hypersecretion of anterior pituitary hormones Flashcards
what are the symptoms for hyperpituitarism associated with
excess production of adenohypophysial hormones
what re the main causes of hyperpituitarism
isolated pituitary tumours - main or ectopic tumours - neuroendocrine tumour secrete peptide hormones similar to from anterior pituitary but not in the anterior pituitary eg carinoid tumour in the gut
effect of a pituitary tumour on the optic chiasm and how this causes bitemporal hemianopia *
fibres that cross through the optic chiasm are what allows you to see the temporal fields
a pituitary mass stretches the optic chiasm causing bitemporal hemianopia, also invade the cavernous sinus so can squash the cranial nerves involved in sight - presents quite late because you can still get around
squash CN IV and VI = diplopia (double vision), III = ptosis (drooping/falling of upper eye lid)
eg in pic the optic chiasm is stretched - invasion into the cavernous sinus and therefore into th CN
can see the internal carotid arteries as 2 black circles
how do you assess a bitemporal hemianopia *
use perimetry every time you see a flash you press a button
what does excess ACTH cause *
cushing’s syndrome
what does excess TSH cause *
thyrotoxicosis the thyroid gland is told to produce too much thyrotrope
what does excess LH and FSH cause *
precocious puberty in children - too much LH, FSH -> testosterone and oestrogen
what does excess prolactin cause *
hyperprolactinaemia
what does excess GH cause *
gigantism in children - don’t have epiphysial bone closure acromegaly in adults - have epiphysial bone closure
when is hyperprolactinaemia physiological
in pregnancy - preparation for lactation in breastfeeding
when is hyperprolactinemia pathological and describe this *
prolactinoma - microadenomas <10mm in diameter
it is the most common functioning pit tumour high
prolactin supresses GnRH pulsatility - therefore teh GnRH is not able to stimultate the production of LH/FSH - this casues some of the symptoms
clinical features of hyperprolactinoma in women *
galactorrhoea out of pregnancy
secondary amenorrheoa or obligomenorrhoea - becasue of shut down of LH and FSH
loss of libido - loss of LH FSH
infertility - because of abnormal periods, itself because of LH FSH
clinical symptoms of hyperprolactinaemia for men *
galactorrhoea- unusual, have to also have abnormally high oestrogen, otherwise cant make the milk
loss of lipido, erectile dysfunction and infertility - becasue of loss of LH adn FSH -> loss of testosterone
describe the principle of treatment for hyperprolactinaemia *
prolactin production is inhibited by dopamine
lactotrophs (in ant pit) have D2 receptors on the surface - dopamine from the hypothalamic dopaminergic neurons binds to these and inhibits prolactin production
therefore hyperprolactinaemia can be trated by supplying a dopamine agonist that can bind and stop prolactin production and reduce the size of the tumour
this is the 1st line treatment
eg bromocriptine and cabergoline
given by oral admin
side effects of dopamine agonists *
nausea and vomiting (settles down), and postural hypotension are more common with bromocriptine
dyskinesias - uncontrolled involuntary movement
depression
pathological gambling, hypersexuality - impulse control disorder - dopamine stimulates the reward pathway in brain
principles of diagnosis of hyperprolactinaemia *
usually diognosed relatively early because people notince when their periods are off, or lactation - women present earlier
what is the main cause of excess GH
a benign growth hormone secreting pituitary adenoma
describe gigantism *
when GH hypersecretion occurs in childhood - grow really tall, above the average
problem is it causes impaired glucose tolerance and therefore DM
describe acromegaly *
insidious in onset
untreated, excess GH is releated to increased morbity and death
How can acromegaly cause death *
increase cardiovascular disease 60% - increase cardiomyopathy (Big baggy heart), furrinmg up of the coronary arteries
resp complications 25% - obstructuve sleep apnoea because tongue etc gets bigger
