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bioanalytical pathology III


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causes of azotemia (general)
1.prerenal: due to decreased perfusion of kidney increased BUN can occur due to protein catabolism
2.renal: due to kidneys inability to excrete BUN/Cr
3.postrenal: due to obstruction of urinary tract leakage/rupture of bladder
caues of prerenal azotemia
cardiac disease
in dehydrated animals (>3%) specific gravity should be:
urine specific gravity the same as that of the ultrafiltrate
categories of proteinuria
1.preglomerular: uncommon, transient functional/physiologic; overflow proteinuria
2.glomerular: damage to glomerulus and diltering selectivity
3.postglumerular: more common than glomerular; renal tublular dysfunction
inflammation/hemorrhage within kidneys, ureters, bladder, urethra or genital tract
causes of proteinuria degree of protein in urine
1.preglomerular: mild
2.tubular damage: mild
3.glomerular damage: mod-severe
4.inflammation: mild- severe
urinary GGT/NAG
both found within renal tubular epithelial cells- released as cells die
GGT shown to be good predictor of aminoglycoside induced nephrotoxicity
general utility is more controversial-with CRF, loss of epithelial cells occurs; a lot of individual variation
fanconi syndrome
tubular defect, glucosuria
A transient/acute rise in blood glucose above the renal threshold will result in detectable glucosuria
F. need a chronic elevation to in blood glucose to detect glucosuria
what interferes with ADH
T/F ketonuria will often precede ketonemia
causes of ketonemia
1.diabetes mellitus-most common
2.high fever (puppies and kittens)
3.starvation; requires prolonged stravation in adults
1.anorexia/poor nutrition- high producers
2.pregnancy toxemia
In what two speicies is a trace amount of bilirubinuria normal
dogs and cattle
when is bilirubinuria significant
dogs: because of low renal threshold, bilirubinuria can precede bilirubinemia
2-3+ particularly in a urine < 1.035 is significant
cattle: anything > a trace amount is significant
all other species: any bilirubin is significant
causes of increased urine pH
1.bacteria can split urea producing NH3-seen with urinary tract infections, retention of urine in bladder, and delayed analysis of contaminated urine
2. systemic alkalosis prandial alkaline tide
causes of decreased urine pH
1.systemic acidosis
4.paradoxic aciduria- Cl, K depletion so H+ excreted
5.increased protein catabolism

name crystal and sigficance

triple phosphate or struvite
small number can be normal
seen with UTIs
seen with Feline Urologic Syndrome

name crystal and signifcance

calcium oxalate dihydrate
can be seen in small numbers in some normal dogs, cats
can be seen in animals prone to calcium oxalate urolith formation
seen in animals with ethylene glycol toxicity (monohydrate form more common)

name the crystal and significance

calcium oxalate monohydrate
can be seen in small numbers in some normal dogs, cats
can be seen in animals prone to calcium oxalate urolith formation
seen in animals with ethylene glycol toxicity (monohydrate form more common)

name the crystal and the significance

calcium carbonate
normal in horses, rabbits, guinea pigs and goats

name the crystal and significance

ammonium biurate
can be seen in animals with portal vascular shunts, rarely seen in small numbers in normal animals

name the crystal and significance

can be seen in concentrated urine of normal dogs
generally indicate increased blood bilirubin levels
cellular casts
always abnormal
WBC: generally indicates pyelonephritis
epithelial: generally indicate tubular necrosis or pyelonephritis

name the structure, significance

fine granular cast
degeneration of cells
suggests renal tubular injury
toxic ischemic

