2. Hypersecretion of anterior pituitary hormones Flashcards
What is hyperpituitarism?
Condition where the symptoms are associated with excess production of adenohypophysial hormones
What is the most likely cause of hyperpituitarism?
Isolated pituitary tumours (adenoma)
Explain bitemporal (heteronymous) hemianopia
- Light from the left visual field hits the right part of the retina and vice versa
- At the optic chiasm, fibres from the inner (nasal) part of both retinae cross
- Therefore, all light from the left visual field is detected by the right side of the brain
- All the light from the temporal fields cross at the optic chiasma for this to happen
- A pituitary tumour could protrude out of the sella turcica and disrupt the fibres coming from the nasal parts of the retinae
- This could lead to a loss of the temporal part of the visual field - bitemporal hemianopia
An excess of what 5 types of pituitary hormones can result what conditions?
- Corticotrophin (ACTH) => Cushing’s disease
- Thyrotrophin (TSH) => Thyrotoxicosis
- Gonadotrophins (LH and FSH) => Precocious puberty in children
- Prolactin => Hyperprolactinaemia
- Somatotrophin (GH) => Gigantism, Acromegaly
What is hyperprolactinaemia?
• Excess circulating prolactin when not due to a physiological cause e.g. pregnancy or breast-feeding
• Associated with pituitary tumours - prolactinoma
- most common type - microadenomas
What happens in hypoprolactinaemia?
- Not really a problem
* Absence of prolactin doesn’t really have any serious physiological consequences
What is the effect of hyperprolactinaemia due to prolactinoma in women?
• Galactorrhoea • Decreased LH and FSH levels leading to: - secondary amenorrhoea - loss of libido - infertility
What is the effect of hyperprolactinaemia due to prolactinoma in men?
• Galactorrhoea (uncommon) • Decreased LH and FSH levels leading to: - loss of libido - impotence - infertility
What does excess somatotrophin lead to in children and adults?
- Children - gigantism
* Adults - acromegaly (growth plates of long bones have fused so height doesn’t increase, but there are other effects)
Outline the onset and development of acromegaly?
- Insidious onset
- Signs and symptoms progress gradually over many years
- If untreated, associated with increased morbidity and mortality due to cardiovascular and respiratory complications
- Increased organ size - increased demand for oxygen - strain on CVS
What parts of the body grow in acromegaly?
- Periosteal bone
- Cartilage
- Fibrous tissue
- Connective tissue
- Internal organs e.g. hepatomegaly
- Prognathism (protrusion of mandible or maxilla)
- Enlarged supraorbital ridges
- Enlarged soft tissues
What are the metabolic effects of acromegaly?
- Increased endogenous glucose production
- Decreased muscle glucose uptake
- Increased insulin production => increased insulin resistance
- Impaired glucose tolerance
- Diabetes mellitus
Apart from growth, what are the other clinical manifestations of acromegaly?
- General coarseness of features
- Hyperhidrosis (excessive sweating)
- Carpal Tunnel Syndrome - increased cartilaginous growth creating pressure on nerve in wrist
- Joint pain
- Galactorrhoea
- Menstrual abnormalities, decreased libido and impotence
- Hypertension
What test is used to test pituitary hypersecretion?
Suppression test
Describe glucose-induced suppression of growth hormone secretion
• Normally, if glucose is given, GH release is inhibited, levels decrease then a there is a sudden rise • In acromegaly: - glucose given - paradoxical rise in GH - back down and levels out
What is the treatment of acromegaly?
• Surgery - transphenoidal hypophysectomy
• Radiotherapy (might lead to hypopituitarism though)
• Chemotherapy
- somatostatin analogues e.g. octreotide
- dopamine agonists e.g. bromocriptine and cabergoline
When is octreotide used?
- As a short-term treatment before pituitary surgery
- Can also reduce size of tumour to make surgery easier
- As a long-term treatment in those no controlled by other means
- Treatment of other neuroendocrine tumours e.g. carcinoid tumours
How is octreotide administered?
- Subcutaneous or intramuscular - 3x per day
- Depot preparation once GH levels are under control
- Adjust dose according to need
Where is octreotide metabolised and what is its half-life?
- Hepatic/renal metabolism
* 2-4 hours half-life
What are the negative side-effects of octreotide?
- GI tract disturbance (somatostatin is produced by the small intestine)
- Initial reduction in insulin secretion (inhibits insulin production by beta cells) - transient hyperglycaemia
- Gallstones (rare)
How is hyperprolactinaemia treated?
- With dopamine receptor agonists (as dopamine is the main hypothalamic influence on prolactin secretion - inhibits secretion)
- DA2 agonists decrease prolactin (and GH) secretion and reduces tumour size
What is bromocriptine and how is it administered?
- DA2 agonist
- Oral administration
- 1 time a day
What percentage of bromocriptine is protein-bound, where is it metabolised and what is its half-life?
- Highly plasma protein-bound - 93%
- Hepatic metabolism
- 7 hours half-life
What are the negative side-effects of bromocriptine?
- Nausea/vomiting/abdominal cramps
- Dyskinesias
- Pschomotor excitation
- Postural hypotension
- Vasospasm in fingers and toes
Apart from its main use, what are the main uses of bromocriptine?
- Suppression of lactation
- Cyclical benign breast tumours
- Acromegaly - but doesn’t have the same beneficial effect on tumour size
- Parkinson’s disease
What is cabergoline, how is it administered and what is its half-life?
- DA2 agonist
- Oral administration, 1-2 times a week
- 45 hour half-life
What are the negative side-effects of cabergoline?
Same as bromocriptine but less pronounced
