Posterior Pituitary Disorder - Exam 3 Flashcards
Posterior pituitary hormones are synthesized in the _____ and travel to the posterior pituitary where they are released
hypothalamus
Hormones released from the posterior pituitary gland are controlled by ???
nerve impulses from hypothalamus that maintain homeostasis
_____ is peptide hormone that is released by posterior pituitary. What are the 2 main functions?
oxytocin
uterine muscle contraction
milk let-down reflex
______ produces milk and ____ releases milk
prolactin= produces milk
oxytocin= releases milk
In SIADH what are the 4 major players and are they increasing or decreasing?
increasing: ADH and urine osm
decreasing: serum Na and blood osm
In DI what are the 4 major players and are they increasing or decreasing?
increasing: serum Na and blood osm
decreasing: ADH and urine osm
What are 5 actions of ADH?
Adjust water permeability of the collecting duct in kidneys
Electrolyte handling
Vascular resistance
Inhibited by cortisol
Stimulates vactor VIII and vWF release from vascular endothelium
The major stimuli to ADH secretion are _____ and effective circulating _____
hyperosmolality
volume depletion
_____ governing secretion of ADH are located in the _____. Where are volume receptors (baroreceptors) found? name two additional causes of increase ADH?
Osmoreceptors
hypothalamus
kidneys, heart, brain
nausea and surgery
In general, the ______ is the primary osmotic determinant of ADH release. What about in uncontrolled diabetics?
plasma sodium concentration
Glucose can also act as an osmole and promote ADH secretion
______ has an inhibitory effect on vasopressin therefore adrenal insufficiency would cause a ____ in vasopressin
Cortisol
rise
ADH is synthesized in the ____ and released by the _____
hypothalamus
secreted by the posterior pituitary
In relation to ADH and water, when ADH is high, water is (excreted/reabsorbed). When ADH is low, water is (excreted/reabsorbed).
high ADH, water is reabsorbed (collecting duct is highly permeable to water)
low ADH, water is excreted (collecting duct is NOT permeable to water)
if you drink a glass of water, _____ drops. hypothalamus sees this drop and signals _____. _____ leads to a large volume of diluted urine
plasma osmolality drops
pituitary gland to slow down the release of ADH
low ADH
What is SIADH characterized by? What is the helpful way to remember it?
SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE
soaked inside
too much ADH, too much water
SIADH is defined by _____ and _____ resulting from inappropriate, continued secretion or action of the hormone despite normal or increased plasma volume
hyponatremia
hypo-osmolality
SIADH is the MC cause of _______ ______ in hospitalized patients
euvolemic hyponatremia
SIADH consists of ____, inappropriately ????, and decreased _____ in a euvolemic patient. Why?
hyponatremia
elevated urine osmolality (>100 mOsm/kg)
serum osmolality
due to RAAS
weight gain
anorexia
NO edema aka NO hypervolumic
N/V
low serum sodium (irritability, confusion, hallucinations, seizures)
What am I?
SIADH
What is SIADH caused by?
inappropriate hypersecretion of ADH from the hypothalamus/pituitary or by ectopic production
What are 4 broad categories of SIADH?
Nervous system disorders
Neoplasms (small cell lung tumor is most common - secretes ADH)
Pulmonary diseases - hypercapnia (too much CO2) can stimulate ADH release
Drug induced - can stimulate release of ADH or potentiate effects
**What is the MC cause of neoplasms that secrete ADH?
small cell lung tumor
** What is a common pulmonary cause of SIADH?
hypercapnia (too much CO2) can stimulate ADH release
What specific drug classes are known to induce SIADH? What state?
psych drugs
post op state secrete too much ADH
How does the severity of SIADH depend on? 2 things
severity of hyponatremia and rate of progression
aka the faster the drop in sodium the worse the s/s
**What are the early s/s of SIADH that can ve seen with the Na serum is less than 125. What are worse s/s? What are they due to?
anorexia, nausea, malaise
headache, muscle cramps, irritability, drowsiness, confusion, weakness, seizures, and coma
These occur as osmotic fluid shifts result in cerebral edema and increased intracranial pressure
HA, confusion, impaired memory are ____ clinical presentation
confusion, disorientation, somnolence, hallucinations, acute psychosis are _____.
