Diabetes insipidus
•Download as PPTX, PDF•
39 likes•10,794 views
Diabetes insipidus : central and nephrogenic
Recommended
More Related Content
What's hot
What's hot (20)
Viewers also liked
Viewers also liked (20)
Similar to Diabetes insipidus
Similar to Diabetes insipidus (20)
More from Pratap Tiwari
More from Pratap Tiwari (20)
Recently uploaded
Recently uploaded (20)
Diabetes insipidus
- 1. Diabetes insipidus Pratap Sagar Tiwari, MD Lecturer, NMC
- 2. Polyuria • Polyuria has generally been defined as a urine output exceeding 3 L/day in adults and 2 L/m2 in children. 1. Primary polydipsia 2. Central DI 3. Nephrogenic DI
- 3. Primary polydipsia • Also called psychogenic polydipsia • Characterized by a primary increase in water intake.
- 4. Antidiuretic hormone • Vasopressin, also known as arginine vasopressin (AVP), antidiuretic hormone (ADH), or argipressin, is a neurohypophysial hormone. • Its two primary functions are to retain water in the body and to constrict blood vessels.
- 5. Central DI • Central DI (also called neurohypophyseal or neurogenic DI) is associated with deficient secretion of ADH. • This condition is most often idiopathic (possibly due to autoimmune injury), or can be induced by trauma, pituitary surgery, or hypoxic or ischemic encephalopathy.
- 6. Clinical manifestation • Patients with untreated central DI typically present with polyuria, nocturia, and, due to the initial elevation in serum sodium and osmolality, polydipsia. • They may also have neurologic symptoms related to the underlying neurologic disease.
- 7. Nephrogenic DI • Characterized by normal ADH secretion but varying degrees of renal resistance to its water-retaining effect. • NDI presenting in adults is almost always acquired with chronic lithium use and hypercalcemia .
- 8. Workup • A normal Na is’t helpful in Dx but, if a/w a UO > 600 mosmol/kg, excludes a diagnosis of DI. • A low Na(<137 meq/L) with a low UO(eg, less than one-half the plasma osmolality) is usually indicative of water overload due to PP. • A high-normal Na (>142 meq/L, dt water loss) points toward DI, particularly if the UO is < PO
- 9. Water deprivation test • Free fluids until 0730 hrs on the morning of the test. • Attend at 0830 hrs for body weight, plasma and urine osmolality • Record body weight, urine volume, UO, PO and thirst score on a VAS q 2 hrs for up to 8 hrs • Stop the test if the patient loses 3% of body weight . • If PO > 300 mOsm/kg and UO < 600 mOsm/kg, then administer DDAVP 2 μg i.m
- 10. Water deprivation test • DI : if PO> 300 mOsm/kg with a UO< 600 mOsm/kg • CDI :if UO rises by at least 50% after DDAVP • NDI :if DDAVP does not concentrate the urine • PP is suggested by low PO at the start of test
- 11. Treatment • The initial AOT is to reduce nocturia, thereby providing adequate sleep, most often by administration at bedtime desmopressin, which is the preferred therapy for CDI. • Once this is achieved, aim for partial control of the diuresis during the day, since complete control can lead to retention of water and hyponatremia. • Other drugs, chlorpropamide, carbamazepine, thiazide diuretics, and nonsteroidal antiinflammatory drugs.
- 12. End of slides References: • Davidson’s 21st edition. • Medscape • Uptodate 21.2 Last slide pic: www.weallhaveuniquebrains.com 1st slide pic :http://nurse-practitioners-and-physician-assistants.advanceweb.com/
Editor's Notes
- In the absence of a glucose-induced osmotic diuresis in uncontrolled diabetes mellitus, there are three major causes of polyuria in the outpatient setting, each of which is due to a defect in water balance leading to the excretion of large volumes of dilute urine (urine osmolality usually below 250 mosmol/kg): primary polydipsia, which is primarily seen in adults and adolescents; central DI; and nephrogenic DI
- This disorder is most often seen in anxious, middle-aged women and in patients with psychiatric illnesses, including those taking a phenothiazine which can lead to the sensation of a dry mouth. Primary polydipsia can also be induced by hypothalamic lesions that directly affect the thirst center, as may occur with an infiltrative disease such as sarcoidosis . The M3-muscarinic receptors (M3R) mediate parasympathetic cholinergic neurotransmission to salivary (and lacrimal) glands. Anticholinergics drug leads to dry mouth.
- The regulation of urine production occurs in the hypothalamus, which produces ADH . After synthesis, the hormone is transported in neurosecretory granules and stored in the posterior lobe of the pituitary gland. In addition, the hypothalamus regulates the sensation of thirst in the ventromedial nucleus by sensing increases in serum osmolarity . The neurohypophysial hormones are oxytocin and vasopressin. They are named for being secreted by the neurohypophysis, i.e. the posterior pituitary gland (hypophysis refers to the pituitary gland), itself a neuronal projection from the hypothalamus. Vasopressin, also known as arginine vasopressin (AVP), antidiuretic hormone (ADH), or argipressin, is a neurohypophysial hormone. Its two primary functions are to retain water in the body and to constrict blood vessels. Vasopressin regulates the body's retention of water by acting to increase water reabsorption in the collecting ducts of the kidney nephron. Vasopressin is a peptide hormone that increases water permeability of the kidney's collecting duct and distal convoluted tubule by inducing translocation of aquaporin-CD water channels in the kidney nephron collecting duct plasma membrane. It also increases peripheral vascular resistance, which in turn increases arterial blood pressure.
