Antidiuretic Hormone Flashcards
Where is ADH released from
posterior pituitary
ADH is released in response to
either low BP or increased salt concentrations
Two conditions that alter ADH levels
SIADH
diabetes insipidous
Other causes of elevated ADH
infection/tumors in CNS or lungs
fluid imbalances after surgery
acute porphyria
Other causes of depressed ADH
damage to pituitary gland
primary polydipsia
SIADH high or low levels of ADH?
higher than normal
Consequences of ADH
increase water reabsorption
which will increase blood pressure
by increasing blood volume
Diabetes insipidus high or low levels of ADH?
lower than normal
ADH is also known as
vasopressin
Conditions associated with SIADH
infections (meningitis)
head injury (subarachnoid hemorrhage)
cancers (small cell lung CA)
drugs (SSRI’s)
What is ADH released in response to
low bloodpressure
increased salt concentrations
Main function of ADH
controls reabsorption of water by kidneys
Consequences of SIADH
water retention
increase BP
increase ECF volumes
Fluid overload in SIADH causes
hyponatremia
S/Sx of SIADH
effects of hyponatremia headaches nausea/vomiting confusion severe: convulsions or coma
Name treatments for SIADH
water restriction
demeclocycline (tetracycline drug blocks effect of ADH)
management of underlying cause
diuretics for fluid retention
Dilution syndrome or fluid overload are results of
SIADH
Condition in which the kidneys are unable to conserve water
Diabetes insipidus
S/Sx of diabetes insipidus
excessive thirst large amounts of very dilute urine loss of potassium severe dehydration heart failure
Two forms of DI
central/neurogenic
nephrogenic
Form of DI caused by lack of ADH due to damage to hypothalamus or pituitary gland
Central/neurogenic
Inherited Central DI involves mutations of what?
AVP gene which encodes vasopressin or ADH
autosomal dominant pattern
Treatments for central DI
Drinking more water
DDAVP (form of vasopressin)
Form of DI involving defect in the parts of kidneys/nephrons that reabsorb water into blood stream causing limited availability for ADH to work at target site
Nephrogenic DI
X-linked defect that causes vasopressin receptor in kidney not to reply
inherited nephrogenic DI
Inherited nephrogenic DI is there enough ADH being produced?
Yes
it is the receptor that is not able to signal appropriately
Drugs that can cause nephrogenic DI
lithium, amphotericin B, demeclocyline
Other causes of nephrogenic DI
drugs
high calcium
polycystic kidney disease
Gene that forms water channels
AQP2 aquaporin-2
mutation of gene prevents water reabsorption
seen in nephrogenic DI
Decreased water reabsorption leads to
polyuria
polydipsia
Lithium toxicity involves
decreasing second messengers that signal AQP2 water channels upon ADH stimulation
reduces number of water channels
thus reducing ablility to reabsorb water
causing polyuria
treatment of nephrogenic DI
drinking enough fluids to match urine output with drugs that lower urine output
low-salt and low-protein diet
Causes of Central/neurogenic DI
head injury or cranial surgery, pituitary surgery
True or false: Vasopressin in given to pts with nephrogenic DI
False
It is given to pts with central or neurogenic because there is a lack of ADH
If given in nephrogenic, no effect because something is wrong with the nephrons
Posterior pituitary not producing enough ADH is it neurogenic or nephrogenic?
Neurogenic or central
Both types of DI respond partially to what type of diuretics
thiazide
agonist for vasopressin which allows for rectification ADH deficit
DDAVP
With DI persons are unable to
concentrate urine
osmolar concentration in 1L of solution
Osmolarity
osmolar concentration in 1kg of water
Osmilality
measurement of urine concentration
urine osmolality
Normal urine osmolality values
50 to 1200 milliosmoles per kilogram (mOsm/kg)
12 to 14 hour fluid restriction: Greater than 850 mOsm/kg
What happens to UO and urine osmolality with polydipsia
urine output increases
urine osmolality is dilute d/yt the increase in water intake, and is generally less than 100 mOsm/kg
