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Neurosurgery > Ch. 9 - Pituitary Tumors > Flashcards

Ch. 9 - Pituitary Tumors Flashcards

1
Q

Incidence of pituitary tumors

A

8-10% of all intracranial tumors

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2
Q

Pituitary adenoma origin

A

From anterior lobe (adenohypophysis)

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3
Q

Microadenoma vs. macroadenoma

A

Micro: < 10mm

Macro: >10mm

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3
Q

Pituitary adenoma spread and consequences

A

Local invasion inferiorly through floor of sella (CSF rhinorrhea)

Superiorly to suprasellar cisterns (compression of optic chiasm, hypothalamus, 3rd ventricle)

Laterally to cavernous sinus (CN disturbance)

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4
Q

Lateral microadenomas are more likely to produce which hormones?

A

Prolactin and GH

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6
Q

Central microadenomas are more likely to produce which hormone?

A

ACTH

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7
Q

Effects of prolactin

A

Breast growth and promotion of lactation; important in spermatogenesis

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8
Q

How is prolactin secretion regulated?

A

Dopamine blocks prolactin secretion (UNLIKE ALL OTHER PITUITARY HORMONES)

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9
Q

Characteristic presentation of prolactinomas

A

Young females with amenorrhea and galactorrhea; males with impotence

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10
Q

Prolactin level suggestive of pituitary adenoma

A

>2000 ng/mL (nl 70-550)

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11
Q

Other pituitary adenomas associated with hyperprolactinemia

A

GH and null cell can cause hyperprolactinemia 2/2 mass effect blocking DA secretion

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12
Q

Consequences of ACTH adenoma

A

ACTH stimulates adrenal cortex to secrete cortisol = CUSHING’S DISEASE

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13
Q

Null cell adenoma histology

A

Chromophobic (no cytoplasmic granules) + accumulation of mitochondria (then called ‘oncocytomas’)

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14
Q

Null cell adenoma presentation

A

Aggressive and grow quickly = visual disturbances

Hormonally silent

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15
Q

Factors affecting presentation of pituitary adenomas

A

Size of tumor + endocrine fxn of secreted hormones

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16
Q

Visual field deficits a/w pituitary adenoma

A

Compression of optic chiasm -> bitemporal hemianopsia

Compression of optic tract -> homonymous hemianopsia

Compression of posterior chiasm -> bilateral central scotomas

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17
Q

Extraocular deficits a/w pituitary adenomas

A

CN3, 4, 6 palsies

CN5 damage 2/2 cavernous sinus invasion causes facial pain

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18
Q

Sxs of hypopituitarism

A

Pre-pubertal: retards development of 2ndary sex characteristics

Post-pubertal: fatigue, muscle weakness, anorexia –> episodic confusion/drowsiness (severe) can be precipitated by stressful events

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19
Q

Sxs of pituitary apoplexy

A

Spontaneous hemorrhage into pituitary tumor = sudden severe HA, transient LOC + extraocular muscle paralysis (looks like SAH + EOM involvement)

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20
Q

What do GH-secreting tumors cause?

A

Kids - gigantism

Adults (30-40) - acromegaly (enlarged hands/feet, coarse/greasy skin, sweat profusely, HTN, cardiac hypertrophy, diabetes)

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21
Q

Cushing’s disease

A

ACTH-producing pituitary adenoma (80% microadenomas)

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22
Q

Cushing’s disease mortality

A

50% at 5 years

23
Q

Cushing’s disease sxs

A

Obesity, thin skin, striae, fat redistribution (moon face, buffalo hump), easy bruising, acne, facial hair, weakness/muscle atrophy, osteoporosis, glucose intolerance

24
Q

Causes of Cushing’s syndrome

A

90% of cases 2/2 Cushing’s disease (ACTH-producing pituitary adenoma)

OTHER: adrenal adenoma/carcinoma or ectopic ACTH (small cell lung CA)

25
Q

Nelson-Salassa syndrome

A

ACTH-producing pituitary adenoma in pt w/ bilateral adrenalectomy -> no negative feedback -> accelerated growth of existing adenoma (usually macroadenoma)

26
Q

Cutaneous findings of Nelson-Salassa syndrome

A

Hyperpigmentation 2/2 beta-MSH production (ACTH breakdown product)

27
Q

How is GH-secreting tumor diagnosed?

A

Glucose suppression test - measure GH following glucose bolus (should suppress normally)

IGF-1 levels - indicator of GH activity

Other: measure GHRH or TRH

28
Q

How is Cushing’s disease diagnosed?

