hypersecretion of anterior pituitary hormones Flashcards

1
Q

what are the symptoms for hyperpituitarism associated with

A

excess production of adenohypophysial hormones

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2
Q

what re the main causes of hyperpituitarism

A

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

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3
Q

effect of a pituitary tumour on the optic chiasm and how this causes bitemporal hemianopia *

A

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

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4
Q

how do you assess a bitemporal hemianopia *

A

use perimetry every time you see a flash you press a button

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5
Q

what does excess ACTH cause *

A

cushing’s syndrome

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6
Q

what does excess TSH cause *

A

thyrotoxicosis the thyroid gland is told to produce too much thyrotrope

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7
Q

what does excess LH and FSH cause *

A

precocious puberty in children - too much LH, FSH -> testosterone and oestrogen

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8
Q

what does excess prolactin cause *

A

hyperprolactinaemia

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9
Q

what does excess GH cause *

A

gigantism in children - don’t have epiphysial bone closure acromegaly in adults - have epiphysial bone closure

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10
Q

when is hyperprolactinaemia physiological

A

in pregnancy - preparation for lactation in breastfeeding

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11
Q

when is hyperprolactinemia pathological and describe this *

A

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

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12
Q

clinical features of hyperprolactinoma in women *

A

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

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13
Q

clinical symptoms of hyperprolactinaemia for men *

A

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

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14
Q

describe the principle of treatment for hyperprolactinaemia *

A

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

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15
Q

side effects of dopamine agonists *

A

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

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16
Q

principles of diagnosis of hyperprolactinaemia *

A

usually diognosed relatively early because people notince when their periods are off, or lactation - women present earlier

17
Q

what is the main cause of excess GH

A

a benign growth hormone secreting pituitary adenoma

18
Q

describe gigantism *

A

when GH hypersecretion occurs in childhood - grow really tall, above the average

problem is it causes impaired glucose tolerance and therefore DM

19
Q

describe acromegaly *

A

insidious in onset

untreated, excess GH is releated to increased morbity and death

20
Q

How can acromegaly cause death *

A

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

21
Q

what grows in acromegaly

A

Soft tissue:

periosteal bone

cartilage

fibrous tissue

connective tissue

internal organs - cardiomegaly, splenomegaly, hepatomegaly

22
Q

descibe the clinical features of acromegaly *

A

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

23
Q

principle of diagnosis for acromegaly *

A

changes are subtle and over a long time - bring in an old picture to see if there is a difference

24
Q

what are the metabolic affects of acromegaly *

A

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
25
Q

what are the clinical features for acromegaly *

A

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

26
Q

describe how prolactin and GH can be co-secreted in acromegaly and explain the furtehr effects of this *

A

tumour secret prolactin and GH

hyperprolactinaemia - cause secondary gonadism

27
Q

describe the GH axis

A

somatostatin and GHRH released from the hypothalamus

GH released by ant pit

GH act on liver

liver produce somatomedins - IGF1

28
Q

describe the diagnosis of acromegaly *

A

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

29
Q

describe the treatment of acromegaly *

A

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

30
Q

describe how presence of glucose in urine fits in with a diagnosis of acromegaly *

A

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

31
Q

describe somatostatin analogues *

A

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.

32
Q

how would you diagnose DM *

A

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