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52 Cards in this Set

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What are the parts of the pituitary gland?
- where do they originate from and what changes occur in their development?
Anterior Pit = Adenohypophysis
- from an ectodermal evagination of pharyngeal epithelium (Rothke's Pouch)
- loses its connections to oral cavity

Posterior Pit = Neurohypophysis
- from ventral evagination of floor of diencephalon
- maintains connections to hypothalamus through pituitary stalk
Pituitary Gland
- where is it located?
- size?
- what important structures is it near?
- situated in base of skull, protected by Sella Turcica ("turkish saddle")

- 6x12 mm

- Lateral to sella = cavernous sinus: houses internal carotids, CN III, IV, V1, V2, VI
- Ant and inf to Sella = sphenoid sinus
- Sup = optic chiasm
What is the pituitary's vascular supply?
- function?
= Hypophyseal Portal System
... delivers hypthalamic releasing hormones to anterior pituitary
What peptide hormones are secreted by the ant pituitary? What controls each of their releases?
ACTH (regulated by CRH from hypothalamus)

GH (regulated by GHRH (mostly) and somatostatin (-) from hypothalamus)

TSH (regulated by TRH from hypothalamus)

LH/FSH (regulated by GnRH from hypothalamus)

Prolactin (TONIC INHIBITION via DOPAMINE from hypothalamus)
ACTH
- secreted by?
- target organ?
- effect?
- excess/deficiency?
- secreted by ant pit
- target: adrenal glands
- effect: stimulates cortisol synth/secretion (cortisol has negative feedback on ACTH secretion)
- excess: Cushing Syndrome
- deficiency: adrenal insufficiency
TSH
- secreted by?
- target organ?
- effect?
- excess/deficiency?
- secreted by ant pit
- target: thyroid
- effect: stimulate TH (T3 and T4) synth/secretion (TH has negative feedback on TSH secretion)
- excess: hyperthryroidism
- deficiency: hypothyroidism
GH
- secreted by?
- target organ?
- effect?
- excess/deficiency?
- secreted by ant pit
- target: multiple tissues (bone, cartilage, muscles, etc.)
- effect: growth! in many tissues (esp liver), stims synth of IGF-1 (somatomedin C), which causes growth (IGF-1 has negative feedback on GH secretion)
- excess: Acrogmegaly (or Gigantism if before epiphyseal plates are closed)
- deficiency: growth retardation or adult clinical sx
Gonadotropins
- secreted by?
- target organ?
- effect?
- excess?
- deficiency?
= LH and FSh
- secreted by ant pit
- target: ovary/testes
- effect: cause estradiol secretion and gametogenesis [females]; testosterone secretion and spermatogenesis [males]
- excess: precocious puberty
- deficiency: hypogonadism
Prolactin
- secreted by?
- target organ?
- effect?
- excess?
- deficiency?
- secreted by ant pit
- target: mammary glands
- effect: initiation and maintenance of lactation
- excess: galactorrhea and amenorrhea
- deficiency: inability to lactate after delivery
Posterior Pituitary
- what hormones does it secrete?
- where are they synthesized?
- secretes Oxytocin and Vasopressin (ADH)
- both synthesized in hypothalamus (supraoptic nuclei and paraventricular nuclei)... travel to neurohypophysis by pituitart stalk
Vasopressin/ADH
- regulation?
- target organ?
- effect?
- excess?
- deficiency?
- regulated by plasma osmolality and "effective" circulating blood volume
- target: collecting tubule of kidney
- effect: increase in water permeability
- excess: SIADH = syndrome of inappropriate secretion of ADH)
- deficiency: central diabetes insipidus
Oxytocin
- regulation?
- target organ?
- effect?
- regulated by neurotransmitters (cholinergic, alpha-adrenergic)
- target: breast and uterus
- effect: milk letdown reflex; contractions of uterus during labor
Pituitary Tumors
- frequency?
- malignant?
- incidental frequency?
= 10% of intracranial neoplasms
- BENIGN (almost always)
- incidental finding in 10-20% people
How are pituitary tumors classified?
classification based on size:
- microadenoma (<1 cm)
- macroadenoma (>1 cm)
What is the difference between Cushing Syndrome and Cushing Disease???
Syndrome - all etiologies
Disease - ACTH-secreting tumor IN THE PITUITARY! most common endogenous etiology
Cushing's Syndrome
- what is?
- cause? (what is most common?)
= constellation of clinical signs/sx caused by chronic glucocorticoid excess

