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Vocabulary practice flashcards covering pathophysiology, laboratory findings, clinical manifestations, complications, and treatment for Diabetes Insipidus (DI) and SIADH.
Diabetes Insipidus (DI)
A disorder characterized by an impaired ADH effect that causes excessive dilute urine.
Central DI
A form of diabetes insipidus resulting from insufficient ADH production or release.
Nephrogenic DI
A form of diabetes insipidus where the kidneys do not respond adequately to ADH.
Clinical Findings of DI
Polyuria, polydipsia, dilute urine, and possible hypernatremia.
Urine Specific Gravity in DI
A diagnostic indicator that is very low, often below 1.005.
Central DI Treatment
Therapeutic management consisting of desmopressin and fluid replacement.
SIADH
Syndrome where excess ADH causes water retention and dilutional hyponatremia.
SIADH Neurologic Risks
Serious complications including confusion, seizures, and cerebral edema.
Serum Sodium in SIADH
Hyponatremia, often presenting below 135mEq/L.
SIADH vs. DI Urine Differentiation
SIADH urine is concentrated, whereas DI urine is dilute.
First-Line SIADH Management
Fluid restriction and treatment of the underlying cause.
Severe Symptomatic SIADH Hyponatremia Treatment
Carefully monitored administration of hypertonic saline.
Osmotic Demyelination
A severe neurological complication risked by the rapid correction of sodium.
Central DI Basic Defect
Insufficient secretion of antidiuretic hormone.
Nephrogenic DI Basic Defect
Failure of the kidneys to respond to antidiuretic hormone.
DI Urine Pattern
Excretion of large volumes of very dilute urine.
Untreated DI Sodium Pattern
Hypernatremia resulting from free-water loss.
Desmopressin
A prescribed agent commonly used for the treatment of central DI.
DI Treatment Monitoring Parameters
Essential monitoring assessments including urine output, serum sodium, weight, and fluid balance.
SIADH Basic Pathophysiology
Excess water retention due to inappropriate ADH activity.
SIADH Sodium Pattern
Dilutional hyponatremia.
SIADH Urine Characteristic
Inappropriately concentrated urine despite low serum osmolality.
Priority in Severe Symptomatic Hyponatremia
Urgent neurologic assessment and prescribed controlled correction.
Caution in Sodium Correction
Controlled sodium replacement required because overly rapid correction risks osmotic demyelination.
Common SIADH Intervention
Fluid restriction implemented when clinically appropriate.
Indicators of Worsening SIADH
Clinical deterioration marked by seizures, severe confusion, or declining consciousness.