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Endocrinology > Pituitary Disorders > Flashcards

Pituitary Disorders Flashcards

1
Q

What is the best imaging modality for the pituitary?

A

MRI

  • Posterior pituitary has bright spot on normal contrast
  • with contrast, both anterior and posterior pituiary are bright
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2
Q

Axes of the Pituitary

  • how they differ?
  • types of disorders
A

Anterior pituitary: hormones SYNTHESIZED and STORED

  • Pituitary tumors
  • Hypofunction
  • Hyperfunction

Posterior Pituitary: Hormones are STORED only (hormones are synthesized by the hypothalamus)

  • Diabetes insipidus
  • SIADH
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3
Q

Hormones produced by Anterior Pituitary

A
  • FSH and LH: stimulated by pulsatile GnRH
  • TSH: stimulated by TRH
  • ACTH: stimulated by CRH
  • PRL: stimulated by TRH; inhibited by dopamine
  • GH: stimulates by GHRH
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4
Q

Hormones produced by Posterior Pituitary

A
  • AVP (Arginine Vasopressin)

- Oxytocin

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5
Q

Hypopituitarism

A
  • Diminished or absent secretion of >1 pituitary hormones
  • Development often slow and insidious
  • Clinical presentation depends upon etiology of hypopituitarism
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6
Q

Hypopituitarism: Invasive causes

A
  • Large pitutiary adenomas more likely to cause hypofunction than small pituitary adenomas (microadenomas)
  • Look for compressive effect: e.g., Vision deficits due to compression of optic chiasm
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7
Q

Sheehan’s Syndrome

A
  • Hypopituitarism due to Infarction
  • Mechanism for ischemia uncertain; believed to be hypotension and vasospasm of the hypophysial arteries, or due to shock

Clinical Symptoms: (75% of gland must be destroyed for symptoms to manifest)

  • Failure to lactate
  • Post-partum menstrual irregularities
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8
Q

Lymphocytic hypophysitis

A
  • IMMUNOLOGIC hypopituitarism that occurs during pregnancy and post-partum period
  • Autoimmune process with infiltration of pituitary by lymphocytes and plasma cells that destroys anterior pituitary
  • Pituitary autoantibodies may be present
  • May result in isolated hormone deficiencies: ACTH deficiency most common
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9
Q

Isolated anterior pituitary hormone deficiencies

A
  1. GH deficiency: usually presents in childhood
    - Decreased muscle mass, increased fat mass; occult
  2. Gonadotropin deficiency:
    - Hypogonadotropic hypogonadism
    - Kallman’s sydrome: defect in GnRH secretion and maldevelopment of olfactory center
    - Amenorrhea, ED, decreased libido
  3. TSH deficiency: incredibly rare; deficiency in TRH
    - Fatigue, wt gain, cold intolerance
  4. ACTH deficiency: incredibly rare; lymphocytic hypophysitis
    - fatigue, weakness
  5. PRL deficiency: sign of severe hypopituitarism
    - Lactation failure
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10
Q

What hormone provides NEGATIVE INHIBITORY CONTROL over Prolactin?

A

Dopamine

  • During damage to anterior pituitary, Prolactin levels are the most resistant to change
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11
Q

Primary (ADDISON’S) vs. Secondary Adrenal Insufficiency

A

Note: aldosterone made by adrenal gland is more under the control of renin angiotensin (secreted by kidney) than ACTH (pituitary)

  • Primary Adrenal Insufficiency (ADDISON’S DISEASE): will have low aldosterone, but high ACTH
  • Secondary: when you have pituitary deficiency with low ACTH production , you are going to get all the manifestation of cortisol decrease but not aldosterone decrease.
  • present with hyponatremia but not hypokalemia
  • tend not to see hypotension as with aldosterone deficiency
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12
Q

Stimulation Testing

  • ACTH Stimulation Test
A
  • Useful for diagnosis of adrenal insufficiency and growth hormone deficiency
  • After measuring baseline ACTH & Cortisol/Alodsterone, administer COSYNTROPIN (analog of ACTH)
  • High baseline ACTH: admin of cosyntropin does not raise cortisol/aldosterone –> Primary Adrenal Insufficiency
  • Low baseline ACTH: admin of cosyntropin does not raise cortisol/aldosterone –> Central (Secondary) adrenal insufficiency
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13
Q

