L5: Urinalysis Flashcards
how to get a clean “catch”
clean nonfoaming disenfectant, allow to dry
discard first voided portion as it may contain urethral contaminants, collect midstream speciman
Dark brown→ black urine
bile/bilirubin due to liver/bile disease
turbidity causes
Crystal precipitation of amorphous material, bacteria, yeast, WBCs, RBCs, mucus, squamous epithelial cells, sperm prostatic fluid, lipids
bile/bilirubin due to liver/bile diseases that can cause brown/black urine
alkaptonuria: lack of homogentisic acid oxidase
malignant melanoma: melanogen
ash tray smell to urine
cigarrete smokers
fruity smell to urine
ketone bodies
putrid, foul smelling urine
bacteria of UTI
Amino acid disorders that change urine smell
Phenylketonuria
Maple syrup urine disease
Normal pH
4.5-8
Urine pH reflects
serum pH
acidic urine pH
4.5-5.5
alkaline urine pH
6.-8.0
Specific gravity
Concentration/weight of dissolved solutes
Ability of kidney to concentrate and dilute urine
normal Specific gravity
1.003-1.035
Isosthenuria
Fixed at 1.010→ kidney disease
→ same SG as initial plasma
normal urine volume
500CC-2000CC/24 hours
oliguria
<500 CC/24 hours
anuria
<100 CC/24 hours
polyuria
Excessive amounts, dilute, SG=1.0-1.002
When does glucose appear in the urine
plasma glucose >150-180 mg/dL exceed renal threshold
false negatives for glucose
ascorbic acid, aspirin
Ketones are
Products of incomplete fat metabolism when carbohydrate stores are diminished
When are ketones present
acidosis: DKA, rapid weight loss, fasting, starvation, pregnancy
Proteins are mostly
albumin
reflect renal endothelial function
Elevated proteins indicate
Early sign of kidney disease
proteins are overestimated in
concentrated urine
proteins are underestimated in
dilute urine
proteins false positive due to
pyridium
can moderately increased albumin be detected by a urine dipstick?
No
Must perform a special test
If a patient has persistently positive proteins on dipstick, the next step is to
quantify albumin:
abumin: creatinine ration
24 hour urine sample
high risk patients to screen for moderately increased albumin
DM
HTN
CVD
causes of blood in urine
hemoglobin or myoglobin
have to centrifuge to determine which
false negatives when hematuria is present
ascorbic acids
hematuria testing sensitivity
5-10 RBC/ .05-.3 mg/DL of hemoglobin
nitrite is produced by
enterobacteriaceae that reduce nitrates→ nitrite
nitrite indicates
UTI
false negatives for nitrite
urine in bladder < 4 hours
different bacteria don’t have enzymes
leukocyte esterase
Released by lysed neutrophils and macrophages
leukocyte esterase + nitrate both positive
increased sensitivity for UTI
false positives for leukocyte esterase
vaginal contamination, trichomonas
bilirubine and urobilinogen
Used in conjunction to determine pathology
Both normally negative
bilirubin turns urine
brown
Hemolytic disease findings
(-) bilirubin
Increased urobilinogen
Hepatic disease findings
(+/-) bilirubin
Increased urobilinogen
Biliary obstruction findings
(+) bilirubin
normal urobilinogen
RBCs in urine appear
refractile discs, shriveled
normal RBCs
0-3 RBC/HPF
cause red urine that isn’t hematuria
beeturia, phenazopyridine, porphyria, other
causes of >3 RBC/HPF:
Renal/lower urinary tract trauma Kidney stones Glomerular damage Tumors UTI Acute tubular necrosis Nephrotoxins Vaginal bleeding Cancer: kidney, bladder, prostate Benign prostatic hypertrophy
If urine is red:
centrifuge it
Red sediment after centrifuging urine means
hematuria
Red supernatant after centrifuging urine
do a dipstick heme
a negative dipstick heme means
the red urine was a false positive
a positive dipstick heme means
myoglobin or hemoglobin: centrifuge blood sample and evaluate plasma color
clear centrifuged plasma color
myoglobinuria
red centrifuged plasma color
hemoglobinuria
WBCs appear
Lobed nuclei and refractile cytoplasmic granules
Normal WBCs
0-5 WBC/HPF
5-10 WBC/HPF
suspicious for UTI
> 20 WBC/HPF
UTI
bacteria
0-4+/HPF
May or may not be significant, depends on method of collection and how long it stands for
Renal tubular and transitional epithelial cells
Slough from tubule lining in small numbers normally
large numbers of renal tubular and transitional epithelial cells
tubular degeneration
Oval fat bodies definition and appearance
Degenerated tubular cells containing abundant lipoproteins
Appear refractile
Exhibit “maltese cross” under polarized light microscopy
Presence of oval bodies
nephrotic syndromes
Squamous epithelial cells
Large polygonal squamous epithelial cells with small nuclei normally present in small numbers
large numbers of squamous epithelial cells
contaminated by skin or external urethra
casts are formed
only in the distal convoluted tubule or collecting duct
RBC/WBC are measured
Number per high power field (hpf)
casts are measured
Number per low power field (lpf)
Hyaline casts
Very pale, slightly refractile. Composed of mucoprotein tamm-horsfall protein secreted by tubule. normal.