Seizures, severe somnolence and coma are _____
mild/moderate
advanced
grave danger!!
PE finding: In SIADH, the patient is typically _____ and _____
euvolemic and normotensive
Edema in a hyponatremic patient makes you think of ???? NOT ____
CHF, cirrhosis or CKD
NOT SIADH
What factors need to be present in order to dx SIADH?
Hyponatremia with corresponding serum hypo-osmolality
Continued renal excretion of Na+
increased urine osm and increased urine sodium concentration
NO volume depletion s/s: aka must have normal skin turgor and blood pressure
NO other cause of hyponatremia
aka it is a dx of exclusion
**How you do you treat the hyponatremia in mild SIADH?
fluid restriction: stop giving fluids and everything should even out
What lab tests would you want to order if you suspect SIADH?
BMP, serum cortisol and TSH
What is the treatment of SIADH based on?
degree of hyponatremia
is the pt symptomatic?
is it acute (less than 48 hours) or chronic?
**Correcting hyponatremia too rapidly may result in ______ with permanent neurologic deficits. The magnitude of ______ rise, rather than the _____ correction rate, has more association with neurologic symptoms.
central pontine myelinolysis (CPM)
**daily plasma sodium
hourly
CPM is a neurological disease caused by ?????, and is characterized by ?????
severe damage of the myelin sheath of nerve cells in the brainstem, specifically the pons
acute paralysis, dysphagia, and dysarthria, and other neurological symptoms.
What is the tx of SIADH in am emergent setting? What is it important to monitor for?
raise serum Na+ levels by 0.5-1 mEq/h, and not more than 10-12 mEq in the first 24 hours (Goal serum sodim is 125-130)
**3% hypertonic saline:
Furosemide: increase excretion of free water
monitor: Neurological symptoms and serum Na+
What is the tx in an acute setting with moderate s/s?
3% hypertonic saline (513 mEq/L)
Loop diuretics (furosemide) with saline
Vasopressin-2 receptor antagonists
(aquaretics, such as conivaptan)
Water restriction
_______ MOA inhibition of the AVP V2 receptor reduces the number of aquaporin-2 water channels in the renal collecting duct and decreases the water permeability of the collecting duct
Vaptans: Conivaptan (Vaprisol) and Tolvaptan (Samsca)
Collectively, agents that competitively block ADH action and increase water excretion are called _____
aquaretics
_____ is a parenteral dual V1a- and V2-receptor antagonist, which is approved for use in hospitalized patients with euvolemic (dilutional) and hypervolemic hyponatremia
conivaptan (Vaprisol)
________ is a selective oral V2 receptor antagonist approved for use in hospitalized patients for hypervolemic and euvolemic hyponatremia
Tolvaptan (Samsca)
What types of pts should you NOT use vaptans with?
avoided in hypovolemic hyponatremia
What is the primary risk with using vaptans? What is a benefit?
excessively rapid rate of correction of serum Na which is why these should only be used by experienced providers
producing water excretion without electrolyte excretion and eliminating the need for fluid restriction
What is the tx for chronic SIADH?
fluid restriction and V2 receptor antagonists
refer to nephro!!!
What is DI characterized by? What are some s/s?
Dry Inside aka decrease in ADH and water is getting peed out
frequent urination
blurry vision
increased hunger
paresthesia in the feet
excessive thirst
extreme fatigue
weight loss
Diabetes insipidus is an uncommon disease characterized by an ____ in thirst and the passage of ????
increase
large quantities of urine of low specific gravity
What is DI caused by ?
deficiency or resistance to vasopressin/ADH
What is primary central DI?
without a lesion on the pituitary or hypothalamus
Many appear to be due to autoimmunity against hypothalamic arginine vasopressin (AVP)-secreting cells: think GENETIC causes
What is secondary central DI?
