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69 Cards in this Set

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Aspects of microscopic examination that should be standardized:
volume of urine analyzed
length and force of centrifugal
re-suspending vol and conc of sediment
vol and amount of sediment examined
terminology and reporting format
Materials for microscopic examination:
- Conical centrifuge tubes, or regular test tubes up to 15 mL.
- Centrifuge
- Pipettes
- slides and coverslips
- microscope
Procedure for microscopic examination:
1. Mix the urine specimen.
2. Transfer about 10-12 mL of urine into a labeled centrifuge tube.
3. centrifuge the specimen at a medium speed (1500-2000rpm) for 3-5 minutes.
4. Discard the supernatant by quick inversion of the tube.
5. Re-suspend the sediment that is at the bottom of the tube, by tapping the tube with your fingers.
6. Take the sediment by Pasteur/disposable pipette from the tube and transfer a drop into the clean and dry slide.
Sources of error in microscopic examination:
Drying of the specimen on the slide.
If the supernatant fluid after centrifugation is not poured off properly, it may decrease conc of urine sediments and false result may be reported.
If the whole sediment with supernatant is discarded during inverting down the tube for a long period, the whole sediments will be discarded and so again false neg result will be reported.
Thus another sample should be collected and the test repeated.
Delineates structure and contrasting colors of the nucleus and cytoplasm.
ID's WBCs, epithelial cells and casts.
Sternheimer-Malbin stain
Enhances nuclear detail.
Diffs WBCs and renal tubular epithelial cells.
Toiuidine blue stain
Lyses RBCs and enhances nuclei of WBCs.
Distinguishes RBCs from WBCs, yeast, oil droplets and crystals.
2% acetic acid
Stains triglycerides and neutral fats orange-red.
IDs free fat droplets and lipid-containing cells and casts.
Lipid stains: Oil Red O and Sudan III
Methylene blue and eosin Y stains eosinophilic granules.
IDs urinary eosinophils
Hansel stain
Stains structures containing iron.
IDs yellow-brown granules of hemosiderin in cells and casts.
Prussian blue stain
frequently used, low light via rheostat control not lowering condenser
bright field
advantageous for low refractive casts, mucous threads and Trichomonas
Phase contrast
crystals and lipids: confirm fat droplets, oval fat bodies and fatty casts
polarizing
3D image- fine structures
interfering contrast
spirochete Treponema pallidum
Dark-field
Organized (formed) elements
RBCs (HPF)
WBCs (HPF)
Bacteria (HPF)
Epithelial cells (LPF)
Casts (LPF)
Parasites (LPF)
Yeast cells (LPF)
Mucus tread (LPF)
Spermatozoa
Miscellaneous substances
Slightly acidic urine
calcium carbonate
acidic, neutral, or slightly alkaline urine crystal
calcium oxalate crystals
alkaline, neutral or slightly acidic urine
triple phosphates
alkaline urine crystals
amorphous phosphate
calcium carbonate
calcium phosphate
In concentrated urine RBCs may be:
crenated
small/shrink
cells lose water
In diluted urine RBCs may be:
turgid and increased in size
absorb water
swell
in alkaline urine RBCs may be:
small or entirely destroyed forming massive of brownish granules
In diluted and alkaline urine RBCS will:
rupture and release the hemoglobin, leaving faint colorless membrane (ghost cells)
High numbers of RBCs indicate:
renal disease
Factors that may result in falsely high RBCs
menstrual bleeding
vaginal bleeding
trauma to peranal area in females
following traumatic catheterization
aspirin
antocoag therapy
WBCs in alkaline urine
may increase their size and become irregular
High WBCs in urine indicate
infection or inflammation in urinary or genital tract
0-5 leukocytes is
normal
5-10 leukocytes is
few
10-20 leukocytes is
moderate
20-30 leukocytes is
many
above 30 leukocytes is
full/field
presence of RBCs
acute/chronic glomerulonephritis
tumor in urinary tract
renal stone
cystitis
prostates
trauma of the kidney
traumatic catherterization
increased WBCs in urine may indicate:
UTI (renal tuberculosis)
all renal diseases
bladder tumor
cystitis
prostates
fever
exercise
very large
abundant irregular cytoplasm rectangular with irregular border
single nucleus
clue cells
squamous epithelial cells
granular with sort of tail.