name the structure and significance

waxy cast
final breakdown of granular casts
suggests intrarenal stasis

name structure and significance

hyaline cast
pure protein
fever/exercise- small #
glomerular disease
leakage enzymes of the liver
indicate hepatocelluar injury
1.alanine aminotransferase (ALT); free in cytoplasm/dog and cat
2.aspartate aminotransferase (AST); some free in cytoplasm, most mitochondrial/dog,cat,horse,cattle
3.sorbitol dehydrogenase (SDH); free in cytoplasm/horse,cattle
4.GLDH, horse,cattle,dog,cat
induced enzymes of the liver
gen indicate cholestasis
1.alkaline phospatase (ALP); membrane bound in many tissues, several different isoenzymes
2.gamma glutamyl transferase (GGT); associated with bile ducts and perilobular hepatic parenchyma, most body cells can synthesize GGT
1.cytoplasmic in high concentrations in dog/cat; rapid release, in acute phase blood levels generally reflect the severity of the injury
2.considered liver specific but severe muscle injury can lead to increases
3.exogenous/endogenous glucocorticoids can result in 2-5 fold increases in dogs
1.present in hepatocytes and muscle of all species; muscle vs liver source
2.rises in AST will generally parallel ALT with liver disease; AST may be slightly more sensitive in dogs/cats
3.steroids have little effect on AST levels
1.induced enzyme; generally requires several days for induction
2.produced by many tissues
3.different isoenzymes; bone, hepatic, glucocorticoid; the 3 major isoenzymes can be differentiatied
ALP in cats
relatively short half-life compared to dog; 6 hours vs 70 hours
2.feline liver extract contains 1/2 as much ALP as canine liver
3.not increased by glucocorticoids or other drugs
4. 2-3 fold elevations in a cat is strong evidence of significant liver disease
drug induced ALP
1.dogs particularly prone to drug effects, cats particularly resistant
2.glucocorticoids are potent inducers of ALP \
3.anti convulsants also can induce ALP; phenobarbitol, primidone, phenytoin
1.pancreas>kidney>hepatocytes>bile duct>intestinal mucosa; pancreatic GGT out GI tract, renal GGT out in urine
2.good indicator of cholestasis; rises parallel those of ALP
3.present in high levels in the colostrum; exception is the horse, all neonates will have higher GGT values
drug induction of GGT
1.only clinically significant in the dog
2.glucocorticoids can result in moderate to large increases
3.anticonvulsants have a lesser effect; mild ranging from none to 2-3x increases
fasting hyperbilirubinemia
particularly prominent in horses; can reach values of 5-7 mg/dl within 4-6 days of anorexia, resolves within 48 hours of refeeding, mechanism not completely resolved
can see up to 3x increases in cattle and lesser increases in other species
gall bladder mucocoele
slow growing mass in common bile duct
progressive occlusion of biliary drainage; cholestasis
back up of bile salts, increased pressure,hepatocellar damage
if bilirubin is up due to cholestasis, ______ will also be up
bile acids
causes of increased bile acids
1.liver damage
2.bile duct obstruction
3.shunting of blood
bile acids in dogs and cats
pre sample after 12 hour fast
post sample 2 hours after feeding; must be a fat meal, measuring both samples improves sensitivity especially in cats
Dog: pre > 20umol/L and post >25umol/L
Cat: pre or post > 20umol/L; very specific indicators of liver disease
normal pre <5, post <10-15
bile acids in ruminants and horses
single sample collected
general rule of thumb
levels > 3-4x upper end of normal
very suggestive of pancreatic injury
general rule of thumb:
> 2x upper end of normal
very suggestive of pancreatic injury
exception is steriods in dogs
the kidney and amylase and lipase
approx. 50-60% of dogs with renal failure have increased amylase and or lipase levels
prerenal azotemia can also lead to increases
glomerular filtration a route of excretion, renal inactivation (?), secondary to uremia (?)
________ levels of enzymes generally higher than serum levels in pancreatitis
panel abnormalities other than amylase and lipase seen in pancreatitis
1.hyperglycemia; combination of stress, excitement glucagon
2.hypocalcemia; not consistly seen
3.increased liver enzymes; cholestasis; bile duct obstruction, inflammation, hepatocyte necrosis, ischemic, toxic damage, ascending inflammation
most sensitive test for pancreatitis in dogs
pancreatic lipase immunoreactivity
most common reason for hyperglycemia
regulation of serum sodium concentration is predominantly in the
aldosterone results in reabsorption of _____ and secretion of ___
aldosterone production is 1.increased with:

