EXPLAINING OF PITUITARY GLAND TUMOURS
Introduction
In order to understanding the pituitary gland tumours it should be first known the important anatomy of the pitiuitary
The pituitary gland or hypophysis cerebri is the master gland in the body
It is an endocrine gland which secreted many hormones in the blood It very small in size a pea sized
It is intracranial structures which present in the middle cranial fossa It is lies in bony cavity like structure called sella trucica
It is composite structure consists of three parts the anterior intermediate and posterior lobe
Hormones secreted by anterior pituitary by its cells
Acidophilic cells secreted somatotropic or growth hormone and prolactin
Basophilic cells secreted adrenocorticotropic hormone (ACTH) , thyroid stimulating hormone (TSH) follicular and luteinzing hormones (FSH and LH
Hormones secreted by posterior pituitary
Oxytocin and vasopressin or antiduritic hormones
Pituitary gland tumours can be classified as follow
Classification of Pituitary tumours
Endocrine active
|
Clinical syndrome
|
Secretory product
|
Acromegaly gigantism
|
Growth hormone GH 20%
|
Somatrophic
|
Cushing,s disease
|
Adrenocorticotrophic hormone ACTH 15%
|
Corticotrophic
|
Amenorrhoea galactorrhoea impotence
|
Prolactin PRL 40%
|
Prolactinoma
|
Hyperthyroidism
|
Thyroid stimulating hormone TSH 1%
|
Thyrotrophic
|
Behaves as endocrine inactive
|
Follicle stimulating hormone FSH Luteinising
hormone LH 1-2%
|
Gonadotrophic
|
Hyothyroidism
|
Alpha subunit 20%
|
Endocrine inactive
|
Pituitary tumours account for 8% of all intracranial tumours. they were classified according to their staining characteristics seen on light microscopy. However, the three types (chromophobe, acidophilic and basophilic) did not correspond closely with the clinical syndromes of pituitary hypersecretion. The subsequent development of immunological staining techniques and electron microscopy provided a more refined classificanon of pituitary tumours. It is now correct to classify pituitary tumours according to their size(microadenomas < 10 mm), mesoadenomas (10-20 mm) and macroadenomas (> 20 mm) and whether they are endocrine active or inactive . These features will also determine their presentation.
Clinical features
The most common endocrine syndromes are Cushing's disease due to adrenocorticotropic hormone (ACTH) secretion, Forbes-Albright syndrome due to prolactin secretion, and acromegaly due to growth hormone secretion.
Pituitary tumours
arise in the sella turcica and can expand up into the suprasellar cisterns,
compressing the optic chiasm above and resulting In visual failure (classically
a bitemporal hemianopia
Careful assessment of the visual fields, visual acuity and optic fundi is therefore essential. They may also invade laterally into the cavernous sinuses on each side, compressing the third to sixth cranial nerves.
Endocrine disturbance is due to either hypopituitarism due to compression on the gland or excess secretion of a particular pituitary hormone.
Prolactin secreting tumours are usually found in younger women and cause loss of libido, infertility, amenorrhoea and galactorrhoea.
Corticotrophin-producing tumours cause Cushing's disease owing to cortisol excess.
The principal features are moon face abdominal striae, buffalo hump, hypertension and diabetes mellitus.
Acromegaly is due to an overproduction of growth hormone.
The disease is disfiguring, causing prognathism and overgrowth of include hypertension, cardomyopathy, diabetes mellitus, excessive sweating, arthralgias and lassitude
Haemorrhage Into a macroadenoma, known as pituitary apoplexy, can precipitate an acute presentation with abrupt headache, hypopituitarism and visual failure decreased mental status, and endocrine dysfunction.
Diabetes Insipidus, a product of direct hypothalamic involvement, is usually indicative of a craninopharyngioma or metastatic lesion and is rarely caused by pituitary adenomas.
Investigations
Diagnosis is confirmed by laboratory assessment of pituitary endocrine function, neuroradiological Imaging and formal visual assessment.
Radioimmunoassay will identify the hormone being secreted. It is important, particularly with acute presentations, to exclude a prolactinoma as (the majority of these will respond rapidly to treatment with the dopamine agonist bromocriptine.
Prolactin levels above 200 ng ml are usually diagnostic. Non-functiomng macroadenomas may cause hyperprolactinaemia due to distortion of the pituitary stalk or impingement on the hypothalamus.
This is because the latter produces prolactin-inhibiting factor, which, under normal circumstances, suppresses prolactin levels to below 15 ng ml .