due to damage of the hypothalamus or pituitary
can be: tumor, hypophysitis, infarction, hemorrhage, anoxic encephalopathy, surgical or accidental trauma, infection (eg, encephalitis, tuberculosis, syphilis), or granulomas (sarcoidosis or multifocal Langerhans cell granulomatosis)
What is nephrogeneic DI causes by?
defect in the* kidney tubules that interferes with water reabsorption
aka: do NOT respond to ADH but there is plenty floating around
present at birth and is due to defective expression of renal vasopressin V2 receptors or vasopressin-sensitive water channels
What are acquired forms of vasopressin-resistant DI due to?
pyelonephritis, renal amyloidosis, myeloma, or Sjögren syndrome
What is gestational DI caused by? How do you tx it?
circulating enzyme destroys native vasopressin
give synthetic desmopressin
intense thirst
craving for ice water
polyuria
large urine volumes
What am I?
How do they maintain fluid balance? What happens if they cannot?
DI
continuing to ingest large volumes of water
hypernatremia and dehydration in patients without free access to water,
What is an aggravating factor of DI?
high-dose corticosteroids because it increases renal free water clearance
What are 3 main tests that we can use to check for DI?
24-hour urine collection for volume and creatinine
Water restriction test
Vasopressin challenge test (supervised)
What would you expect the results of the 24-hour urine collection for volume and creatinine to be in a pt with DI? What is the exception?
urine volume should be greater than 2 liters
urine sodium and urine osm should be low (aka the urine is SUPER DILUTE)
urine volume will be less than 2 Liters if the pt is hypernatremic
What is the expect result of water restriction test for a DI pt? For vasopressin challenge test? describe the test.
urine with stay dilute
when given ADH ->
Central DI: volume should go down and concentration should go up! aka urine osmolality should increase/go back to normal
Nephogenic: no change
Desmopressin acetate 0.05–0.1 mL (5–10 mcg) intranasally (or 1 mcg subcutaneously or intravenously) is given, with measurement of urine volume for 12 hours before and 12 hours after administration
During the vasopressin challenge test what will pts with central DI report?
notice a distinct reduction in thirst and polyuria
need to order _____ to look for a lesion in DI
MRI
What tests do you need to order to dx nephrogenic DI? What is the expected result?
Measurement of serum vasopressin is done during fluid restriction and desmopressin challenge;
vasopressin level is high in nephrogenic DI and we don’t see a change in urine osmolality
What is a way to distinguish central DI from other non DI potential causes?
restrict fluids
there will be no change in DI pts and in the other causes it will cause lab values to normalize
What is the tx for mild DI? Central and gestational DI?
mild: adequate fluid intake
central and gestational: Desmopressin acetate
**What are the SE of Desmopressin acetate?
hyponatremia, agitation, emotional changes, depression, increased risk of suicide
**What is the difference between micro and macro adenoma? What s/s are common with each?
Microadenomas (< 1 cm in diameter): complaints related to hormone excess
Macroadenomas (> 1 cm in diameter): impinge on the optic chiasm or other structures, and may or may not affect hormones
Somatotrope is an adenoma affecting what hormone?
Growth hormone
_____ is the classic visual field defect in a patient with an expanding pituitary mass
Bitemporal hemianopia: aka they lose vision on both temporal sides
What is the best way to eval a pituitary adenoma?
MRI of the brain
Ophthalmologic exam
Laboratory studies based on the clinical presentation aka what hormone is being affected
What is the tx for a pituitary adenoma?
Transsphenoidal Surgery
radiation: usually reserved for post-surgical management due to its slow onset of action
medication based on what hormone is affected
What are 4 possible complications of transsphenoidal surgical resection?
hypopituitarism
Permanent diabetes insipidus
cranial nerve damage
nasal septal perforation
visual disturbances
CSF leak
carotid artery injury
hypothalamic damage
meningitis
Name the treatment of choice for the following conditions:
prolactinomas
acromegaly
TSH secreting tumors
ACTH-secreting tumors
prolactinomas -> dopamine agonists
acromegaly -> somatostatin analogues and GH receptor antagonists
TSH-secreting tumors -> somatostatin analogues
ACTH-secreting tumors -> surgery and/or radiation