2.decreased with:
1.angiotensin II (renin)
decreased Na intake
2.atrial natriuretic peptide (from atrial myocytes)
increased Na intake
1.made by juxtaglomerular cells of afferent arterioles
2.activated by decreased renal perfusion pressure, decreased distal tubular delivery of NaCL, and dietary depletion of sodium, excess K
3.angiotensinogen to angiotensin I to angiotensin II = release of aldosterone, enhances reabsorption of Na and water (stimulates Na/H antiporter in proximal tubule
atrial natruiretic peptide
released in response to volume expansion
blocks: aldosterone production, angiotensin, response to ADH
causes of hypernatremia
1.sodium excess (rare)- concurrent water restriction or lack of urine concentration typically needed
a) excess intake: salt poisoning- ingestion or adminstriaton of hypertoic fluids
b)decreased renal excretion of sodium = hyperaldosteronism seen in cushings animals
2.decreased ECF water:
a)decreased intake: water deprivation/ defective thirst response
b) loss:
-insensible losses (respiratory or skin losses: fever, panting hyperventalition)
-kidney: diabetes insipidus, osmotic diuresis
-GI loss: osmotic diarrhea/ ruminal acidosis
causes of hyponatremia
1.sodium deficiency
a)GI loss
b)renal loss: nephropathies, prolonged diuresis, hypoadrenocorticism, ketonuria = anions pull the cations with them
c)sweating in horses
d)third space loss: repeated drainage of chylous effusions,, acute internal hemorrhage or acute exudation
2.water excess:
a)disorders that cause edema (usually normonatremic)
b)hypovolemia promotes thirst and increased intake: cangestive heart failure, hepatic fibrosis, nephrotic syndrome
c)inappropriate secretion of ADH (rare)
d)administration of Na poor fluids
shifts bt ICF and ECF
1.plasma hyperosmalality: draws fluid from ICF to ECF, also loss if osmotic diuresis or ketonuria
2.damage to membranes of muscle cells: sodium shifts from ECF to ICF
3.Na poor fluid added to body cavity (uroperitoneum):shifts of sodium from intravascular to extravascular space
often in attempt to maintain electroneutrality:
1.associated with hypernatremia
2.associtated with HCO3 loss:
a)alimentary loss
-vomiting diarrhea
-cattle with loss of saliva
b)renal loss
-proximal tubular acidosis
-distal tubular acidosis
c)respiratory alkalosis (retention of H+ decreased conservation of HCO3)
1.associated with hyonatremia
2.associated with increased HCO3
a)metabolic alkalosis
-loss of sequestration of HCL: vomiting, sequestration with DA, pyloric obstruction, functional obstruction
clinical signs associated with K imbalances manifest as
cardiac and skeletal muscle dysfunction
causes of hyperkalemia
1.inreased intake
a)metabolic acidosis
b)massive tissue breakdown/exertion
c)insulin deficiency
d)in vitro effects
4.decreased urinary excretion
a)urethral obstruction
b)ruptured bladder
c)anuric or oliguric renal failure
e)repeated drainage of chylous effusions
one of the most common electrolyte disturbances in critically ill patients
causes of hypokalemia
1.decreased intake
b)insulin or glucose containing fluids
4.GI loss: vomiting, SI diarrhea
5.renal loss:
a)CRF- esp cats
b)distal renal tubular acidosis
c)post obstructive diuresis
d)diabetic ketoacidosis
e)diuretic administration
f)mineralocorticoid excess (rare)
isotonic dehydration
proportional loss of NaCl and water:some diarrheas and renal diseases
.PCV and TPincrases
.Na Cl normal
.no change in osmolality-therefor no shift bt ICF and ECF: decearse in ECF volume
hypertonic dehydration
water loss greater than NaCl loss
1.diabetes insipidus
2.osmotic diuresis
3.water depervation
.PCV and TP increase
.Na and Cl increase
water moves from ICF to ECF to maintain volume
hypotonic dehydration
NaCL loss greater than water loss
1.secretory diarrhea
3.third space loss
4.equine sweat
.PCV and TP increased
.Na and Cl decrease or WNL
water shifts from ECF to ICF- leads to volume depletion
increased HCO3 in blood
1.loss of H+: in/from GI tract
2.hypochloridemia: if Cl is not present for tubluar resorption with Na, H+ exchanges with Na instead, H+ secretion = production of HCO3 for resorption
3.hypokalemia: promotes K-H transporter
K reabsorption = H secretion = HCO3 generation
4.respiratory acidosis
decreased HCO3 in blood
1.excess H+: HCO3 is used up buffering it
a)excess production of acid: lactate, ketones
b) decreased renal excretion of H+: renal failure, distal tublar acidosis, uroperitoneum or UT obstruction, hypoaldosteronism
2.HCO3 loss:
a)alimentary loss-intestinal and pancreatic secretions
