- Flashcards
what is polyuria
pee more than usual
what happens to blood pressure in adrenal insufficiency
decreases
conductor of the endocrine orchestra
pituitary
structures of hormones
polypeptide, glycoprotein, steroid or amine
what causes release of hormones
intracellular calcium
hypothalamic releasing hormones are released into the
pituitary portal system
only unbound/bound hormone is biologically active
unbound
cell surface receptors contain – secretions
hydrophobic
most peptide hormones activate via
G protein coupled receptors
steroid and thyroid hormones act via
nuclear receptors
TRH and TSH increases release of
T3 and T4
Role of TSH
stimulates increased iodine uptake by the thyroid
t3 and t4 bind to what kind of receptors
nuclear
secondary gland failure is due to
pituitary disease
in secondary gland failure, the pituitary hormone is not
suppressed so negative feedback not really working in pituitary disease
hormones are measured by
biochemical assays in lab
not possible to measure
hypothalamic hormones
circulating levels of most hormones are
very low
how do immunoassays work
highly specific antibodies bind to hormone and this interaction is measured
immunoassays definitely have their
limitations
in women who are pregnant or on the pill can give false impression of
in women who are pregnant or on the pill can give false impression of
hypercortisolaemia due to high oestrogen levels
in people with diabetes mellitus may give impression of
androgen deficiency due to Low testosterone levels
in people with diabetes mellitus may give impression of
androgen deficiency due to Low testosterone levels
thyroid hormones show what kind of secretion
continuous with very little variation
GH, Lh and FSH show
pulsatile secretion
cortisol levels vary greatly with highest levels being in the morning and lowest
overnight
stress increases
acth and cortisol, GH, prolactin, adrenaline and noradrenaline
secretion of – and – is increased during sleep
GH and prolactin
what 2 hormones decreases after digestion of food
testosterone and GH
testosterone should be. measured
before 11am in the fasting state
cortisol should be checked
between 8 and 10 am to exclude hypoadrenalism and and at midnight to exclude cushings
what hormones vary with menstrual cycle
Lh/FSH, oestrogen and progesterone
renin and aldosterone vary with
sodium , age and posture
dexamethasone decreases
cortisol
dopamine restricts production of
prolactin
ADH and oxytocin are secreted in hypothalamus but are stored in
posterior pituitary
oxytocin produces
milk ejection and uterine myometrial contraction
most common cause of pituitary disease
pituitary tumours
most common presentation of prolactinoma
galactorrhea(milky nipple discharge), amenorrhoea (lack of period), erectile dysfunction, hypogonadism(sex glands produced little if any sex hormones)
central obesity associated with
cushings disease
nelsons syndrome occurs
post adrenalectomy
excess acth secretion occurs in
cushings disease and nelsons syndrome
acidophil
acromegaly
basophil
Cushings disease and nelson syndrome
usual treatment of choice for pituitary tumour
surgery via transphenoidal route and large tumours through trans cranial route usually transfrontal
what drugs can cause shrinkage of particular tumour types
somatostatin analogue eg octreotide and or dopamine agonists eg cabergoline particularly in prolactinomas
replacement therapy for adrenal
hydrocortisone
replacement for deficiency in gonadal in male and what for female
male - testosterone and female - oestrogen/ progestogen
replacement for fertility
HCG plus FSH
if thirsty given
desmopressin
if breasr deficiency eg prolactin inhibition give
dopamine agonist eg cabergoline
reduction of excess hormone for acromegaly treatment drug
somatostatin analogue
dopamine agonists for
prolactinomas
most common mass lesion of pituitary
pituitary adenomas
another pituitary mass lesion
craniopharyngioma
arises from rathkes pouch
craniopharyngioma and is a cystic tumour
often from tumour growth where there is multiple deficeiceis in these hormones what hormones first affected
GH and gonadatrophins
last affected
tsh and acth
hypoadrenalism causes
mild hypotension, hyponatraemia and cardiovascular collapse during severe intercurrent stressful illness
– leads to loss of libido (sex drive), sexual hair, amenorrhoea dn erectile dysfunction and eventually osteoporosis
hypogonadism
pallor with hairlessness
panhypopituitarism
loss of smell
kallmanns syndrome
3 zones of the adrenal cortex
zona glomerulosa, fasciculata and reticularis
zona glomerulsoa secretes
aldosterone
inner medulla synthesises, stores and secretes
catecholamines
zona fasciculata and reticularis produce
glucocorticoids, cortisol, sex steroids and androgen
catecholamines such as
adrenaline and noradrenaline
main role of mineralocorticoids
on extracellular balance of sodium and potassium in kidney
glucocorticoids main effects on
carbohydrate metabolism
what contains melanocytes stimulating hormone
ACTH
circulatimg acth stimulates – in the adrenal
cortisol
crH - acth - —–
cortisol
following adrenalectomy or other adrenal damage eg Addisons disease, cortisol secretion is absent or reduced and acth levels will
rise
— secretion is mainly controlled by the renin angiotensin system
mineralcorticodi
– increases in response to stress
cortisol
administration of dexamethasone does what to CRH and ACTH levels and thus cortisol
decreases them
dexamethasone test for
cushings syndrome
for stimulation tests what is given
synthetic ACTH to stimulate adrenal cortisol production
cushings syndrome most often iatrogenic Fromm administering what
steroids
Cushings disease is caused by excess secretion of ACTH from a
pituitary adenoma
cushings syndrome divided into 2 categories
- increased circulating ACTH from the pituitary known as cushings disease (65%) or ectopic non pituitary tumour acth producing tumour from elsewhere in the body (10%)
- excess of cortisol secretion by an adrenal tumour(25%)
pigmentation in cushings only occurs
with acth dependent causes most frequently in ectopic acth syndrome
– is common in all causes of cushings syndrome
hypertension
what is common with ectopic acth secretion in cushings
hypokalaemia and impaired glucose tolerance and pigmentation
signs more specific to Cushings
plethora (moon face), thin skin, bruising, proximal myopathy
confirm diagnosis for cushings with
48hr low dose dexamethasone test
why is overnight dexamethasone test used as more of an initial screening test in cushings
as has a higher false positive rate and takes less time.
