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oleh; ;
Dr. Bakti H Simanjuntak SpB (K) V
o The pituitary gland, or hypophysis, is
an endocrine gland
o Produce number of hormones which control
the secretions of many other endocrine glands
o Its anatomical position is important in
ophthalmological view
The anterior pituitary
(adenohypophysis) arises
from Rathke's pouch, an
upward growth from the
ectodermal roof of the
stomodeum
The posterior pituitary
(neurohypophysis) arises
from a downward growth
from the floor of the
diencephalon
Occupies a cavity of the
sphenoid bone called
sella turcica at the
middle cranial fossa
Roof is formed by
diaphragma sellae
The stalk of pituitary is
attached above to the
floor of third ventricle
Size of a pea (< 8 mm)
It weighs about 0.5 gm.
Anterior Lobe:
• FSH
• LH
• ACTH
• TSH
• Prolactin
• GH
Posterior Lobe:
• ADH
• Oxytocin
Benign tumors of pituitary gland
Etiology is unknown
10-15% of all primary brain tumors
75% of adenomas are endocrinogically
secreting
25% of those with MEN-I develop pituitary
adenomas
Hormones Clinical features
Secreting (75%) Chromophobes
(50%)
Prolactin Female: Infertility,
amenorrhea,
galactorrhea
Male :
Hypogonadism,
impotency, sterility,
↓libido,
gynecomastia,
galactorrhea
Acidophils (20%) GH Acromegaly(adult)
Gigantism(child)
Basophils(5%) ACTH, FSH & TSH Cushing disease,
FSH & TSH tumors
Nonsecreting
(25%)
Microadenoma < 10 mm diameter Secreting adenoma
Macroadenoma > 10 mm diameter Mass effects
Non secreting
Localized mass effects
• Chiasmal syndromes
• Compression of other adjacent structures
~ Cavernous sinus (paresis of 3rd, 4th or 6th CNcausing
disorders of extraocular motility)
~ Hypopituitarism (direct pressure, vascular damage)
~ Papilloedema (raised ICP, very rare)
Endocrine effects
• Hypersecretion
Growth Hormone ACTH
Female
• Infertility-amenorrhea- galactorrhea
Male
• Hypogonadism, impotence, sterility, ↓ libido,
gynecomastia, galactorrhea
Growth hormone deficit
• In children: dwarfism
• In adults: weakness, overweight , reduced cardiac output, low blood
sugar levels, and reduced exercise tolerance
TSH deficit
• Hypothyroidism
ACTH deficit
• Underactive adrenal gland, which causes low blood
pressure, hypoglycemia, fatigue, weight loss, vomiting, and low stress
tolerance
ADH deficit
• Diabetes Insipidus
Blurred vision
Headache
Diplopia
Colour desaturation
Visual field defect
Optic atrophy
Post fixation blindness
Visual hallucination
See-Saw nystagmus
Bitemporal hemianopia
Incongruous homonymous hemianopia
Bitemporal central scotoma
Diffuse scotoma
Junctional scotoma
Classic defect in
pituitary adenoma
Occurs in central
chiasmal defect
Superotemporal field
affected first
↓
Lower temporal
field defect
Occurs in optictract
lesion
Occurs in post.
Chiasmal lesion
Compressing only the
macular fibers
Bitemporal central
scotoma
Central scotoma in one
eye with superotemporal
visual field loss in the
other eye
Caused by compression
to anterior loop to the
decussating nasal fibers
in posterior optic nerve
(Von Wilbrand's knee)
Bow tie atrophy Diffuse atrophy
Large adenoma leading to haemorrhage or
infarction of pituitary gland
Occur in pregnancy
Compresses hypophysial portal vessels
Presentation: hyperacute chiasmal syndrome
Treatment : high dose steroid / surgery
Visual acuity
RAPD
Color vision
Ocular motility
Fundus examination
Endocrinological evaluation
• Serum prolactin
• FSH
• TSH
• GH
• Insulin stress test
Ocular investigation
• Visual Field Analysis
• Hess / Lees chart
Imaging
• MRI / CT scan of brain
• X-ray skull (Ant. & Lat. view)
Referral to Endocrinologist &Neuro-surgeon
Observation
Medical therapy
• Dopamine agonists – Cabergoline/Bromocriptine
Surgery
• When mass causing severe compression
• Endoscopic - Transphenoidal, transfrontal
• Craniotomy
• Visual recovery is tri-phasic
Trans-
sphenoidal
Surgery
Radiotherapy
Transfrontal
Observation
Medical therapy
Radiotherapy
• Following incomplete removal of tumour
• Primary treatment
Gamma knife stereotactic radiotherapy
• Close proximity to the optic nerve
• Cavernous sinus invasion
Surgery Radiotherapy Medical
Non-functioning
adenoma
1st line 2nd line -
Prolactinoma 2nd line 2nd line 1st line
Acromegaly 1st line 2nd line 2nd line
Cushing’s
disease
1st line 2nd line -
Medical therapy –
• Monthly for large tumors or during pregnancy for
tumors of any size
• 6 month intervals in microadenoma for 1 year,
then yearly
Surgery –
• Immediately postoperatively
• 4-6 weeks postoperatively
• 4 months intervals for a year
• Yearly for 5 years
• Every 2 years
Radiotherapy –
• At the midpoint and end of radiotherapy
• 3 months interval for a year
• 6 months interval for a year
• Yearly
Evaluation -
• Visual acuity
• Fundoscopy
• Visual field
• Imaging
Pituitary adenomas occurs with a wide
spectrum of clinical features
Should be managed between different
specialists
Neuro-ophthalmological manifestations are
frequent and varied
Physicians must be aware about these in order
to refer patients to ophthalmologist for early
diagnosis and treatment
K - 29 EMB BDH  ; pituitaryadenoma.pptx

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K - 29 EMB BDH ; pituitaryadenoma.pptx

  • 1. oleh; ; Dr. Bakti H Simanjuntak SpB (K) V
  • 2. o The pituitary gland, or hypophysis, is an endocrine gland o Produce number of hormones which control the secretions of many other endocrine glands o Its anatomical position is important in ophthalmological view
  • 3. The anterior pituitary (adenohypophysis) arises from Rathke's pouch, an upward growth from the ectodermal roof of the stomodeum The posterior pituitary (neurohypophysis) arises from a downward growth from the floor of the diencephalon
  • 4. Occupies a cavity of the sphenoid bone called sella turcica at the middle cranial fossa Roof is formed by diaphragma sellae The stalk of pituitary is attached above to the floor of third ventricle Size of a pea (< 8 mm) It weighs about 0.5 gm.
