Pituitary Gland Flashcards
What makes up the anterior pituitary?
Adenohypophysis -stains red-blue -Reticulin Network 3 cell types 1. acidophils (red) 2. basophils (blue) 3. chromophobes (pale)
What makes up the posterior pituitary?
Neurohypophysis
- resembles neural tissue,
1. glial cells
2. nerve fibers
3. nerve endings
4. intra-axonal neurosecretory granules
-ADH and oxytocin synthesized in hypothalamus and transported to post pituitary where processing is completed
Anterior pituitary adenoma
General Symptom
Histology
Sporadic vs Familial
Pathogenesis
most common cause of hyperpituitarism
micro 1cm
Symptom
Mass Effect:
-bitemporal hemianopsia
-headache
Histologically:
- monomorphism
- absence of reticulin network
- Majority Sporadic
- 5% familial-MEN1 (parathyroid, pancreas, pituitary)
Pathogenesis:
GNAS1 Gene mutation
-constitutive activation of stimulatory G protein
-unchecked cellular proliferation
Prolactinoma
Prolactin Secreting Adenomas
Symptoms
Causes
Treatment
Most common functioning adenoma
Female:
- Galactorrhea
- Amenorrhea, infertility-elevated prolactin inhibits LH surge
Male:
-Impotence, infertility
Causes:
- hypothalamic/stalk pathology
- hypothalamic dopamine inhibits prolactin - drugs
- pregnancy, breast feeding
Treatment:
- Dopamine agonist
- bromocriptine, cabergoline - surgery for macroadenomas
Somatotroph Cell Adenoma
(Growth hormone secreting adenoma)
Symptoms
Diagnosis
Treatment
- 2nd most common type of functioning adenoma
- persistent GH stimulation–stimulation of hepatic insulin-like growth factor in liver
Symptoms
- prepubertal-gigantism
- post pubertal- acromegaly
Diagnosis
- elevated insulin like growth factor
- elevated growth hormone
- lack of growth hormone suppression by oral glucose
Treatment:
Surgery
Somatostatin(growth hormone-inhibitory hormone) analogs
-octreotide, lantreotide
Adrenocorticotroph hormone producing adenoma
(corticotroph adenoma)
Cushing disease
Nelson syndrome
Secrete ACTH
Clinically silent vs hypercortisolism
Cushing DISEASE
- hypercortisolism via pituitary adenoma
- hyperpigmentation-prohormone melanocyte stimulating hormone
- buffalo hump
- osteopenia
- hypertension
- glucose intolerance
- hyperlipidemia
- increased susceptibility to infections
- depression
Nelson Syndrome:
- adrenal glands removed for treatment of hypercortisolism due to cushing’s
- unknown presence of corticotroph microadenoma
- no inhibitory effect of adrenal corticosteroids on pituitary adenoma
- adenoma continues to grow into a clinically aggressive mass
- -mass effect-visual field defects, headache, cavernous sinus invasion
- -hyperpigmentation-marked elevated levels ACTH produced by adenoma
- -no cortisol secreted
What are consequences nonfunctioning pituitary adenomas?
- Null cell
- true hormone negative - clinically silent though producing hormone
- mass effect
Is pituitary carcinoma and LH, FSH, TSH secreting adenomas extremely rare?
yes
What can cause hypopituitarism?
- nonfunctional pituitary adenoma
- mass effect
- pituitary apoplexy-acute hemorrhage into adenoma - ischemic injury
A. sheehan syndrome-postpartum necrosis of anterior pituitary-obstetrical hemorrhage, shock(hypotension—vasospasm—ischemic necrosis)
-initial clinical clue: lactation failure-life threatening secondary adrenal insufficiency!
B. Ischemic necrosis
-Destruction of greater than 75 percent of pituitary (DIC, sickle cell disease, traumatic injury, shock) - radiation, surgery, trauma
- inflammatory conditions
- empty sella syndrome
-enlarged sella turcica not filled with pituitary tissue
Primary: defect in diaphragm of sella leads to csf leak-increased csf pressure-pituitary atrophy
Secondary: identifiable disease/therapy which results in empty sella - Infiltrative lesion
- TB, sarcoid, hemochromatosis, metastases - Hypothalamic disease
- Hypopituitarism of posterior pituitary dysfunction (ie diabetes insipidus)????????
Posterior Pituitary Syndromes
Describe ADH deficiency
ADH deficiency
Diabetes insipidus
1. Central-ADH deficinecy-pituitary, hypothalamic pathology-response to ADH analog (desmopressin)
2. Nephrogenic-renal tubules unresponsive to ADH-no response to ADH analogue (desmopressin)
- excessive loss of free water-polyuria–dilute urine
- compensatory increased thirst-polydypsia
- patient unable to compensate with free water-hypernatremia-dehydration-inappropriately low urine specific gravity
Posterior Pituitary Syndromes
Describe ADH excess
What could cause it
ADH excess
- SIADH
- euvolemic hyponatremia-total body water increased, blood volume remains nearly normal-no peripheral edema
From:
- ectopic secretion-small cell carcinoma lung (paraneoplastic syndrome)
- non-neoplastic lung pathology
- CNS injury
- Drugs-SSRI, carbamazepine, chlorpropamide, cyclophosphamide
- idiopathic
How does Rathke pouch from the pituitary? What can vestigial remnants of Rathke’s pouch lead to?
Histology
Distribution
- future anterior pituitary grows from roof of pharynx/ or ectoderm;
a neurohypophyseal bud forms from diencephalon - rathke pouch detaches from roof of pharynx and merges with neurohypophyseal bud
Remnants lead to Craniopharyngioma
- Benign tumor
- Primary suprasellar location
- 10-20 percent intrasellar
Histology: Solid, cystic components Calcifications common Palisading of squamous epithelial cells -Keratin
Distribution
-bimodal: children/ young adults and older than 60
-tend to recur after resection
What are rathke cleft cysts
Sellar/suprasellar tumors
- Developmental failure of rathke’s pouch obliteration
- lined by cuboidal epithelium with cilia and or goblet cells
- growth may compromise pituitary gland
Germ cell tumors/ dermoid cyst
sellar/suprasellar tumors
- Primary CNS tumors arise along midline (pineal and suprasellar)
- rests of germ cells vs migrate late in development