tests for cushings
48hr low dose dexamethasone test
24hr urinary free cortisol measurements
circadian rhythm
classic ectopic acth syndrome of cushings is
pigmentation ,weight loss, hypokalaemia, diabetes and plasma acth levels above 200ng/L
in cushings severe hirsutism suggests
adrenal tumour
for a dexamethasone test, failure of significant plasma cortisol suppression suggests an
ectopic source of acth ( or an adrenal tumour)
exaggerated ACTH and cortisol response to CRH suggests
pituitary dependent cushings disease
untreated cushings syndrome can cause death from
venous thromboembolism, hypertension, MI, infection and heart failure
drugs to control cortisol hypersecretion prior to surgery
usual drug is metyrapone but ketocanazole can also be given
treatment of choice for cushings disease
transphenoidal removal of the tumour
what is mainly used after failed pituitary surgery in
external pituitary irradiation
what is last resort in treatment of cushings disease
bilateral adrenalectomy
cushions due to adrenal adenomas should be
resected laparoscopically
if source of acth is not clear in cushings , cortisol hyperesecretion should eb controlled with medical therapy until diagnosis eg
metyrapone or ketoconazole
what occurs after 20% of cases after bilateral adrenalectomy for cushings disease
nelson syndrome
when is there destruction of the entire adrenal cortex
Addisons disease
if entire adrenal cortex is destructed then what are reduced
glucocorticoid, mineralocorticoid and sex steroid production
what generally remains intact in hypothermic pituitary disease
mineralocorticoid secretion also sex steroid
in Addisons disease, reduced cortisol levels lead through feedback to increased CRH and __ production, the latter being directly responsible for the hyperpigmentation
ACTH
Addisons disease is usually caused by
autoimmune disease
most common cause of primary adrenal insufficiency in kids is
congenital adrenal hyperplasia
most common cause of primary adrenal insufficiency in kids is
congenital adrenal hyperplasia
what is the predominant sign in Addisons
pigmentation (dull, slaty, grey-brown) especially of new scars and palmar creases and postural systolic hypotension
if adddisons disease is suspected, investigation is
urgent
what is given to suspected add-ons disease if hypotensive or seriously ill
hydrocortisone and IV saline
random cortisol. measurement of below – during the day is highly suggestive of Addisons
100nmol/L
ACTH stimulation test should be performed in
Addisons
absent or impaired cortisol response to acth stimulation test confirms presence of hypoadrenalism but does not
differentiate Addisons from acth deficiency or iatrogenic suppression by steroid medication
what may be normal but classical seen in Addisons
hyponatraemia, hyperkalaemia and high urea
long term treatment of Addisons is with
glucocorticoid and mineralocorticoid replacement
is measuring cortisol levels during the day for Addisons while on replacement therapy recommended as an assessment for dose adequacy
NO
patients should double dose of steroid in Addisons during
intercurrent illness
long term steroid therapy can lead to
acth suppression
hydrocortisone needs to be started before
t4 replacement
in secondary hypoadrenalism, acth levels are
low
disorder resulting in a defiency of an enzyme in the cortisol synthetic pathway
congenital adrenal hyperplasia
in CAH, as cortisol secretion is reduced,
acth is increased causing adrenal hyperplasia
what test for congenital adrenal hyperplasia
synacthen test
long term steroids (greater than 3 weeks) will often mimic
cushings syndrome
steroids can affect endocrine system by causing what
weight gain and glycosuria(urine contains lots of glucose)/hyperglycaemia/ diabetes
what accounts for 5-10% of all hypertension
primary hyperaldosteronism
what is characterised by excess aldosterone, leading to sodium retention, potassium loss and the combination of hypokalaemia and hypertension
primary hyperaldosteronism
secondary aldosteronism is when there is
excess renin
most common cause of primary hyperaldosteronism
bilateral adrenal hyperplasia followed by conns syndrome ( adrenal adenomas)
usually presentation for primary hyper aldosteronism is simply
hypertension
screening test for primary hyperaldosteronism
plasma aldosterone :renin ratio
2 main causes of hyperaldosteronism
adrenal adenoma or hyperplasia
how to treat an adenoma and hypoerplasia causing primary hyperaldosteronism
adenoma - laparoscopically
hyperplasia- aldosterone anatoginst (spironolactone)
increase in levels in urine of — is a marker of abnormal hyper secretion of them
catecholamines
rare tumours of the sympathetic nervous system
pheochromocytoma and paraganglioma
metabolism of virtually all nucleated cells of many tissues is controlled by the
thyroid hormones
thyroid gland moves on
swallowing
embryonically what originates from the base of the tongue and descends into the middle of the neck
thyroid gland
does thyroid gland have rich blood supply
yes
thyroid gland consists of
follicles
colloid is the
iodinated glycoprotein thyroglobulin
parafollicular cells contain
c cells
what is a prohorome
T4
iodine + thyroglobulin =
T3 and t4
majority of t3 and t4 in plasma is bound to hormone binding proteins
true
only – hormone is available for action in the target tissues where t3 binds to nuclear receptors
free