Treatment for Adrenal Deficiency

A
  • Administer Glucocorticoids (e.g., hydrocortizone or prednisolone
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14
Q

Treatment for TSH Deficiency

A
  • administer Levothryoxine

** If adrenal insufficiency is suspected with hypothyroidism, treat with glucocorticoids (steroids) prior to levothyroxine

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15
Q

Pituitary Adenomas (Clinical presentation)

A

Early manifestations: Signs of hypogonadism and oligomenorrhea/amenorrhea

Late manifestations:

  • Mass effect: headache, peripheral visual deficit
  • Specific symptoms of hormone hypersecretion
    • Lactotrophs (60%)
    • Somatotrophs (20%) - acromegaly
    • Corticotrophs (10%) – Cushing disease
    • Thyrotrophs
    • Gonadotrophs
  • Pituitary insufficiency once tumor becomes big enough
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16
Q

Bitemporal Hemianopsia

A
  • Bilateral peripheral visual deficit
  • due to compression of optic chiasm
  • often compressed by mass effect of pituitary adenomas
17
Q

Prolactinoma

A
  • Prolactin-secreting tumors
  • Microprolactinoma 10 mm in size; More common in men (present late)
  • PRL level correlates with size of prolactinoma

Presentation: Prolactin increases milk production, decreases GnRH

  • menstrual irregularities
  • Galactorrhea (perform a thorough physical exam)
  • visual field defects (33% with macroadenomas)
  • Headache
  • libido-potency failure (dereased gonadal function)

Treatment:

  • DOPAMINE inhibits prolactin secretion
  • Limiting factor for radiotherapy: need at least 5mm space from pituiary to optic chiasm
18
Q

Dopamine Agonists

A
  • Bromocriptine : D1 and D2 receptors
  • Cabergoline : more specific for D2 receptor
  • long half life & long duration of action
  • Contraindications: uncontrolled HTN or known sensitivity to ergot derivatives
  • Metabolized in the liver
  • Advise to take at bedtime: nausea, headache, dizziness, mental fogginess
19
Q

Treatment of Primary Hypothyroidism with elevated prolactin secretion

A
  • Treat primary hypothyroidism first
  • hypothyroidism will cause increase in TRH and TSH
  • TRH will override inhibitory effect of dopamine, and stimulate excess secretion of prolactin
  • Prolactin levels should normalize after treatment of primary hypothyroidism with levothyroxine
20
Q

Acromegaly

A
  • Due to excess GH secretion, typically caused by pituitary adenoma

Findings: large tongue, hands & feet; enlarged angled jaw; deep voice; impaired glucose tolerance (insulin resistance)
- No linear growth because fused long bone epiphyses

Diagnosis:

  • increased serum IGF-1; GH stimulates HEPATIC secretion of IGF-1
  • Glucose suppression test: oral glucose load (75g) and measure GH at baseline, 1h and 2h
    • Normal: GH very low
    • GH excess: GH does not suppress
  • Imaging after biochemical confirmation to determine etiology of GH excess (majority of cases pituitary adenoma > 1 cm)

Tx: Surgery is first line

21
Q

Gigantism

A
  • excess GH secretion in children
  • increased linear bone growth
  • Concomitant hypogonadism also delays epiphyseal closure
22
Q

What suppresses GH release?

A
  • Glucose
  • Somatostatin: GH inhibitory hormone
  • Pegvisomant: GH receptor antagonist
23
Q

Cushing’s Disease

A
  • Pituitary adenoma secreting excess ACTH
  • Insidious onset of symptoms of cortisol excess:

Presentation:

  • Obesity, central fat distribution, moon facies
  • HTN
  • glucose intolerance
  • gonadal dysfunction
  • proximal muscle weakness
  • easy bruising, striae
  • hirsutism, acne

Diagnosis: 24 HOUR URINE FREE CORTISOL

Treatment: transsphenoidal surgery +/- medical therapy

24
Q

Gonadotropin-secreting adenoma

A
  • Usually secrete FSH>LH

Clinical presentation: hypogonadism and hypopituitarism due to large size at time of diagnosis

No medical therapy available: primary treatment is surgical

**Note that if patient presents with elevated FSH and LH, diagnosis likely primary gonadal failure (or menopause)

25
Q

TSH-oma

A
  • Incredibly rare!
  • Presentation: Hyperthyroidism with goiter without exopthalmopathy (Graves’)
  • Lab: Elevated TSH and thyroid hormones

