Diabetes Insipidus Flashcards
DI
general
Condition in which the body is unable to control the balance of water → excretion of large volumes of dilute urine
Affects 1 in 25,000 people
Can affects people of any age, but is mostly seen in adults
DI
Types
Types:
Central diabetes insipidus (CDI)
Nephrogenic diabetes insipidus (NDI)
Gestational diabetes insipidus
Dipsogenic diabetes insipidus (primary polydipsia)
DI
Potential complications
Severe dehydration
Electrolyte imbalance
ADH
normal functioning
Normal osmolality range
Osmoreceptors of the hypothalamus sense changes in osmolality of the blood (Normal: 275 to 295 mOsm/kg)
Osmolality
Concentration of dissolved particles
Major particles include: glucose, sodium, and blood urea nitrogen (BUN)
Increased plasma osmolality (due to dehydration)
Stimulate the sense of thirst
Stimulate the release ADH from the posterior pituitary
ADH acts on the distal tubule to reabsorb water → decrease plasma osmolality (concentrate urine)
Central Diabetes Insipidus
general
Also referred to as neurogenic diabetes insipidus
Characterized by a decreased production by the hypothalamus or decreased release of antidiuretic hormone (ADH) from the posterior pituitary resulting in a variable degree of polyuria
Central Diabetes Insipidus
Causes
Causes:
Idiopathic 30-50%
Assumed to be caused by autoimmune damage to ADH-producing cells
Acquired
Cancerous or noncancerous tumors in the brain or pituitary gland
Head injury
Prior surgery (trans-sphenoidal) or radiation at or around the hypothalamus or pituitary gland
Infections: encephalitis or meningitis
Rare familial (autosomal dominant gene mutation) and congenital diseases
Nephrogenic diabetes insipidus
general
Characterized by a decrease in urinary concentrating ability as a result of resistance to the action of ADH
Nephrogenic diabetes insipidus
causes
Drug induced
Causes:
Hereditary (children)
X-linked inheritance for a mutation in the vasopressin V2 receptor gene
Mutation in the aquaporin-2 gene
Dysfunction of the aquaporin-2 water channel
Drug-induced
Often reversible
Chronic ingestion of lithium
Leads to dysfunction of the aquaporin-2 water channel
Acute or chronic kidney disease
Reduction in maximum renal concentrating ability due to fewer nephrons or damage to tubules
Examples: pyelonephritis, polycystic kidney disease, amyloidosis
Gestational diabetes insipidus
general
Transient ADH resistance in the second half of pregnancy due to release of vasopressinase by the placenta (breaks down vasopressin)
Dipsogenic Diabetes Insipidus
general
Also known as psychogenic polydipsia
Cause by drinking excessive amounts of water
Related to a psychologic problem (schizophrenia)
Causes a decreased blood osmolality and the hypothalamus decreases the release of ADH as a normal physiological response and the kidneys produce excessive amount of urine (polyuria)
DI
Clin man
Polyuria
Degree of polyuria correlates with the degree of ADH deficiency or resistance
Defined as > 3 L urine output/day in adults (age-specific in children); Severe: 10-15 L/day
Nocturia → daytime sleepiness
Polydipsia (due to ↑ serum sodium and ↑ plasma osmolality)
Hypotension
Dehydration
Headache, dry mucous membranes, light-headed, muscle cramps, confusion, weakness
DI
Neurologic symptoms relating to hypernatremia
Irritability
Seizures
Altered mental status → coma
DI
volume of urine in 24hr for Dx
24-hour urine volume
> 3 L/day in adults
>2 L/day in children
Rule out DI if < 2 L/day in 24 hours in the absence of hypernatremia
central DI
ADH lab finding for Dx
↓ serum ADH levels
Water deprivation test/ADH stimulation test
Water deprivation test/ADH stimulation test
Plasma and urine osmolality are measured before water restriction
No water intake for 2–3 hours
Hourly measurements ofplasma andurine osmolality after this interval
If there is no increase inurineosmolality, an ADH analog (desmopressin) is administered
Ifurine osmolalityincreases → CDI (= lack of central ADHsecretion)
Ifurine osmolality stays low → NDI (= defect inkidneys)