CAUSES:
** most common = chronic high-dose glucocorticoid (steroid) inkate
- pituitary tumor (Cushing's Disease) = most common endogenous etiology
What are the different endogenous causes of Cushing's Syndrom?
ACTH-dependent: increased ACTH
- pituitary tumor (Cushing's Disease)
-other

ACTH-independent: increased cortisol
- adrenal adenoma/carcinoma
- other

Pseudo-Cushing's Syndrome
- alcoholism
- major depressive disorder
What are some of the main signs/sx of Cushing's Syndrome?
- central obesity (with thin arms/legs)
- moon facies
- increased supraclavicular fat pads (buffalo hump)
- hirsutism on face
- acne
- hyperpigmentation
Diagnosis of Cushing's Syndrome
- which is best??
1. Urinary Free Cortisol Measure
- BEST TEST!
- (+) is value of cortisol is >3x upper limit of normal
- requires 24-hr urine sample

2. Overnight Low-Dose Dexamethasone Suppression Test
- take 1 pill at 11 p.m. --> should have negative feedback on ACTH secretion and shut down adrenals, thus reducing cortisol to <3ng/dL by 8 a.m.
- If (+) is value >3 ng/dL at 8 a.m.
**many false-positives (due to obesity, alcoholism, depression) --> must confirm (+) with urine free cortisol test

3. Loss of Diurnal Variation of Cortisol Secretion
- Normally, highest cortisol levels are in the morning and cortisol is lowest at 11 p.m.
- (+) if cortisol is ALWAYS high
What is Dexamethasone?
- use?
= synthetic cortisol
- used to test for Cushing's Syndrome bc has a much longer t1/2 than natural cortisol
How do you differentiate between ACTH-dependent and ACTH-independent Cushing's Syndrome?
Check plasma ACTH!

< 5 pg/ml = ACTH-independent (Adrenal Cushing's Disease - bc no problem with ACTH from pituitart, just extra cortisol secreted from adrenals)
... do CT of adrenals

> 10 pg/ml = ACTH-dependent (Pituitary or Ectopic Cushing's)

5-10 pg/ml = Not difinitive

**Ectopic Cushing's has much higher ACTH than Cushing's Disease (pit tumor)
What is Ectopic Cushing's Disease?
ACTH secreted by neuroendocrine tumors...
- Bronchial Carcinoids = most common
- other: SCC of lungs, islet cells tumor of pancreas, pheochromocytoma, medullary carcinoma of thyroid
How do you differentiate between Pituitary v. Ectopic Cushing?
1. High Dose Dexamethasone Suppression Test
- most ppl with pituitary tumors will suppress ACTH secretion after high dose dexa... ectopic patients will not

2. Petrosal Sinus Sampling
- catheter inserted into petrosal sinus which drains pituitary venous system (measures ACTH coming directly from pit) - if pituitary tumor, will have high ACTH; if ectopic, ACTH will be low/normal
- INVASIVE (last resort)
What is the next step after a patient tests positive for Cushing's?
MRI of pituitary!!

