pituitary tumours AD Flashcards
Describe the anatomy of the pituitary tumour
- Lies in the sella turcica- a small cavity on the upper surface of the sphenoid bone
- Covered in dura mater (forms the sella diaphragm or roof of pituitary fossa)
- The pituitary stalk passes through an orifice in the sella diaphragm.
Describe the hormones produced by the anterior pituitary, their stimulators from the hypothalamus, and what they act on. (6)
- CRH from hypothalamus -> ACTH pituitary -> Adrenal glands : steroid production- cortisol, aldosterones, sex hormones.
===inhibited by glucocorticoids - TRH from hypothalamus -> TRH from pituitary -> t3 and t4 from thyroid
====inhibitors are T3/4, dopamine, somatostatin, glucocorticoids. - GHRH from hypothalamus=> GH from pituitary -> targets the liver, bones and other tissues to increase IGF-I production, growth induction, insulin antagonism.
==== inhibitors are somatostatin - GnRH from hypothalamus => LH, FSH from Pituitary => ovaries: ovulation (release of oestrogen and testosterone from adrenal)
===> inhibited by sex steroids - TRH from hypothalamus AND oestrogen => PL from pituitary -> acts on the breast and other tissues to produce milk.
====> It is inhibited by dopamine.
Describe the pathophysiology of pituitary tumours
Multiple oncogene abnormalities may be involved in the pituitary tumorigenesis. G-protein abnormalities, ras gene mutations, p53 gene deletions, mutations and rearrangements, and the association of pituitary tumours with the syndrome of multiple endocrine neoplasia have been described and are involved in the development of adenomas in the pituitary gland.
what are the specific types of pituitary adenomas?
- Benign, monoclonal tumours of anterior pituitary
- Microadenomas 1cm confined to sella
- Macroadenomas with suprasellar expansion
- Invasive macroadenomas with lateral expansion
what is the pathogenesis of pituitary adenomas?
• Hereditary (multiple endocrine neoplasia 1 MEN1) • Genetic Mutations o Signal transduction mutations (eg GSP) o Activated oncogenes (eg p27) o Disrupted paracrine growth factor • Environmental
What are the clinical manifestations of pituitary adenoma?
• Undersecretion of pituitary hormones • Over secretion of pituitary hormones • Neurological manifestations o Visual deficit (bitemporal hemianopia) o Headaches o Diplopia (cranial nerve palsies) o CSF rhinorrhea – if dura is damaged, leak Optic chiasm can be affected => damage to the nasal part of the optic nerve, leading to temporal field deficit (ie. bitemporal haemianopia)
What is a lactotroph andenoma?
Secretion of excessive prolactin which RESULTS IN THE INHIBITION OF GRH LEADING TO A DECREASE LH AND FSH
Females: present earlier, complain of galactorrhoea, infertility, oligo and amenorrhoea. Often present as microadenoma
Male: Decreased libido, impotence, rarerly gynecomastia, galactorrhoea, neurological symptoms, often present in macroadenoma phase.
lactotroph andenoma
- examination
OE they will have signs OF OTHER pituitary HORMONE excess or DEFICIENCY!!!
What investigations would you perform on lactotroph adenoma?
- Prolactin levels
- TFTs and other pituitary hormones
- MRI * often microadenomas**
What are other causes of high PROLACTIN levels you need to rule out?
Other causes of high prolactin levels • Pregnancy • Chest wall stimulation, injury • Drugs (metoclopramide, antidepressants, verapamil) • Pituitary stalk compression • Hypothyroidism
How would you treat a lactotroph adenoma?
- Dopamine agonists
- (Bromocryptine or cabergoline)
- Observatiion
- Surgery if unresponsive to medication and neurological manifestations
What would you expect to see in a Gonotrophic adenoma?
ually clinically silent ‘non functioning’. Secrete inefficiently and variably.
May not find anything because they may secrete intact FSH and or/ alpha and beta subunits
What are the clinical signs of gonotrophic adenoma?
- Incidental imaging
- Neurological symptoms due to mass effect
- Rarely hormonal hypersecretion (may present with pelvic pain due to ovarian hyperstimulation)
- Rarely hormonal deficiencies due to compression
What are some of the features of GH excess
Skin/Connective tissue • Skin thickening/hyperhidrosis, Bone changes (Thickened extremities- facial changes, Prognathism/malocclusion, Sinus enlargement, Arthralgia, Arthritis, Accelerated osteoarthritis, ?increased risk of colonic malignancy) Respiratory • 3 fold increase in resp deaths • Upper and small airway narrowing • Obstructive sleep apnoea syndrome • Increased anaesthetic risk Cardiovascular • HTN • Septal/ventricular hypertrophy • Cardiomegally • Cardiomyopathy Neurological • Visual field loss • Headaches (>50% of patients) • Tumour related o Due to dural stretch o May persist after cure • Entrapment neuropathy • Peripheral neuropathy • Myopathy Metabolic • Insulin resistance o Which can lead to diabetes (due to impaired glucose tolerance) • Hypercalciuria o Raised 1,25 VD • Hypertryglicerideamia
How do you clinically diagnose Acromegally?
caused by pituitary adenoma
Confirm biochemical diagnosis
• IGF-1 : secreted from the liver, will be persistently elevated .
• Glucose tolerance test – 75g glucose, GH should suppress to <4mU/L (in acromegally it remains HIGH)
Rise in GH following TRH or LHRH adminstration