Diagnosis of Cushing's disease is made by radioimmunoassay of adrenocorticotrophic hormone (ACTH) in the peripheral blood and petrosal venous sinus sampling to detect a brain-peripheral concentration gradient
With the exception of some patients with Cushing's disease MRI of the sella will confirm diagnosis of an intrasellar mass the resolution of MRI will also detect all but the smallest less than 2 mm tumours and any extrasellar extension
Treatment
Treatment depends on the endocrine disturbance present and the effect of compression of adjacent neural structures.
For prolactinomas, dopamine agonist therapy should be commenced which may causes shrinkage of it.
Surgical excision
Is reserved for macroadenomas compressing the optic chiasm, growth hormone-secreting tumours causing acromegaly and ACTH-secreting tumours causing Cushing's disease
Surgery is indicated in patients with prolactinomas who are not responding to medical treatment or when unwanted side-effects occur or has persistent mass effect or endocrinal dysfunction .
This is usually performed via a trans-sphenoidal route, although the Transcranial route can be used.
The aim is to preserve normal pituitary function if possible Surgery should be covered with parenteral hydrocortisone, and frequently vasopressin is required
Radiotherapy
Is used for subtotal resections and for persistent hypersecretion of pituitary hormones.
The long-term follow-up of non-functioning pituitary adenomas has shown to be recurrent indicating that there is perhaps a more extensive role for this modality and that postoperative patients should be more closely followed up.
tags:pituitary,tumours,explaining,gland
Careful assessment of the visual fields, visual acuity and optic fundi is therefore essential. They may also invade laterally into the cavernous sinuses on each side, compressing the third to sixth cranial nerves.
Endocrine disturbance is due to either hypopituitarism due to compression on the gland or excess secretion of a particular pituitary hormone.
Prolactin secreting tumours are usually found in younger women and cause loss of libido, infertility, amenorrhoea and galactorrhoea.
Corticotrophin-producing tumours cause Cushing's disease owing to cortisol excess.
The principal features are moon face abdominal striae, buffalo hump, hypertension and diabetes mellitus.
Acromegaly is due to an overproduction of growth hormone.
The disease is disfiguring, causing prognathism and overgrowth of include hypertension, cardomyopathy, diabetes mellitus, excessive sweating, arthralgias and lassitude
Haemorrhage Into a macroadenoma, known as pituitary apoplexy, can precipitate an acute presentation with abrupt headache, hypopituitarism and visual failure decreased mental status, and endocrine dysfunction.
Diabetes Insipidus, a product of direct hypothalamic involvement, is usually indicative of a craninopharyngioma or metastatic lesion and is rarely caused by pituitary adenomas.
Investigations
Diagnosis is confirmed by laboratory assessment of pituitary endocrine function, neuroradiological Imaging and formal visual assessment.
Radioimmunoassay will identify the hormone being secreted. It is important, particularly with acute presentations, to exclude a prolactinoma as (the majority of these will respond rapidly to treatment with the dopamine agonist bromocriptine.
Prolactin levels above 200 ng ml are usually diagnostic. Non-functiomng macroadenomas may cause hyperprolactinaemia due to distortion of the pituitary stalk or impingement on the hypothalamus.
This is because the latter produces prolactin-inhibiting factor, which, under normal circumstances, suppresses prolactin levels to below 15 ng ml .
Diagnosis of Cushing's disease is made by radioimmunoassay of adrenocorticotrophic hormone (ACTH) in the peripheral blood and petrosal venous sinus sampling to detect a brain-peripheral concentration gradient
With the exception of some patients with Cushing's disease MRI of the sella will confirm diagnosis of an intrasellar mass the resolution of MRI will also detect all but the smallest less than 2 mm tumours and any extrasellar extension
Treatment
Treatment depends on the endocrine disturbance present and the effect of compression of adjacent neural structures.
For prolactinomas, dopamine agonist therapy should be commenced which may causes shrinkage of it.
Surgical excision
Is reserved for macroadenomas compressing the optic chiasm, growth hormone-secreting tumours causing acromegaly and ACTH-secreting tumours causing Cushing's disease
Surgery is indicated in patients with prolactinomas who are not responding to medical treatment or when unwanted side-effects occur or has persistent mass effect or endocrinal dysfunction .
This is usually performed via a trans-sphenoidal route, although the Transcranial route can be used.
The aim is to preserve normal pituitary function if possible Surgery should be covered with parenteral hydrocortisone, and frequently vasopressin is required
Radiotherapy
Is used for subtotal resections and for persistent hypersecretion of pituitary hormones.
The long-term follow-up of non-functioning pituitary adenomas has shown to be recurrent indicating that there is perhaps a more extensive role for this modality and that postoperative patients should be more closely followed up.
tags:pituitary,tumours,explaining,gland
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