Note: do NOT do MRI before dx Cushing's (bc 10-20% ppl will have a pituitary incidentaloma pit tumor, but it might not be causing the Cushing's)
What is treatment for Cushing's?
surgical resection
-- if ectopic, resect tumor
-- if adrenal, do unilateral adrenalectomy

...sometimes followed by radiation
Acromegaly
- what is?
- cause?
= excessive production of GH
- 99% due to pituitary tumor
What is Gigantism?
due to GH-secreting tumoes arising in childhood -- bc epiphyses are not yet closed
What are some clinical sx of acromegaly?
- enlarged facies
- acral enlargement
- heel pad thickness >22 mm
- prognathism/malocclusion (enlargement/forward protrusion of jaw)
- arthralgias
- carpal tunnel syndrome (englarged bones press agains median n)
- HTN, diabetes (GH increases blood vol and insulin resistance)
- sweating!!!!
- oily/greasy skin
- skin tags
- sleep apnea (due to enlargement of oral cavity)
What are some of the major long-term consequences of acromegaly?
What is the #1 cause of death?
CV Disease:
**# cause of death = cardiomyopathy
Neuropathy
Arthropathy
- bones do not shrink after surgery
- soft tissue changes return to normal
Hypertension
***High risk of Colon Cancer
What is the mnemonic for the long-term effects of acromegaly?
CHANC

c= cardiomyopathy
h= hypertnsion
a= arthropathy
n=neuropathy
c= colon cancer
Diagnosis of Acromegaly?
- what is the best test?
- what is the gold standard?
- why are they not the same??
1. High levels of IGF-1 (somatomedin C)
- *BEST TEST!!
- 10-15% false negatives

2. Failure of GH fall after OGTT (Oral Glucose Tolerance Test)
- **Gold standard - but difficult to do, so done second
- give oral glu (1 g/kg), then measure GH every 30 min for 2 hours
- normally, glu has negative feedback on GH release... if have tumor, GH doesn't fall
- GH > 1 ng/ml = ACROMEGALY

3. If test positive, do MRI of pituitary
Treatment of Acromegaly?
1. Transspehnoidal Surgery = 50% curative
2. Adjunctive tx if necessary
- somatostatin analogues (e.g., SANDOSTATIN) --> inhibits GH secretion and shrinks what's left of tumor
- Radiation
- (occasional) dopamine agonists, GH receptor antagonists

***Screen for colon cancer/polyps
Prolactinomas
- micro or macroadenomas
- sx
**most common secretory pit tumor!!
= micro OR macroadenomas

SX
women: amenorrhea, infertility, galactorrhea
men: decreased libido, impotence, (sometimes) galactorrhea
both: (if macro) mass effects - headache, vision changes, etc (due to compression)
What are the most common secretory pituitary tumors??
PROLACTINOMAS
Diagnose Prolactinoma?
- High Prolactin
- Abnormal pituitary MRI
- Must exclude other etiologies of high prolactin... (esp bc 10-20% ppl have pit incidentalomas)
What are other etiologies of high prolactin besides prolactinoma?
- primary hypthyroidism
- renal failure
- cirrhosis (can't metab estradiol --> stims prolactin secretion)
- pregnancy
- stress (bc prolactin is a stress hormone)
- drugs - dopamin antagonists
- non-functioning pit adenomas or infiltration of h-p axis (e.g., sarcoidosis)- compression of pit stalk prevents dopamine from traveling down to pit
Treatment for Prolactinoma?
***Almost always medical!
- Dopamin agonists - e.g., Bromocriptine or Cabergoline
--> shrink tumor

- surgery and radiation ONLY for pts who don't respond to drugs
Thyrotrope Adenoma
- frequency?
- clinical presentation?
- tx?
- RARE (<1% all pit tumors)

- 2 clinical presentations:
(1) Hyperthyroidism - goiter, other classic sx -- High T3/T4 BUT inappropriately normal/elevated TSH
(in normal hyperthyroidism, T3/T4 feedback inhibit TSH, so TSH is LOW)
(2) mass effects - headache, abnormal visual fields