Red cell casts indicate
Glomerular or renal tubular injury
GLOMERULONEPHRITIS
White cell casts indicate
Acute pyelonephritis, glomerulonephritis
Renal tubular cast cells
Injury to tubular epithelium: acute tubular necrosis
granular casts
Cellular casts which remain in tubules break down so that cells forming them degenerate into granular disease
coarse→ finely granular→ waxy cast
granular casts indicate
abnormality, but not specific
uric acid crystals indicate
Acidic urine, form secondary to hyperuricema
Crystine crystals indicate
Cystinuria: rare genetic cause of kidney stones
struvite crystals indicate
Crystalluria: secondary to infection by urease producing bacteria in alkaline urine
Calcium oxalate crystals
Form independent of pH, cause kidney stones, 2 forms: monohydrate/dihydrate
Urine culture indicates UTI when
> 100,000 colonies/ml
UTI still possible with fewer colonies esp if sx dysuria, frequencia, pyuria
major intracellular cation
serum potassium
potassium is excreted by
kidneys, controlled by distal nephron
who not to administer K+ to
impaired kidney function
Effects of aldosterone
- Increases renal sodium reabsorption
2. Increases renal potassium excretion
Hyperkalemia
> 5.0MEQ, >6.0–6.5 dangerous
Hyperkalemia presentation
Serum potassium >7
Ascending muscle weakness→ flaccid paralysis
Conduction abnormalities and arrhythmias
Mild hyerkalemia ECG
5.5-6.5 mEq/L peaked T waves
Moderate hyperkalemia ECG
6.5-8.0 mEq/L prolonged QRS complex
Severe hyperkalemia ECG
Vfib, asystole
Pseudohyperkalemia
due to hemolysis at venipuncture site→ repeat k+
Causes of hyperkalemia due to inadequate excretion of K+
- Renal failure → check BUN/Creatinine
- Medications:
aldosterone antagonist
K+ sparing diuretics
ACEI/ARBS
3. Hypoaldosteronism: Addison’s disease (adrenal insufficiency) Congenital Adrenal hyperplasia NSAIDS Renal tubular dysfunction
Causes of hyperkalemia due to Redistribution of K+: ICF→ ECF
- Tissue damage (rhabdomyolysis)
- Acidosis
- Decreased insulin
.1 decrease in pH causes
such as acidosis
.5-1.0 increased K+
causes of hyperkalemia due to excessive administration of K+
Rx K+ supplements
K+ containing salt substitutes, exp. In patient with some renal impairment
To rapidly correct hyperkalemia
Calcium chloride, IV (antagonizes K+)
Shift K+ from ECF to ICF
Sodium bicarb IV→ increases pH
Insulin + D50W → insulin shifts K+ into cells, D50W prevents hypoglycemia
to slowly correct hyperkalemia
Loop or thiazide diuretics
→ beware in decreased renal function
Hemodialysis if: kidney failure, very severe, refractory
when to send a hyperkalemic patient to the ER/ICU for monitoring
K+ >6.5
treat the underlying cause of hyperkalemia:
Stop meds: K+ sparing diuretic, ACEIs, ARBs, K+ supplements
Addison’s→ mineralocorticoid replacement
Hypokalemia is defined as
<3.5 mEq/L, <3→ dangerous
Hypokalemia presentation
Ascending muscle weakness/paralysis
Respiratory failure
Muscle cramping
Rhabdomyolysis
GI: N/V/A→ vomiting causes further hypokalemia
EKG: arrhythmias, U waves, flattened T waves, ST depression
To rapidly correct hypokalemia
- Cardiac monitor
- IV potassium chloride (KCl)
- Check K+ every 2-4 hours
To slowly correct hypokalemia
orally
When correcting hypokalemia, be sure to
Check for hypomagnesemia: low K+ difficult to correct if not also corrected
Inadequate intake of K+ hypokalemia
usually in a patient who takes thiazide/loop diuretic→ use supplements/K+ rich foods to prevent
GI tract loss of K+ hypokalemia
Upper GI: vomiting, NG suction
→ metabolic alkalosis→ promotes K+ loss
Lower GI: diarrhea
→ metabolic acidosis
____ promotes K+ loss
metabolic alkalosis
Renal losses of K+ hypokalemia
Diuretics
Bicarb excretion
Mineralocorticoid excess:
Hyperaldosteronism
Cushing’s syndrome
Redistribution of K+ from ECF to ICF hypokalemia
Metabolic alkalosis
Insulin administration
B adrenergic agonists
→ induce uptake of K+
→ promote insulin secretion
Hypokalemic periodic paralysis
.1 increase in pH causes
such as alkalosis
K+ decrease by .5-1.0 mEq/L
pH and K+ have a _____ relationship
inverse