seen with no leukocyte and mucus trade
few in number
catheterization
cells from renal pelvis
oval in shape
seen with leukocytes and filaments
catheterization
cells from urethra
smaller than epis
larger than leukocytes
very granular
refractive and clear nucleus
with proteins or casts
increase=necrosis of renal tubules
renal epithelial cells
RTE absorbe lipids present in filtrate
make RTE highly refractile
with free floating fat droplets
ID with Sudan III or Oil Red O
Polarizing light: maltese cross
oval fat bodies
Presence of epithelial cells in large number indicates:
actue tubular damage
acute glomerulonephritis
silicate overdose
UTI (with large number of leukocytes)
Immunologic disorder affecting other major organs
Kidneys filter immune components- deposit on glomerular membranes
Results in damage to basement membranes and capillaries
Glomerular disorder
(immunologic origin)
exposure to chemicals
electrical membrane changes, chronic inflammation, basement membrane damage
glomerular disorder
(non immunologic origin)
Affecting glomerulus:
sterile
inflammatory
RBCs, protein and casts
glomerulonephritis
sudden onset
following strep A infection
affect glomerular function
Fever, edema, oliguria, and hematuria
RBC casts and dysmorphic RBCS
acute post-steptococcal glomerulonephritis (AGN)
Immune systemic disorder
system lupus erythematosus (SLE)
Permanent damage to capillaries
proliferation in bowman's capsule
marked proteinuria
Rapidly progressive glomerulonephritis (Crescentic)
cytotoxic autoantibody against glomerular and alveolar basement membranes
hematuria, proteinuria, and RBC casts
Goodpasture syndrome
(glomerulonephritis)
immune response to antineutrophilic cytoplasmic antibody (ANCA) that binds to neutrophils
granulomas-infection
pulmonary- then renal
elevated BUN/creatinine
wegener's granulomatosis
(glomerulonephritis)
children- caused by immune response following viral infection
RBC casts
renal complications
vascularture
red rash
henoch-sshonelein purpura
(glomerulonephritis)
AKA Berger disease
IgA complexes don't deposit on the glomerular membrane
most common
increased levels of IgA
microhematuria
>20 years with lack of symptom
IgA nephropathy
(chronic glomerulonephritis)
massive proteinuria
high levels of serum lipids
hypoproteinemia
edema
increased passage of proteins
increased prod of lipids
sodium retention
4+ protein
oval fat bodies
nephrotic syndrome
podocytes of glomerular dysfunction
allow protein to filter
children- edema, hematuria
corrected with corticosteroids
minimal change disease (lipid nephrosis)
only affects a PORTION of glomeruli
associated with heroine, analgesic use, and AIDS
focal segmented glomerulosclerosis
inherited disorders
males
during respiratory infections
hematuria
abnormality in hearing and vision
thinning areas of glomeruli
URI
alport syndrome
AKA kemmelstiel-wilson disease
most common cause of end stage renal disease
membrane thickening
proliferation of mesangial cells
deposit of cells in glycosylated proteins
diet and exercise management
waxy broad casts and glucosuria
diabetic nephropathy
do casts increase or decrease flow?
increase
primary disorder dealing with damage to renal tubules
ischemia
toxic damage due to tubules via ultrafiltrate (antibiotics)
lack of blood flow (necrosis of tubules)
presence of RTE
acute tubular necrosis (ATN)
failure to inherit gene for tubular reabsorption
systemic condition affecting tubular reabsorption
hereditary and metabolic tubular disorders
PCT reabsorption failure
changes in cellular energy required for transport
associated with cystinosis, toxic build up, or autoimmune (multiple myeloma)
faconi syndrome
sex linked recessive gene or acquired thru medication (lithium and amphotericin B)
sickle cell anemia and polycystic disease
ADH disruption
low SpG, pale yellow color, polyuria
nephogenic diabetes insipidus
autosomal recessive
reabsorption of glucose is decreased
increased urine glucose conc.
normal glucose in serum
renal glycosuria or glucosuria
affects renal intersitial tissues and renal tubules
infections and inflammation
UTI's
WBCs and bacteria
tubulointersitial disease
Upper UTI has ___ casts and lower UTI has ____ casts.
WBC
no WBC
untreated lower UTI leads to upper tract infection
antibiotic treatment and management of underlying conditions can resolve
acute pyelonephritis
leads to permanent damage
caused by congenital defects that result in urinary structural defects
children
WBC casts
granular, waxy and broad casts
chronic pyelonephritis
pyelonephritis has what kinds of casts?
WBC
inflammation of renal tubules and renal intersitium
rapid onset- fever, skin rash
allergic reaction- penicillin, methicillin, ampicillin, cephalosporin, sulfonamides
increased eosinophils
actue intersitial nephritis (nephrons)
sudden loss of renal function
usually reversible
decreased GFR, azotemia (BUN/creatinine)
presence of RTE, casts, ATN, WBCs
acute renal failure
gradual progression
marked decrease GFR
azotemia
electrolyte imbalance
isothenuric urine (kidney cannot dilute or conc urine)
abundance of granular, waxy and broad casts
chronic renal failure
kidney stones
form in pelvis of the kidney, ureters and bladder
vary in size/PAINFUL
some may be passed others need lithotripsy
pH, stasis, clumps of crystal
renal lithiasis