Urinalysis and Body Fluids Exam 1 Flashcards
Two dominant manifestations of acute glomerulonephritis and give examples of various causes of this condition:
- Proteinuria ex. streptococcal infection
- Hematuria with RBC casts
i. e streptococcal infection, immune complex diseases.
* chronic glomerulonephritis is a slow progressing disease.
What are two clinical manifestations of acute tubular necrosis and what is it often associated with:
Manifestations: -decreased urine flow
-inability to produce urine
-loss of many tubular epithelial cells into
urine
Often associated with reduced blood supply to renal tubes.
3 manifestations of nephrotic syndrome
- proteinuria
- Hypoproteinemia (low protein in blood)
- edema (fluid retention)
common causes of urinary obstruction
- stones
- tumors
- congenital malformation
- stricture from infection
explain pyelonephritis
severe kidney infection that often originates from a bladder infection.
What are 2 main clinical findings in urine that may indicate diabetes mellitus and what would you expect to see in regards to SG
Glucose (glycosuria) Ketone bodies (ketonuria)
Both high SG/high volume
Unconjugated Bilirubin
Not found in the urine. Travels to the liver where it is separated from albumin and is insoluable in water.
i.e. free or indirect
Conjugated Bilirubin
Conjugated in the liver by esterfication with glucuronic acid. water soluble.
i.e. direct bilirubin and bilirubin diglucronide
Urobilinogen
conjugated bilirubin travels to the bile duct to the small intestine. 99.9% excreted into feces. Absorbed into the intestinal mucosa and travels back to the liver.
Healthy patient bilirubin and urobilinogen
bilirubin-negative
urobilinogen- normal or decreased
Hemolytic disease bilirubin and urobolinogen
bilirubin- negative
urobolinogen-normal or increased
Hepatic Disease bilirubin and urobolinogen
bilirubin- positive or negative
urobolinogen-normal or increased
Biliary obstruction bilirubin and urobolinogen
bilirubin- positive
urobolinogen- low or absent
PKU
Lack phenylalanine hydroxylase for the conversion of phenylalanine to tyrosine
Phenylalanine accumulates and it’s metabolite phenylpyruvic acid appears in the urine
mousy odor
*phentest = dark green/blue green color
alkaptonuria
-Lacks homogenistic acid oxidase. Homogenistic acid accumulates in the blood and body fluids and is found in urine.
-urine darkens upon standing
Occurs in middle-age
*clinitest-orange
maple syrup disease
Lacks enzyme needed in branched-chain amino acid metabolism. Excessive accumulation of valine, leu one, insole icons and their keto & hydroxy acid in urine, blood, CSF. Causes keto acidosis, vomiting, seizure and lethargy.
*acetest-purple
urine smells like burnt sugar
Fanconi’s syndrome
- proximal convuluted tuble function is impaired
- failure to reabsorb glucose, water, phospurus, potassium and calcium
cystinuria
-cystine crystals in the urine
-inability of renal tubes to reabsorb cystine as well arginine, lysine and ornithine due to inherited trait.
Frequent cystine calculi(stones)
galactosemia
-lack of enzyme necessary to convert galactose to glucose
-detected in early infancy as diarrhea, vomiting and failure to thrive occurs
Positive on clinitest and negative on dip stick for glucose.
Define hematuria and name some conditions that may cause it:
presence of an abnormal # or RBC’s which often accompanies disease or the urinary system
- glomarular disease
- tubular disease
- vascular disease
Physical changes that occur as urine specimen remains at room temperature
- color darkens or changes
- clarity decrease
- odor-foul smelling