MRI: Pituitary adenomas usually large
Treatment: surgical; Somatostatin analogs can be helpful

26
Q

Multiple Endocrine Neoplasia Type 1

A

3 P’s:

  1. Pituitary adenomas (prolactinoma, growth hormone)
  2. Parathyroid adenomas (or hyperplasia)
  3. Pancreatic tumors (gastrinoma, insulinoma)

Presentation: commonly with kidney stones and stomach ulcers

Autosomal dominant inheritance of MEN1 gene from chromosome 11

27
Q

MEN 2A

A

2P’s

  1. Parathyroids
  2. Pheochromocytomas
  3. Medullary thyroid carcinomas: secrete calcitonin
28
Q

MEN 2B

A

1P:

  1. Pheochromocytoma
  2. Medullary thyroid carcinoma
  3. Oral/intestinal ganglioneuromatosis
29
Q

Pituitary Apoplexy

A
  • Caused by HEMORRHAGIC NECROSIS of a tumor or pituitary gland infarction
  • Can be presenting sign of a pituitary adenoma
  • An endocrine EMERGENCY

Clinical presentation:

  • Sudden-onset headache (mostly frontal)
  • Visual (acuity, field) loss
  • Ophthalmoplegia
  • Meningismus
  • Altered mental status
  • Vomiting
  • Fever
  • Nausea, vomiting
  • Hypotension
30
Q

Empty Sella Syndrome

A
  • Sella turcica partially filled with CSF, causing Sella to enlarge and pituitary to flatten
  • Partial empty sella: congenital incompetence of diaphragm sellae surrounding normal pituitary
  • occurs after pituitary surgery or radiation therapy
  • Usually middle-aged obese women
  • Associated with systemic HTN or benign intracranial hypertension
  • Pituitary function almost always normal
31
Q

Function of AVP

A
  • with low BP, induces AQP channel formation at collecting duct to allow reabsorption of water into the vasculature
  • without AVP, water is lost in the urine
32
Q

Central diabetes insipidus

A
  • Def: Deficiency of AVP

Spontaneous DI

  • Infiltrative diseases (sarcoidosis, histiocytosis)
  • Lymphocytic hypophysitis (or lymphocytic infundibuloneurohypophysitis)
  • Head trauma
  • Neurosurgery
  • *Sellar lesions and pituitary adenomas are NOT common causes of DI
    • If sellar lesion present with DI, suggests metastatic disease (vs. primary anterior pituitary adenoma)

Clinical presentation: always thirsty; frequent urination

Lab: Hypernatremia and serum hyperosmolality, with inappropriately dilute urine (low urine osmolality)

Dx: Water deprivation test: can they concentrate their urine?

33
Q

SIADH

A
  • Syndrome of Inappropriate ADH secretion
  • Elevated urine sodium excretion while on normal salt and water intake
  • Hypoosmolality of ECF and plasma

Clinical: will be euvolemic

  • no orthostasis, tachycardia, decreased skin turgor, dry mucous membranes to suggest hypovolemia
  • no edema, ascites to suggest hypervolemia

Common causes:

  • Tumors
  • CNS disorders
  • Drug-induced
  • Pulmonary diseases
  • Prolonged exercise (marathon running)

Management:

  • Treat the underlying disorder
  • Fluid restriction
  • IV hydration likely to worsen hyponatremia as patient will retain more free water
34
Q

Panhypopituitarism

A
  • Typically, GH production falls 1st, followed
    by FSH/LH, TSH, and ACTH last
  • Order not followed in all cases
  • ADH deficiency rare with pituitary disease,
    more common after surgery on pituitary
  • PRL will be least affected b/c under inhibitory control of dopamine
Causes:
 Pituitary non-functional tumor
 Compression of stalk
 Post-partum shock (Sheehan’s syndrome)
 Inflammation (autoimmune lymphocytic
hypophysitis)
35
Q

Craniopharyngiomas

A
  • Tumor that arises from epithelial remants of Rathke’s pouch in the sella turscia
  • presents as a supratentorial mass in children
  • may compress the optic chasm
  • calcifications are common
  • may have keratin-filled cysts

Endocrinology (11 decks)

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