A
  1. Hypercortisolemia on 24 hr urine cortisol
  2. Dexamethasone suppression test (high-dose will suppress pituitary adenoma but NOT ectopic or adrenal ACTH source)
  3. Administer CRH and measure differential ACTH level in periphery/pertrosal sinus
29
Q

Scan of choice for pituitary adenomas?

A

High resolution CT/MRI with contrast

30
Q

Appearance of pituitary micro vs. macroadenoma on CT?

A

Micro: hypodense, upward bulging, deviation of pituitary stalk, thinning of sella

Macro: contrast-enhancing lesion in sella, best seen on coronal section

31
Q

Appearance of pituitary micro vs. macroadenoma on MRI?

A

Micro: T1 - hypointense T2 - hyperintense

Macro: T1 - isointense T2 - hyperintense

32
Q

Ddx of pituitary adenoma

A

Craniopharyngioma (pituitary gland embryonic tissue) OR suprasellar meningioma (part of sella turcica)

Uncommon: optic nerve/hypothalamus glioma, aneurysm, Rathke’s cleft cysts

33
Q

Indications for surgical excision of pituitary adenomas

A
  1. Large tumors compressing adjacent structures (esp. visual pathways)
  2. GH-secreting (causing acromegaly)
  3. ACTH secreting (causing Cushing’s)
  4. Refractory prolactinomas
34
Q

Surgical approaches to pituitary adenomas

A

Transphenoidal vs. transcranial excision

35
Q

Post-operative management of pituitary excision

A

Fluid balance and hormonal status!

Endocrine deficiency replacement with (1) parenteral hydrocortisone and (2) vasopressin for transient DI

36
Q

Indications for postoperative radiotherapy in pituitary adenomas

A

Subtotal excision or residual hormone secretion

37
Q

Medical tx of micro prolactinomas

A

Bromocriptine = dopamine agonist; significant side effects (n/v, postural hypotension)

38
Q

Craniopharyngioma origin

A

Epithelial remnants of Rathke’s pouch

39
Q

Craniopharyngioma histology

A

Cystic tumor with yellow fluid (cholesterol crystals)

  1. Adamantinous - all children have this type
  2. Papillary - 1/3 of adults, rare in children
40
Q

Craniopharyngioma presentation

A
  1. Elevated ICP (3rd ventricular obstruction) - HA, vomiting, papilledema
  2. Visual impairment - papilledema vs. chiasmal compression (direct)
  3. Endocrine abnormalities - hypogonadism, stunted growth, DI
41
Q

Craniopharyngioma appearance on CT

A

Cystic tumor in suprasellar region with curvilinear calcification

42
Q

DDx of craniopharyngioma

A

Rathke’s cleft cyst

43
Q

Craniopharyngioma tx

A

Pterional craniotomy vs. bifrontal craniotomy (top-down approach since tumor is suprasellar)

44
Q

Empty sella syndrome

A

Communicating extension of subarachnoid space into pituitary fossa

2/2 defect in diaphragma sella OR pituitary surgery/radiotherapy OR increased ICP = herniation of subarachnoid space

Considered ANATOMICAL VARIANT

45
Q

Classic pt with empty sella syndrome

A

Obese, hypertensive, middle-age woman

46
Q

Sxs of empty sella syndrome

A

HA, spontaneous CSF rhinorrhea

47
Q

Tx of empty sella syndrome with CSF rhinorrhea

A

Repair leak in floor of sella with crushed muscle and fascia lata + CSF shunt

48
Q

Anterior pituitary lobe vs. posterior lobe development

A

Anterior lobe - Rathke’s pouch

Posterior lobe - infundibulum (floor of diencephalon)

49
Q

Hormones released by anterior pituitary? Posterior pituitary?

A

Anterior - GH, TSH, ACTH, prolactin, LH, FSH

Posterior - ADH, oxytocin

50
Q

What is the most common pituitary adenoma?

A

Prolactinoma (40%) > GH adenoma (20%) = non-secreting adenoma (20%) > ACTH adenoma (15%)

51
Q

Population most commonly affected by craniopharyngiomas

A

Children and young adults; almost half occur in first 20 years of life

52
Q

Identify the lesion

A

Pituitary macroadenoma

53
Q

Identify the lesion

A

Craniopharyngioma

54
Q

Identify the lesion

A

Empty sella syndrome

Neurosurgery (21 decks)

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