B4W3 Flashcards
Describe the path from pituitary secretion to effector or AVP
released from the posterior pituitary, goes into circulation, V2 receptors on the basolateral surface of the collecting duct, to increase AQP2 insertion in apical membranes, for increasing water reabsorption
What are the stimuli for vasopressin release
serum osmolality (even slight changes in the osmolality)
NE
Dopamine
Hypoxia
Acidemia
What are the functions of vasopressin
water balance, (increases) BP maintenance, platelet function (induces aggregation), thermoregulation (in fever)
match hypo/hypertonic plasma with the type of plasma that they will have
hypo = dilute urine = limited ADH, limited thirst
hyper = conc urine = conc ADH, conc thirst
Match ECV volume with whether or not RAAS and ADH will be secreted
High ECV volume = low RAAS activation, low ADH activation
Low ECV volume = high RAAS and ADH activation
What is thirst responding to
hyperosmolarity
What are the general lab guidelines for diagnosing hyponatremia
<135 mEq/L Na level
Hyponatremia is also referred to as
Hyperaquaremia
What are the labs that you want to order when diagnosing hyponatremia, and what would you expect to see
Serum sodium, urine Osm, Urine (Na)
What are the types of hyponatremia (very general)
Pseudohyponatremia (manifesting as hypertriglyceridemia), isotonic, hypertonic, potomania (low P(Na), normal U(Osm)
Symptoms of hyponatremia
nausea, balance problems, gait instability, neurological symptoms, coma, seizures, death, brain herniation
In terms of hyponatremia, compare acute and chronic hyponatremia in terms of risk
acute = very dangerous with greater risk of complications and cerebral edema (massive H2O intake, underlying CNS pathology, PO)
chronic = greater risk from treatment than the actual pathophysiology
Determine the severity of hyponatremia based off their lab values
mild = 130-135
moderate = 120 - 130
severe = < 120
What is the physiological adaptation that the body completes in order to stop hyponatremia
cerebral adaptation (brain tries to regulate volume by reaching osmotic eq between ICF and ECF) (swelling activates carrier proteins and electrolyte pumps to decrease brain swelling
When is cerebral adaptation helpful
acute hyponatremia
What are the goals of correction of hyponatremia
prevent further Na decline
prevent brain herniation
relieve symptoms
AVOID OVERCORRECTION
What is the goal rate of mEQ/L for correction of hyponatremia
4-6 mEq/L over 1 24 hour period
What receptors are responsible for regulation of ECF volume
baroreceptors in kidney, carotid arch, and atria
Evaluate the U(osm), U(v), and P(Osm) of a SIADH patient
U(osM) = high conc
U(v) = low
P(osm) = low
What associated lab values will be low when evaluating a SIADH patient
urea, BUN
What are the causes of SIADH
-increased hypothalamic production ( pulmonary disease, medication, surgery, infection, cancer)
-malignancy (cancer)
-drugs (MDMA)
-exogenous AVP
what are the treatments of SIADH
-treat underlying disease
-free water deprivation
-hypertonic saline
- high solute diet (loop diuretics with salt/urea tablets)
- vasopressin antagonist (but risk hepatoxicity)
Do salt or urea tablets benefit a SIADH hypertensive patient
urea
Compare and contrast Central and nephrotic DI on their pathophysiology, symptoms, and urinalysis
patho: central (no ADH secretion), nephrotic (resistant ADH)
symptoms: both have polyuria, nocturia, polydipsia (central has some neurological implications
urinalysis: low U(Na), low U(OsM), low specific gravity
