DEFINITION
To measure a urine cortisol:creatinine ratio (UCCR), a single midstream free-catch urine sample is used; cortisol and creatinine are both measured and the concentrations converted into the same units; the UCCR is simply the ratio of the two values.
A normal UCCR is less than approximately 10–30 × 10-6 depending on the laboratory; this value has no units and is typically reported without the scientific notation, e.g. 10 × 10-6 would be reported as 10.
Tuesday, April 5, 2011
Urine Cortisol: Creatinine Ratio
DEFINITION
To measure a urine cortisol:creatinine ratio (UCCR), a single midstream free-catch urine sample is used; cortisol and creatinine are both measured and the concentrations converted into the same units; the UCCR is simply the ratio of the two values.
A normal UCCR is less than approximately 10–30 × 10-6 depending on the laboratory; this value has no units and is typically reported without the scientific notation, e.g. 10 × 10-6 would be reported as 10.
To measure a urine cortisol:creatinine ratio (UCCR), a single midstream free-catch urine sample is used; cortisol and creatinine are both measured and the concentrations converted into the same units; the UCCR is simply the ratio of the two values.
A normal UCCR is less than approximately 10–30 × 10-6 depending on the laboratory; this value has no units and is typically reported without the scientific notation, e.g. 10 × 10-6 would be reported as 10.
Urinary Tract Obstruction
DEFINITION
Restricted flow of urine from the kidneys through the urinary tract to the external urethral orifice
PATHOPHYSIOLOGY
Excess resistance to urine flow through the urinary tract develops because of lesions affecting the excretory pathway, which cause increased pressure in the urinary space proximal to the obstruction and may cause abnormal distension of this space with urine. Ensuing pathophysiologic consequences depend on the site, degree, and duration of obstruction. Complete obstruction produces a pathophysiologic state equivalent to oliguric acute renal failure.
Perforation of the excretory pathway with extravasation of urine is functionally equivalent.
SYSTEMS AFFECTED
Renal/Urologic
Gastrointestinal, Cardiovascular, Nervous, and Respiratory systems as uremia develops
Restricted flow of urine from the kidneys through the urinary tract to the external urethral orifice
PATHOPHYSIOLOGY
Excess resistance to urine flow through the urinary tract develops because of lesions affecting the excretory pathway, which cause increased pressure in the urinary space proximal to the obstruction and may cause abnormal distension of this space with urine. Ensuing pathophysiologic consequences depend on the site, degree, and duration of obstruction. Complete obstruction produces a pathophysiologic state equivalent to oliguric acute renal failure.
Perforation of the excretory pathway with extravasation of urine is functionally equivalent.
SYSTEMS AFFECTED
Renal/Urologic
Gastrointestinal, Cardiovascular, Nervous, and Respiratory systems as uremia develops
Ureterolithiasis
OVERVIEW
Occurrence of a urolith (calculus) within a ureter; most ureteroliths originate in the renal pelves and so commonly occur in association with nephroliths. Most uroliths that enter the ureter continue to the bladder without impedance, but uroliths may cause partial or complete obstruction of the ureter, resulting in dilation of the proximal ureter and renal pelves and subsequent destruction of renal parenchyma.
SIGNALMENT
Dogs and cats
Breed, age, and sex predispositions vary with type of nephrolith.
See Nephrolithiasis
Occurrence of a urolith (calculus) within a ureter; most ureteroliths originate in the renal pelves and so commonly occur in association with nephroliths. Most uroliths that enter the ureter continue to the bladder without impedance, but uroliths may cause partial or complete obstruction of the ureter, resulting in dilation of the proximal ureter and renal pelves and subsequent destruction of renal parenchyma.
SIGNALMENT
Dogs and cats
Breed, age, and sex predispositions vary with type of nephrolith.
See Nephrolithiasis
Traumatic Myocarditis
OVERVIEW
Traumatic myocarditis is the term applied to the syndrome of arrhythmias that sometimes complicates blunt trauma; it is a misnomer, because myocardial lesions (if present) are more likely to take the form of necrosis than inflammation.
Direct cardiac injury is not required for development of posttraumatic arrhythmia; extracardiac conditions are likely to have equal or greater etiologic importance.
Ventricular tachyarrhythmias occur in most affected patients; supraventricular arrhythmias and bradyarrhythmias are uncommon. Ventricular rhythms that complicate blunt trauma are often relatively slow and detected only during pauses in the sinus rhythm; they are most appropriately referred to as AIVRs. The QRS complexes are wide and bizarre; the rate is > 100 bpm but generally < 160 bpm. Usually, these rhythms are electrically and hemodynamically benign.
Dangerous ventricular tachycardias can also complicate blunt trauma and can also evolve from seemingly benign AIVRs, compromising perfusion and placing the patient at risk for sudden death.
Traumatic myocarditis is the term applied to the syndrome of arrhythmias that sometimes complicates blunt trauma; it is a misnomer, because myocardial lesions (if present) are more likely to take the form of necrosis than inflammation.
Direct cardiac injury is not required for development of posttraumatic arrhythmia; extracardiac conditions are likely to have equal or greater etiologic importance.
Ventricular tachyarrhythmias occur in most affected patients; supraventricular arrhythmias and bradyarrhythmias are uncommon. Ventricular rhythms that complicate blunt trauma are often relatively slow and detected only during pauses in the sinus rhythm; they are most appropriately referred to as AIVRs. The QRS complexes are wide and bizarre; the rate is > 100 bpm but generally < 160 bpm. Usually, these rhythms are electrically and hemodynamically benign.
Dangerous ventricular tachycardias can also complicate blunt trauma and can also evolve from seemingly benign AIVRs, compromising perfusion and placing the patient at risk for sudden death.
Traumatic Myocarditis
OVERVIEW
Traumatic myocarditis is the term applied to the syndrome of arrhythmias that sometimes complicates blunt trauma; it is a misnomer, because myocardial lesions (if present) are more likely to take the form of necrosis than inflammation.
Direct cardiac injury is not required for development of posttraumatic arrhythmia; extracardiac conditions are likely to have equal or greater etiologic importance.
Ventricular tachyarrhythmias occur in most affected patients; supraventricular arrhythmias and bradyarrhythmias are uncommon. Ventricular rhythms that complicate blunt trauma are often relatively slow and detected only during pauses in the sinus rhythm; they are most appropriately referred to as AIVRs. The QRS complexes are wide and bizarre; the rate is > 100 bpm but generally < 160 bpm. Usually, these rhythms are electrically and hemodynamically benign.
Dangerous ventricular tachycardias can also complicate blunt trauma and can also evolve from seemingly benign AIVRs, compromising perfusion and placing the patient at risk for sudden death.
Traumatic myocarditis is the term applied to the syndrome of arrhythmias that sometimes complicates blunt trauma; it is a misnomer, because myocardial lesions (if present) are more likely to take the form of necrosis than inflammation.
Direct cardiac injury is not required for development of posttraumatic arrhythmia; extracardiac conditions are likely to have equal or greater etiologic importance.
Ventricular tachyarrhythmias occur in most affected patients; supraventricular arrhythmias and bradyarrhythmias are uncommon. Ventricular rhythms that complicate blunt trauma are often relatively slow and detected only during pauses in the sinus rhythm; they are most appropriately referred to as AIVRs. The QRS complexes are wide and bizarre; the rate is > 100 bpm but generally < 160 bpm. Usually, these rhythms are electrically and hemodynamically benign.
Dangerous ventricular tachycardias can also complicate blunt trauma and can also evolve from seemingly benign AIVRs, compromising perfusion and placing the patient at risk for sudden death.
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