-Tx: Surgery
Gonadotrope Adenoma
- what does it secrete?
- nick name? why?
- clinical presentation?
- tx?
- secretes FSH, LH, or alpha subunit

- aka: "nonfunctioning adenoma" - no obvious clinical sx related to these hormones

- 2 clinical presentations due to macroadenoma
(1) mass effects - headache, abnormal visual fields
(2) hypopituitarism - deficiency of other pit hormones

- Tx: Surgery
Diabetes Indipidus (DI)
- types?
- sx?
- onset?
- due to insufficient secretion of ADH (CENTRAL/NEUROGENIC)
or
- due to resistance of the kidney to ADH action (NEPHROGENIC)

- sx: polyuria and polydyspia
- pts with central DI have predilection for cold or iced drinks

- Central DI - abrupt onset
- Neph DI - slow onset
Causes of Central DI
- most common?
1. congenital (autosomal dominant)
2. acquired
- iatrogenic (following surg) = most common!
- trauma
- neoplasms
- ischemia (Sheehan's Synd)
- granulomas (Sarcoidosis)
- infections (TB)
- autoimmune
- idiopathic
..... really, any destruction of hypothalamic area
Causes of Nephrogenic DI
1. Congenital (x-linked)
2. Acquired
- renal disease - e.g, sickle cell, polycystic kidney disease, amyloidosis, obstructive uropathy
- **Electrolyte disorders: HYPOKALEMIA, HYPERCALCEMIA
- **Drugs: LITHIUM, demeclocycline

...anything that affects kidneys
Diagnosis of DI?
- how do you determine which type?
- polyuria (high)
- urine specific gravity (low)
- urine osmolality (low)
... = DILUTE URINE

**Differentiate Central DI from Nephrogenic DI...
- give ddAVP (synthetic ADH) --> if respond, must be central DI; if don't respond (nephrogenic DI bc kidneys don't use the ADH you just gave them)
What is ddAVP?
= synthetic ADH
- given to differentiate btwn central and nephrogenic DI
Treatment of DI?
- central?
- nephrogenic?
Central: give ddAVP

Nephrogenic: NSAIDs and Thiazides
Hypopituitarism
- most common cause?
- 2 common types?
= deficiency of one or multiple pituitary hormones
(partial or panhypopituitarism=all)
- GH, FSH, LH first to be lost...
- TSH, then ACTH, then ADH last

- Macroadenoma = most common cause!

- 2 types:
-- Sheehan's Syndrome
- Pituitary Apoplexy
Sheehan's Syndrome
- what is?
- cause?
- clue to dx?
= ischemic pituitary necrosis following childbirth
- assoc'd with postpartum hemorrhage and hypotension
- **clue to dx: failure to lactate
Pituitary Apoplexy
- what is/cause?
- presentation?
= hemorrhagic infarction of pituitary adenoma
- presents ACUTELY with headaches, change in mental status, opthalmoplegia, visual loss
- variable degrees
Diagnosis of Pituitary Apoplexy?
- MRI of hypothalamus/pituitary - will show bleeding
- endocrine testing - assess for deficiencies
Treatment of Pituitary Apoplexy?
Depends on etiology...
- possibly neurosurgery
- hormone replacement (if deficiency)
Pituitary Incidentalomas
- what are?
- frequency?
- most common one?
- other causes?
- Found incidentally by imaging the brain or on autopsy
- 10-20% people not suspected to have pituitary disease
- most common = microadenoma
- could also be: craniopharyngioma germ cell tumor, glioma, metastases from breast, lung, etc.......
Pituitary Incidenalomas
- workup/follow-up?
- Must exclude hormonal hypersecretion: PRL, IGF-1, TSH, Free T4, overnight dexamethasone suppression test, etc
- Use LH/FSH levels as a marker to see if tumor shrinks after pregnancy

If macroadenoma, must rule out hypopituitarism
- test visual fields

**Follow up with periodic MRI: 6 months, 1, 2, 5 years