cancer - 15% - supraphysiological level everyday - so have to have regular bowl screening and colonsocpies to check for polyps
what grows in acromegaly
Soft tissue:
periosteal bone
cartilage
fibrous tissue
connective tissue
internal organs - cardiomegaly, splenomegaly, hepatomegaly
descibe the clinical features of acromegaly *
subtle presentation - occur slowly so difficult to pick up
hyperhidrosis (excessive sweating), headache - hallmarks of active acromegaly
enlargement of supraorbital ridge, nose hands (spade shaped, square fingers), thick lips
general courseness of features
ring and shoe size increase
enlargarged tongue - macroglossia
mandible grows - protusion of lower jaw (prognathism) - gap between teeth
carpel tunnel syndrome - median nerve compression in bony tunnel in either wrist by the growth of soft tissue - pins and needles in hands
barrel chest
kyphosis - convex curvature of spine
painful joints - enlarged so rub together
principle of diagnosis for acromegaly *
changes are subtle and over a long time - bring in an old picture to see if there is a difference
what are the metabolic affects of acromegaly *
excess growth hormone stimulates increased endogenous glucose production and less glucose is taken into the muscles for storage
therefore the blood glucose conc rises so there is increased insulin secretion - leads to insulin resistance
- >impaired glucose tolerance
- > DM
what are the clinical features for acromegaly *
obstructuve sleep apnoea - bone and soft tissue changes narrow the upper airway (larynx and pharynx) - collapse during sleep - dont get into REM sleep
hypertension - direct effect of GH or IGF1 on vascular tree, and GH increases Na and so water reabsorption from urine -> increase BP
cardiomyopathy - because of: DM, toxic effects of GH on myocardium - heart cant pump
increased risk of cancer - colonic polyps
describe how prolactin and GH can be co-secreted in acromegaly and explain the furtehr effects of this *
tumour secret prolactin and GH
hyperprolactinaemia - cause secondary gonadism
describe the GH axis
somatostatin and GHRH released from the hypothalamus
GH released by ant pit
GH act on liver
liver produce somatomedins - IGF1
describe the diagnosis of acromegaly *
GH pulsitile - random measurement unhelpful
do dyanmic tests - because the hormones are on axis we can see if there is an apprpriatee response
measure IGF1 - if GH is always high there will be high IGF1 - clinical hallmark, also has a longer half life so can see what GH has been like recently
paradoxical rise in GH after oral glucose load (ie failed suppression which is normal)
MRI pituitary - show adenoma
describe the treatment of acromegaly *
trans-sphenoidal surgery is sthe first line thrrough cribiform fascia, craniotomy if tumour is large
somatostatic analogues can shrink tumour and reduce GH - eg octerotide
dopamine agonists can work on 30% of teh adonomas - if they secrete prolactin too eg carbergoline
GHR antagonist - block the receptors pegvisomant, IGF1 will be controlled but GH will be high
radiotherapy - if surgeon can’t remove it all - side effect: hypopituitarism
describe how presence of glucose in urine fits in with a diagnosis of acromegaly *
glucose in urine shows DM becasue it shows high blood glucose - that surpasses the glucose threshold of 10mmol/L meaning it is not reabvsorbed into the blood - it acts as an osmotic diuretic making the patient thirsty - this is becasue excess GH leads to type 2 DM
describe somatostatin analogues *
endocrine cyanide
short acting injection/monthly depot
GI side effects becasue stop all enzymes - nausea, diarrhoea, gall stones
given pre-treatment - make surgeyr easier
given while waiting for radiation to take effect.
how would you diagnose DM *
oral glucose test - come in fasting, have 75g glucose and measure glucose after 2hours >11.1 diabetes 7.8-11.1 impaired glucose tolerance - prediabetes (includes the fasting glucose as well)
simple fasting glucose- 6.1-7 impaired fasting glucose 7.1< diabetes
see if glucose is in the urine with a dipstick
