Diabetes insipidus is caused by a deficiency or insensitivity to antidiuretic hormone (ADH), leading to the production of large amounts of dilute urine and an inability to concentrate urine. The main types are central DI, caused by a lack of ADH production, and nephrogenic DI, caused by kidney insensitivity to ADH. Symptoms include polyuria, polydipsia, and nocturia. Diagnosis involves fluid deprivation and desmopressin tests. Central DI is managed with desmopressin replacement while nephrogenic DI is more difficult to treat.
Diabetes insipidus is caused by a deficiency or insensitivity to antidiuretic hormone (ADH), leading to the production of large amounts of dilute urine and an inability to concentrate urine. The main types are central DI, caused by a lack of ADH production, and nephrogenic DI, caused by kidney insensitivity to ADH. Symptoms include polyuria, polydipsia, and nocturia. Diagnosis involves fluid deprivation and desmopressin tests. Central DI is managed with desmopressin replacement while nephrogenic DI is more difficult to treat.
Diabetes insipidus is caused by a deficiency or insensitivity to antidiuretic hormone (ADH), leading to the production of large amounts of dilute urine and an inability to concentrate urine. The main types are central DI, caused by a lack of ADH production, and nephrogenic DI, caused by kidney insensitivity to ADH. Symptoms include polyuria, polydipsia, and nocturia. Diagnosis involves fluid deprivation and desmopressin tests. Central DI is managed with desmopressin replacement while nephrogenic DI is more difficult to treat.
Diabetes insipidus is caused by a deficiency or insensitivity to antidiuretic hormone (ADH), leading to the production of large amounts of dilute urine and an inability to concentrate urine. The main types are central DI, caused by a lack of ADH production, and nephrogenic DI, caused by kidney insensitivity to ADH. Symptoms include polyuria, polydipsia, and nocturia. Diagnosis involves fluid deprivation and desmopressin tests. Central DI is managed with desmopressin replacement while nephrogenic DI is more difficult to treat.
DIABETES INSIPIDUS • ADH (Vasopressin) deficiency (central Dl) or insensitivity to ADH (nephrogenic) q inability to concentrate urine Q production of large amounts of dilute urine.
ETIOLOGIES 1. Central DI: .J.ADH production: MC type. Idiopa thic MC, autoimmune destruction of posterior pituitary, head trauma, tumor (brain or pituitary), infection, sarcoid granuloma.
2. Nephrogenic DI: partial or complete insensitivity to ADH
CLINICAL MANIFESTATIONS 1. Polyuria, polydipsia, nocturia (enuresis in ch ildren). 2. Hypernatremia if severe or .J. oral water intake.
DIAGNOSIS 1. Fluid deprivation test: establishes the dx of diabetes insipidus DI: continued production of dilute urine ! Urinary osm <200 & low specific gravity< 1.005
2. Desmopressin (ADH) Stimulation test: differentiates be tween
nephrogenic & central DJ. - Central DI: q reduction in urine output (iUos m) indicating a response to ADH
- Nephroge nic Dl : q continued production of dilute urine
(no response to ADH)
MANAGEMENT 1. Ce ntra l Dl: des mop ressin/ DDAVP (synthetic ADH); carbamazepine, chlorpropamid e (i' es ADH)
2. Nephrogenic Dl: sodium/protein res trictio n, in creased water
intake q hydroch lorothiazide, indomethacin. Difficult to treat.
223 Chapter 7 - Endocr ine M nemonics D IABETES INSIPIDUS: If you keep saying NA to ADH you will pee and drink so much you will DI
Body keeps saying N A to ADH: Either due:
deficiency of ADH (central) or insensitivity to ADH (nephrogenic)
• HyperNAtremia Polyuria and Polydipsia
PRESENCE OF ADH ABSENCE OF ADH
Due to hyperosmolarity Due to hypoosmolarity or hypovolemia • Thirst inhibited • Thirst stimulated • Increased urine volume • Decreased urine volume
NORMAL PHYSIOLOGY OF ADH
224 Chapter 7- Endocrine Mnemonics
DIABETIC KETOACIDOSIS • DKA part of a spectrum representing the metabolic consequences of insulin deficiency & excess of counterregulatory hormone excess in response to stress ful triggers occurring especially in patients with Type I DM.
• Stressful triggers: infectio ns (MC cause), noncompliance with
3. Physical Exam: tachycardic, tachypneic hypote ns ive, fever if
infection, decreased skin turgor. Kussmaul respirations (deep, rapid breaths), ketotic breath (fruity, acetone odor). Acetone is the chemically neutral by-product of fatty acid metabolism. Acids produced are acetoacetate &
DIAGNOSIS 1. Serum glucose: >250 mg/dL; increased serum osmolarity 2. arterial pH < 7.3 (high an ion gap metabolic acidosis) 3. serum bicarbonate <15 mEq/L 4. ketonuria & ketonemia
MANAGEMENT 1. IV fluids 2. Ins ulin given until anion gap closes. Glucose added when serum glucose <250 to prevent hypoglycemia. 3. Potassium replacement to prevent hypokalemia
DKA -characte rized b y De hyd ra tion 4K's & Ac idosis
4K' s of DKA: Ke tone m ia, d ecrease in to ta l body K+, Ke to tic bre a th , K ussma ul res pira tio ns Management: You must S I P to survive th e d eh y d ratio n of DKA! S a lin e J st step I ns ulin Potassium 225
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