  • 5. Anterior Lobe: • FSH • LH • ACTH • TSH • Prolactin • GH Posterior Lobe: • ADH • Oxytocin
  • 6.
  • 7. Benign tumors of pituitary gland
  • 8. Etiology is unknown 10-15% of all primary brain tumors 75% of adenomas are endocrinogically secreting 25% of those with MEN-I develop pituitary adenomas
  • 9. Hormones Clinical features Secreting (75%) Chromophobes (50%) Prolactin Female: Infertility, amenorrhea, galactorrhea Male : Hypogonadism, impotency, sterility, ↓libido, gynecomastia, galactorrhea Acidophils (20%) GH Acromegaly(adult) Gigantism(child) Basophils(5%) ACTH, FSH & TSH Cushing disease, FSH & TSH tumors Nonsecreting (25%)
  • 10. Microadenoma < 10 mm diameter Secreting adenoma Macroadenoma > 10 mm diameter Mass effects Non secreting
  • 11. Localized mass effects • Chiasmal syndromes • Compression of other adjacent structures ~ Cavernous sinus (paresis of 3rd, 4th or 6th CNcausing disorders of extraocular motility) ~ Hypopituitarism (direct pressure, vascular damage) ~ Papilloedema (raised ICP, very rare) Endocrine effects • Hypersecretion
  • 13. Female • Infertility-amenorrhea- galactorrhea Male • Hypogonadism, impotence, sterility, ↓ libido, gynecomastia, galactorrhea
  • 14. Growth hormone deficit • In children: dwarfism • In adults: weakness, overweight , reduced cardiac output, low blood sugar levels, and reduced exercise tolerance TSH deficit • Hypothyroidism ACTH deficit • Underactive adrenal gland, which causes low blood pressure, hypoglycemia, fatigue, weight loss, vomiting, and low stress tolerance ADH deficit • Diabetes Insipidus
  • 15. Blurred vision Headache Diplopia Colour desaturation Visual field defect Optic atrophy Post fixation blindness Visual hallucination See-Saw nystagmus
  • 16. Bitemporal hemianopia Incongruous homonymous hemianopia Bitemporal central scotoma Diffuse scotoma Junctional scotoma
  • 17. Classic defect in pituitary adenoma Occurs in central chiasmal defect Superotemporal field affected first ↓ Lower temporal field defect
  • 18. Occurs in optictract lesion Occurs in post. Chiasmal lesion Compressing only the macular fibers Bitemporal central scotoma
  • 19. Central scotoma in one eye with superotemporal visual field loss in the other eye Caused by compression to anterior loop to the decussating nasal fibers in posterior optic nerve (Von Wilbrand's knee)
  • 20. Bow tie atrophy Diffuse atrophy
  • 21.
  • 22. Large adenoma leading to haemorrhage or infarction of pituitary gland Occur in pregnancy Compresses hypophysial portal vessels Presentation: hyperacute chiasmal syndrome Treatment : high dose steroid / surgery
  • 23. Visual acuity RAPD Color vision Ocular motility Fundus examination
  • 24. Endocrinological evaluation • Serum prolactin • FSH • TSH • GH • Insulin stress test Ocular investigation • Visual Field Analysis • Hess / Lees chart
  • 25. Imaging • MRI / CT scan of brain • X-ray skull (Ant. & Lat. view)
  • 26. Referral to Endocrinologist &Neuro-surgeon Observation Medical therapy • Dopamine agonists – Cabergoline/Bromocriptine Surgery • When mass causing severe compression • Endoscopic - Transphenoidal, transfrontal • Craniotomy • Visual recovery is tri-phasic
  • 28. Radiotherapy • Following incomplete removal of tumour • Primary treatment Gamma knife stereotactic radiotherapy • Close proximity to the optic nerve • Cavernous sinus invasion
  • 29. Surgery Radiotherapy Medical Non-functioning adenoma 1st line 2nd line - Prolactinoma 2nd line 2nd line 1st line Acromegaly 1st line 2nd line 2nd line Cushing’s disease 1st line 2nd line -
  • 30. Medical therapy – • Monthly for large tumors or during pregnancy for tumors of any size • 6 month intervals in microadenoma for 1 year, then yearly Surgery – • Immediately postoperatively • 4-6 weeks postoperatively • 4 months intervals for a year • Yearly for 5 years • Every 2 years
  • 31. Radiotherapy – • At the midpoint and end of radiotherapy • 3 months interval for a year • 6 months interval for a year • Yearly Evaluation - • Visual acuity • Fundoscopy • Visual field • Imaging
  • 32. Pituitary adenomas occurs with a wide spectrum of clinical features Should be managed between different specialists Neuro-ophthalmological manifestations are frequent and varied Physicians must be aware about these in order to refer patients to ophthalmologist for early diagnosis and treatment