Page 682 - Small Animal Internal Medicine, 6th Edition
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654    PART V   Urinary Tract Disorders



                   TABLE 38.1
  VetBooks.ir  Causes of Polyuria and Polydipsia Seen in Small Animal Practice   CONFIRMATORY TESTS

                                      MECHANISM OF POLYURIA AND POLYDIPSIA
             DISEASE
             Chronic renal disease (S)*  Osmotic diuresis in remnant nephrons    ECC, CBC
                                      Disruption of medullary architecture by structural   Biochemistry profile
                                        disease                                  Urinalysis
                                                                                 Radiography
                                                                                 Abdominal ultrasonography
                                                                                 Iohexol clearance
             Hyperadrenocorticism     Defective ADH release and action           LDDST
               (W)*                   Psychogenic                                Plasma ACTH concentration
                                                                                 Abdominal ultrasonography
             Diabetes mellitus (S)*   Osmotic diuresis caused by glucosuria      Blood glucose concentration
                                                                                 Urinalysis
             Hyperthyroidism (W)*     Increased medullary blood flow, MSW        Thyroxine
                                      Psychogenic                                Technetium scan
                                      Hypercalciuria
             Pyometra (W)             Escherichia coli endotoxin                 History
                                      Immune complex glomerulonephritis          Physical examination, CBC, abdominal
                                                                                  radiography
             Postobstructive diuresis (S)  Elimination of retained solutes       History
                                      Defective response to ADH                  Physical examination
                                      Defective sodium reabsorption              Urinalysis
             Hypercalcemia (W)        Defective ADH action                       Serum calcium concentration
                                      Increased medullary blood flow
                                      Impaired NaCl transport in loop of Henle
                                      Hypercalcemic nephropathy
                                      Direct stimulation of thirst center
             Liver disease (W)        Decreased urea synthesis with loss of medullary   Liver enzyme levels
                                        solute                                   Serum bile acids
                                      Decreased metabolism of endogenous hormones   Blood ammonia
                                        (e.g., cortisol, aldosterone)            Liver biopsy
                                      Psychogenic (hepatic encephalopathy)
                                      Hypokalemia
             Pyelonephritis (W)       E. coli endotoxin                          Urinalysis
                                      Increased renal blood flow                 Urine culture
                                      MSW                                        CBC
                                      Renal parenchymal damage                   Excretory urography
                                                                                 Abdominal ultrasonography
             Hypoadrenocorticism (W)  Renal sodium loss with MSW                 Serum sodium and potassium
                                                                                  concentrations
                                                                                 ACTH stimulation
             Hypokalemia (W)          Defective ADH action                       Serum potassium concentration
                                      Increased medullary blood flow and loss of
                                        medullary solute
             Diuretic phase of        Elimination of retained solutes            History
             oliguric ARF (S)         Defective sodium reabsorption              CBC
                                                                                 Biochemistry profile
                                                                                 Urinalysis
                                                                                 Abdominal ultrasonography
                                                                                 Renal biopsy
             Partial urinary tract    Redistribution of renal blood flow         History
             obstruction (S)          Defective sodium reabsorption              Physical examination
                                      Renal parenchymal damage
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