b)renal loss- proximal tubular acidosis, defect in HCO3 conservation
-abnormal Na resorption
-carbonic anhydrase inhibitor
c)in vitro loss
increased anion gap =
addition of acid
anion gap
The difference between the sum of the measured cations and anions in the plasma or serum calculated as follows: (Na + K) -(Cl + HCO3) = &lt; 20 mmol/l. Elevated values may occur in diabetic or lactic acidosis; normal or low values occur in bicarbonate-losing metabolic acidoses.
causes of respiratory alkalosis
extrathoracic: PO2 is normal = fear, pain, anxiety
intrathorcic: PO2 is decreased = pulmonary disease
causes of respirtory acidosis
1.severe pulmonary disease
2.CNS disease that decreas respiratory rate
3.airway obstruction
4.pleural effusion/masses
5.neuromuscular disorders
creatine kinase (CK) kinetics
increase rapidly after muscle injury, peaks in 6-12 hours
very short half life
can return to normal in 24-48 hours after an acute injury
AST in muscle injury
increases more slowly than CK, stays elevated longer
ALT in muscle injury
liver specific in dogs and cats but can also be increased with severe muscle injury
hemoglobin vs myoglobin in urine
1.+ Hb dipstick
2.remains in serum (serum has red color)
3.precipitates with ammonium sulfate (no longer + Hb on dip stick)
1.+ Hb dipstick
2. cleared from serum (serum clear)
3.does not precipitate
parathyroid hormone (PTH)
increase serum Ca:
1.increased renal distal convoluted tubular reasborption
2.osteoclast activation
3.increased production of activated vitamin D
decreased serum P
1.does casue increased release from bone, but promotes renal excretion, as long as GFR is normal net effect is a decrease
vitamin D
results in increases in both serum Ca and P
kidney converts to active form (driven by PTH)
negative feed back of PTH
causes of hypocalcemia
1.decreased protein
2.renal failure:minority of cases dogs, cats, cattle
4.milk fever
6.intestinal malaborption
7.ethylene glycol toxicosis
8.blister beetle toxicosis in horses
causes of hypercalcemia
2.malignacy, PTH related protein secreting tumor
3.increased vitamin D: some rodenticides, some plants, granulomatous inflammtion
4.local osteolysis: mulitple myeloma, lymphomas
5.renal failure: common in horses/uncommon in other species
causes of increased P
1.decreased GFR: with azotemia (exception equine)
2.increased intestinal absorption (increased vit D)
3.young animals
4.severe myopathies
causes of decreased P
1.increased PTH or PTHrp: results in urinary loss
2.decreased intestinal absorption: malabsorption, decreased vitamin D
3.diuresis: fluid overload, osmotic diuresis in diabetes mellitus
upper GI bleeding
trypsin like immunoreactivity
1.most sensitive test for EPI
2.speicies speific (dog and cat only as of now)
3.dogs with EPI have<2.5ug/L
4.dogs with intestinal disease gen. >5.0ug/L
5.gray zone 2.5-5.0ug/L: may be due to sample exposure to extreme heat in transit, recovering from an episode of pancreatitis, food not with held, early EPI cats <8ug/L = EPI
vitamin B12 and folate
folate is absorbed in proximal SI and B12 absorbed in distal SI
both decreased: gen malabsorption
folate decreased: proximal SI defect
B12 decreased: distal SI defect
increased folate and decreased B12: bacterial overgrowth
proximal duodenal obstruction and hyperglycemia
seen in ruminants
can have incredibly high blood glucose
compared to more typical displaced abomasum glucose<200
levels represents the BG concentration during the previous 2-3 weeks
good indicator of inflammation in ruminants and horses
will also increase with dehydration
plasma protein/fibrinogen ratio
equine: <15 suggest inflammation
ruminant: <10 suggests inflammation
causes of panhypoproteinemia
1.blood loss
2.protein lossing enteropathy-leak from GI
3.severe exudative skin dz
4.severe burns
hypoalbuminemia without decrease in globulin
1.hepatic failure
4.selctive loss due to glomerular disease
5.loss of both albumin and globulin, but have increased production of immunoglobins
hypoglobulinemia without decreases albumin
1.failure of passive transfer
increased albumin
always dehydration
globulin fractions
-increased with acut inflammation
-acute phase protein
-acute inflammtion/acute phase protein
-liver disease
-nephrotic syndrome
-poly- chronic antigenic stimulation, immune mediated disease, liver disease
-mono-multiple myeloma, B cell lymphoma, small number of canine ehrlichia cases
decreased albumin with increased globulins
albumin is negative acute phase protein, decreased synthesis with inflammation requires > 1 week in duration

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