ICR: Polyuria & Diabetes Mellitus

Increased daily volume of urine normal volume per day ranges from 500 ml to 2000 ml true polyuria is defined as a 24 hour urine volume in excess of 2500 ml

Direct attention toward disorders of increased bladder irritability (cystitis, urethritis, spastic neurogenic bladder) or an overfilled bladder with incomplete emptying (sensory neurogenic bladder, prostatism)

Diabetes mellitus - as serum glucose level rises above the max concentration from which 100% of the filtered glucose can be reabsorbed, glucose begins to spill into the urine, obligating increased renal water excretion to wash it out

A slight (to extreme) decrement in ECF volume and a slight to extreme) increment in serum osmolality

Urine dipstick for glucose

If urine volume is abnormally high, you are dealing with another form of diabetes - diabetes insipidus

1) Central DI - due to deficient vasopressin release in response to increasing serum osmolality 2) Nephrogenic DI - due to subnormal renal responsiveness to vasopressin 3) Disogenic DI - due to oral water intake sufficient to lower serum osmolality below the threshold for vasopressin release

Commonly associated with renal tubular diseases, and in reversible form, is commonly due to hypokalemia and hypercalcemia. May also be medication-induced, as with treatment with lithium.

Presence of symptoms (polyuria, polydipsia, weight loss, hyerphagia, blurry vision) and significant glucosuria Confirmatory testing with a fasting glucose greater than or equal to 126 mg/dl OR a random glucose greater than 200

Due to autoimmune destruction of pancreatic islet beta cells, thus, the endogenous insulin reserve is effectively absent. If untreated, patients will experience ketosis even in the fed state, and can develop ketoacidosis when confronted with mild physiologic stress

Insulin replacement therapy is the ONLY treatment option

Due to a complex, variable spectrum of impaired insulin sensitivity at the level of hepatic muscle and fat tissue (insulin RESISTANCE) plus RELATIVE insulin deficiency (not an absolute deficiency) Thus, the endogenous insulin reserve is present but very limited If untreated, patients may exhibit symptomatic diabetes, but will not have ketosis in the postprandial state. Patients may develop ketoacidosis during extreme physiologic stress, but will resist ketosis during minor illnesses.

Diet + exercise to restore insulin sensitivity Oral hypoglycemic drugs (knowing the specific drugs is not listed in the objectives, so I'm not putting them in)

Islet cell and GAD (glutamic acid decarboxylase) antibodies low endogenous insulin as measured by an absent C-peptide response to physiologic stimuli (feeding, IV glucose, etc)

Absernce of serm islet cell and GAD antibodies Measurable endogenous insulin response to physiologic stimuli (the C-peptide ranges are detectable but inappropriately low to markedly elevated)