DIABETES INSIPIDUS Flashcards by Simone Glavas

what is diabetes insipidus?

condition where the body is unable to control the balance of water -> excretion of large volumes of dilute urine

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what is the age epidemiology for diabetes insipidus?

can be seen in any age but mostly seen in adults

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what are the types of diabetes insipidus?

central diabetes insipidus
nephrogenic diabetes insipidus
gestational diabetes insipidus
dispogenic diabetes insipidus (primary polydipsia)

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what are the 2 potential complications of diabetes insipidus?

severe dehydration
electrolyte imbalance

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in normal functioning of ADH, what do osmoreceptors in the hypothalmaus do?

they sense changes in osmolality of the blood (normal: 275-295)

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what is osmolality?

concentration of dissolved particles
major particles include: glucose, sodium, and BUN

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what happens when there is increased plasma osmolality (due to dehydration)?

this stimulates the sense of thirst
stimulates release of ADH from posterior pituitary

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what does ADH act on?

and what happens to plasma osmolality?

the distal tubule to reabsorb water leading to decreased plasma osmolality (concentrate urine)

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what is central diabetes insipidus also known as?

neurogenic diabetes insipidus

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what is central diabetes insipidus characterized by?

a decreased production by the hypothalamus or decreased release of ADH from the posterior pituitary resulting in a variable degree of polyuria

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what is the most common cause of central diabetes insipidus?

idiopathic (30-50%)
- assumes to be caused by autoimmune damage to ADH-producing cells

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what are the types of acquired central diabetes insipidus?

cancerous or noncancerous tumors in the brain or pituitary gland
head injury (pance)
prior surgery (trans-sphenoidal) or radiation at or around the hypothalamus or pituitary gland
infections: encephalitis or meningitis
rare familial (auto dom gene mutation) and congenital diseases

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what is nephrogenic diabetes insipidus characterized by?

decrease in urinary concentrating ability as a result of resistance to action of ADH

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what are the hereditary causes of nephrogenic diabetes insipidus?

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

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what are the drug-induced causes of nephrogenic diabetes insipidus?

CHRONIC INGESTION OF LITHIUM
-leads to dysfxn of the aquaporin-2 water channel

often reversible

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what are the acute or chronic kidney disease causes of nephrogenic diabetes insipidus?

also, why is there a reduction in renal concetrating ability?

reduction in maximum renal concentrating ability d/t fewer nephrons or damage to tubules
- examples: pyelonephritis, polycystic kidney disease,
  amyloidosis

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what are the 2 other types of diabetes other than nephrogenic DI and central?

gestational DI
dipsogenic DI

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what is gestational diabetes insipidus?

transient ADH resistance in the second half of pregnancy d/t the release of Vasopressinase by the placenta (breaks down vasopressin)

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what is dipsogenic diabetes insipidus also known as?

psychogenic polydipsia

what is the cause of dipsogenic diabetes insipidus?

drinking excessive amounts of water

what is dipsogenic diabetes insipidus related to?

psychologic problems (schizophrenia)

what is the pathophsy of dipsogenic diabetes insipidus?

dipsogenic diabetes insipidus 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)

what is the clinical presentation of diabetes insipidus?

polyuria
polydipsia
nocturia-> daytime sleepiness
hypotension
dehydration
neuro sx relating to hypernatremia

what is polyuria characterized by?

> 3L urine output/day in adults (age-specific in children); severe: 10-15 L/day
degree of polyuria correlates with the degree of ADH deficiency or resistance

what sx can you see in someone who is dehydrated?

HA, dry mucus membranes, light-headed, muscle cramps, confusion, weakness

what neuro sx related to hypernatermia can be seen clinically in patients with DI?

1. irritability 2. seizures 3. AMS-> coma

what are the dx tests that can be done for DI?

1. 24-hr urine volume 2. serum sodium level 3. serum ADH level 4. plasma osmolality 5. urine osmolality

in the 24-hr urine volume test, what levels are considered polyuria?

>3L/day in adults >2L/day in children R/O DI if <2L/day in 24 hrs in absence of hypernatermia

what level will be decreased in central DI?

decreased ADH levels

what does hypernatremia indicate?

either CDI or NDI

what does hyponatremia indicate?

dipsogenic diabetes insipidus (primary polydipsia)

what plasma osmolality implies CDI or NDI?

>300

what plasma osmolality implies primary polydipsia?

< or equal to 280

what urine osmolality suggests complete CDI or NDI?

<300

what is the diagnostic water deprivation test/ADH stimulation test?

-plasma and urine osmolality are measured before water restriction - no water intake for 2-3 hours - hourly measurements of plasma and urine osmolality after this interval

what if there is no increase in urine osmolality during the water deprivation test/ADH stimulation test? | what do you give

an ADH analog (desmopressin) is administered

what if urine osmolality increases during the water deprivation test/ADH stimulation test?

CDI (lack of central ADH secretion)

what if urine osmolality stays low during the water deprivation test/ADH stimulation test?

NDI (defect in kidneys)

what is the important first step before treating DI?

stop any possible meds that could cause or aggravate DI

what is the first line for central DI?

desmopressin (DDAVP) -synthetic ADH/vasopressin -preferred med in most patients -given at minimum dose to reduce nocturia; admin at bedtime

what does desmopressin have a risk for?

HYPONATREMIA- causes N/V, HA, lethargy, seizures, and coma

what is the first line treatment for nephrogenic DI?

thiazide diuretics -> hydrochlorothiazide (HCTZ)

what does HCTZ do?

decrease polyuria (increase proximal tubule sodium and water reabsorption and less water delivered to the ADH-sensitive collecting tubules)

what is the 2nd line tx for nephrogenic DI that can also be used in combo with HCTZ?

NSAID (Indomethacin)

what does indomethacin do?

increase renal concentration of urine by inhibiting renal synthesis of prostaglandins (ADH antagonists)

what is another treatment option other than central DI or nephrogenic DI treatments?

fluid replacement - thirst intact- replace water losses orally - electrolyte abnormalities do not normalize through oral water intake: >IV dextrose and water <500 mL/hr with serum glucose monitoring >risk for hyperglycemia