Diabetes insipidus and Hyperparathyroidism Flashcards
Diabetes insipidus
- caused by:
- what happens
- symptoms
- either a lack of ADH or a lack of response to ADH
- prevents the kidneys from concentration urine –> polyuria, polydipsia
- polyuria, polydipsia, nocturia, enuresis
Vasopressin secretion
- regulated by the osmotic pressure of body fluids
- control is mediated by osmoreceptors that are sensitive to small changes in plasma concentration of sodium and its anions
- osmoreceptors are insensitive to other solutes, ex: urea and glucose
below the threshold –> suppressed to levels that permit the development of a maximum water diuresis
above the threshold –> levels rises in direct proportion to plasma osmolarity, reaching levels sufficient to affect pa maximum antidiuresis
Vasopressin actions (2)
- reduce water excretion by promoting concentration of urine
- it does that by increasing the hydro osmotic permeability of cells that like the tubules and ducts of the kidney
What happens in the absence of vasopressin?
- cell are impermeable to water and reabsorb little
- lack of reabsorption results in the excretion of very large volumes of maximally dilute urine = water diuresis
Antidiuretic effect of vasopressin is mediated via…?
G protein coupled V2 receptors that increases intracellular cAMP –> inducing translocation of aquaporin 2 water channels into the apical membrane
The resultant increase in permeability permits an influx of water that diffuses out of the cell through AQP 3 and AQP 4 channels on the basal-lateral surface
Thirst (2)
- vasopressin cannot reduce water loss below a certain minimum level –> evaporation from skin and lungs is necessary to ensure adequate intake –> preventing dehydration
- regulated by an osmotat that is situated in the hypothalamus and is able to detect very small changes in the plasma concentration of sodium and its anions
Diabetes Insipidus (DI) (5)
- definition
- lab values
- will the patient present with clinical signs of dehydration?
- a decrease in 75% or more in the secretion or action of vasopressin
- production of abnormally large volumes of dilute urine
- 24h urine volume >40 ml/kg/ body
- osmolarity <300
-nope, it is uncommon –> unless thirst or compensatory increase of fluid intake is impaired
DI classification (4)
Pituitary - decreased production of ADH
-acquired, congenital malformations, genetic
Gestational
Nephrogenic - collecting ducts don’t respond to ADH
Primary polydipsia - normal ADH –> drink too much water –> too much urine –> patient doesn’t have DI
-psychogenic or dipsogenic
DI
-pathophysiology
Pituitary, gestational, nephrogenic
- polyuria –> decrease in body water –> increase in plasma osmolarity and sodium –> thirst and compensatory mechanisms
- hypernatremia and signs of dehydration do not develop
Primary polydipsia
- pathogenesis is the reverse
- abnormal cognition or thirst –> excessive fluid intake –> increase in body water –> reduces plasma osmolarity/sodium, vasopressin secretion and urine concentration
Nephrogenic DI
- vasopressin is normal or elevated
- urine osmolarity is low (<300)
Pituitary DI
- basal plasma vasopressin is low or undetectable (<1 pg/mL)
- MRI - T1 images - pituitary “bright spot” is always absent or abnormally small
Primary polydipsia
-MRI - T1 image - pituitary “bright spot” is present
Treatment of DI
-Uncomplicated pituitary DI
-desmopressin (synthetic analogue of vasopressin)
Desmopressin
-IV, subcutaneous injection, nasal inhalation or orally
Treatment of DI
- Primary polydipsia
- Nephrogenic
-not treated safely with desmopressin - because eliminating polyuria does not eliminate the urge to drink
- polyuria and polydipsia are not affected by desmopressin
- thiazide diuretic and/or amiloride + low sodium diet and a prostaglandin synthesis inhibitor
Factors involved in calcium and bone metabolism
- Parathyroid hormone - increases reabsorption of calcium from intestine and kidneys, increases osteoclast activity
- Vitamin D - increases intestinal calcium reabsorption, bone resorption and plasma calcium
- Calcitonin - decreases bone turnover and plasma calcium
- Sex steroids
- Growth hormone and insulin-like factors
- Thyroid hormone - increases bone resorption
- Prolactin - increases renal calcium reabsorption
- Glucocorticoids - increases bone resorption, decrease bone synthesis
- Inflammatory cytokines - increases bone resorption
