + K + H secretion
Causes:
adrenal hyperplasia, adrenal adenoma or familial.
the most common cause of 2’ hypertension.
50% of cases due to an adenoma, remaining idiopathic or bilateral hyperplasia.
high morbidity/ mortality if untreated. (HTN + hypokalaemia)
S+S: often found when being refractory to Rx.
cramps, HTN, ileus (hypoK) fatigue, polyuria+ dipsia
NO EDEMA- Spontaneous naturesis
Ix and Rx of conns sydrome
Bloods: hypokalaemia + HTN
hypernatraemia/ normal
metabolid alkalosis- H+ ions being kicked out in the kidney.
urinary potass excretion elevated
Aldosterone:renin ratio- establish high aldosterone
then Image kidneys- CT
Rx:
adrenalectomy- if unilateral- not suitable for non adenomatous
aldosterone antagonisis- spironalactone
cushing disease vs cushing syndrome
cushing disease is a specific type of cushing syndrome where a pituitary tumour causes increaced secretion of ACTH- stimulates cortisol production.
which hormones come from the anterior / posterior parts of the pituitary
ANT: GH, prolactin, FSH, LH, TSH, ACTH
post: ADH, Oxytocin.
clinical summary of pituitary tumours
derived from glandular tissue
mainly sporadic, but MEN1 is a risk factor
S+S- bitemporal hemianopia
diplopia
headache
most common endocrine manifestations are GH and ACTH.
if non functional- are bigger + visual symptoms more frequently present.
discuss order of hormone loss in mass effecting pituitary tumours
fertility- LH FSH go first
GH
TSH
ACTH- most maintained
surgery or radiotherapy to Rx mass effect tumours.