- The Wolfram or DIDMOAD syndrome is characterized by CDI, diabetes mellitus, optic atrophy, and deafness; it is inherited as an autosomal recessive trait with incomplete penetrance.
- Hypercalcemia — A renal concentrating defect may become clinically apparent if the plasma calcium concentration is persistently above 11 mg/dL (2.75 mmol/L) [1]. This defect, which is generally reversible with correction of the hypercalcemia, may be associated with reductions both in sodium chloride reabsorption in the thick ascending limb of the loop of Henle, thereby interfering with the countercurrent mechanism, and in the ability of ADH to increase collecting tubule water permeability . Hypokalemia — Persistent severe hypokalemia (plasma potassium concentration usually below 3 meq/L) can impair urinary concentrating ability. As with hypercalcemia, both decreased collecting tubule responsiveness to ADH (which may be mediated by decreased expression of aquaporin-2) and diminished sodium chloride reabsorption in the thick ascending limb have been demonstrated in experimental animals .
- Plasma sodium and urine osmolality — Each of the three causes of polyuria — primary polydipsia, central DI, and nephrogenic DI — is associated with an increase in water output and the excretion of a relatively dilute urine. With primary polydipsia, the polyuria is an appropriate response to enhanced water intake; in comparison, the water loss is inappropriate with either form of DI. Measurement of the plasma sodium concentration and the urine osmolality may be helpful in distinguishing between these disorders: A normal plasma sodium concentration is not helpful in diagnosis but, if associated with a urine osmolality more than 600 mosmol/kg, excludes a diagnosis of DI. A low plasma sodium concentration (less than 137 meq/L) with a low urine osmolality (eg, less than one-half the plasma osmolality) is usually indicative of water overload due to primary polydipsia. A high-normal plasma sodium concentration (greater than 142 meq/L, due to water loss) points toward DI, particularly if the urine osmolality is less than the plasma osmolality . In adults with DI and no cognitive impairment, true hypernatremia (plasma sodium concentration greater than 150 meq/L) should not occur because the initial loss of water stimulates thirst, resulting in an increase in intake to match the urinary losses . An exception to this general rule occurs when DI is due to a central lesion that also impairs thirst, thereby causing hypodipsia or adipsia; in this setting, the plasma sodium concentration can exceed 160 meq/L . Adipsic DI is associated with significant morbidity including obesity, sleep apnea, venous thrombosis during episodes of hypernatremia, thermoregulatory dysfunction, seizures, and significant mortality .
- The initial aim of therapy is to reduce nocturia, thereby providing adequate sleep, most often by the administration at bedtime of desmopressin, which is the preferred therapy for central DI. Once this is achieved, one aims for partial control of the diuresis during the day, since complete control can lead to retention of water and hyponatremia. Chlorpropamide — Chlorpropamide, an oral hypoglycemic agent, is the most commonly used antidiuretic drug after desmopressin ; it appears to act by enhancing the renal response to ADH or to desmopressin. Studies in animals suggest that this response may be mediated by enhanced sodium chloride reabsorption in the thick ascending limb (thereby increasing the degree of medullary hypertonicity) and/or by increased collecting tubule permeability to water; how these changes occur is unclear. Carbamazepine or clofibrate — Carbamazepine (used to treat seizures and tic douloureux) in a dose of 100 to 300 mg twice daily and clofibrate (used in the treatment of hyperlipidemia) in a dose of 500 mg every six hours can ameliorate the polyuria in partial central DI . Carbamazepine appears to enhance the response to ADH , whereas clofibrate may increase ADH release. The effect of thiazide diuretics is presumably mediated by a hypovolemia-induced increase in proximal sodium and water reabsorption, thereby diminishing water delivery to the ADH-sensitive sites in the collecting tubules and reducing the urine output. The thiazide effect is additive to that of the other modalities. Thiazides also tend to modestly raise the plasma glucose concentration, thereby decreasing the likelihood of hypoglycemia in patients who are also treated with chlorpropamide. NSAIDs — Nonsteroidal antiinflammatory drugs (NS.AIDs) increase urinary concentrating ability by inhibiting the renal synthesis of prostaglandins, which are ADH antagonists . PROBLEM WITH INTRAVENOUS FLUID REPLACEMENT — When thirst is intact and there is free access to water, most patients with central DI can replace their water losses orally. Patients who are unable to drink water must be treated with intravenous dextrose and water (because intravenous sterile water without dextrose causes hemolysis). There is a potential complication if this is performed before the polyuria is corrected by the administration of desmopressin. In adults, the intravenous administration of dextrose and water at more than 1000 mL/hour delivers glucose at a rate that exceeds endogenous metabolic capacity for glucose even in patients without diabetes mellitus, possibly leading to severe and symptomatic hyperglycemia . Thus, intravenous rates of fluid replacement with dextrose in water should be limited to a maximum of 500 to 750 mL/h and serum glucose levels should be monitored.