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Clin Path > Urinary Ch 9 D&P > Flashcards

Urinary Ch 9 D&P Flashcards

1
Q

Structure of the urinary tract of birds?

A

They lack a urinary bladder and urine comes out thru the cloaca, which is a common opening for the urinary, digestive and repro tracts in birds.

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2
Q

What does bird urine contain that mammal urine does not?

A

A solid component of urates, pasty white to yellow substance.
Some normal bird urine may also appear cloudy, opaque or flocculent.

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3
Q

Four things that will make urine an abnormal color?

A

Blood > red urine (clears when centrifuged)
Bilirubin > dark yellow to brown urine
Hemoglobin and Myoglobin > red to red brown urine
Porphyrins > Colorless but produce pink flourescense in acid urine when exposed to UV light

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4
Q

What does yellow green urates in birds mean?

A

Hemolysis or liver disease. (biliverdinuria)

ALso mixing of the urine with feces as well as diet like when eating blue purple fruit or berries.

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5
Q

What may cause tan to brown discoloration of urine and urates in birds?

A

Lead toxicosis can cause chocolate milk appearance to urine.

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6
Q

How is the normal urine or horses unique in appearance and why?

A

It cloudy due to calcium carbonate crystals and mucus.

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7
Q

What about the ammonia content of urine?

A

Ammonia, formed by urease splitting bacteria, may be prominent in retained or old urine samples.
This may have a strong odor.

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8
Q

An acetone odor of urine suggests what?

A

Ketosis

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9
Q

How is urine volume controlled, trace the flow of urine thru the tubules?

A

Enters proximal tubule same osmolality as plasma > Reabsorption of water in proximal tubules secondary to resorption of Na, Glc, etc > Enters loop of Henle Iso-osmotic relative to plasma > descending Loop of H permeable to water but not solutes > Water leaves tubule in dLofH > ascending LofH permeable to solutes but not water so solutes resorbed including ACTIVE Chloride txport > Urine entering distal tubule is Hypo osmotic compared to plasma > Enters distal tubules and collective ducts and water is absorbed in excess of solute (to concentrate urine) under control of ADH and requires a hypertonic medulla. MAJOR CONTROL OF URINE VOLUE OCCURS AT THIS LEVEL.

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10
Q

What is the BLUF in regards to how urine is concentrated within the renal tubules?

A

1st glc and Na absorbed and water follows (isotonic compared to plasma)
2nd in des L of H water absorbed
3rd in asc L of H solutes absorbed and chloride making filtrate hypoosmotic
4th Water resorbed in distal tubule and CD, which concentrates the urine under control of ADH.

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11
Q

What maintains medullary hypertonicity in the kidney?

A

Counter current multiplier of the Loop of Henle and Vasa recta (I think these flow in the opposite direction, and I think urea and Na also play an important role).

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12
Q

Normally urine volume and specific gravity / osmolality are inversely related, in what conditions is this not true?

A
  • Diabetes mellitus > polyuria and high SG d/t glucosuria (Glc increases urine SG)
  • Acute and chronic renal disease
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13
Q

What does specific gravity reflect, and what does the value depend on?

A

Reflects particle number in solution, size and weight.

Its a valid reflection of osmolality.

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14
Q

Adequate renal concentrating ability is based on a urine specific gravity of what in dogs and cats?

A

Greater than 1030 in dogs

Greater than 1035 in cats

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15
Q

What is the simplest definition of renal failure?

A

Azotemia in an animal with inadequately concentrated urine.

May be primary renal dz or secondary to other dz and may be reversible or irreversible.

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16
Q

What is isosthenuria?

A

USG is in the range of the glomerular filtrate/plasma = 1.008 - 1.012. The kidney is neither concentrating nor diluting the urine.

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17
Q

*What is hyposthenuria and what does it tell you?

A

USG less that 1.008
Kidney retains some water balance function as the solute is being resorbed in excess of water.
But may indicate some kind of polyuric renal disease where fluid cannot be absorbed.

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18
Q

Two things that can falsely elevate the USG of urine?

A

Glucose and protein.

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19
Q

How much protien is in the urine normally?

A

Only trace amounts most, including albumin, is resorbed in renal tubules.

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20
Q

What is Tamm-Horsfall protein?

A

Along with IgA, it is secreted by tubules into the urine in clinically undetectable amounts.

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21
Q

Reagent strips for urine protein detection detect which proteins?

A

Best for Albumin, DO NOT reliably detect globulins or Bence Jones proteins with myeloma.
The intensity of the green to blue color is proportional to the protein concentration.

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22
Q

Which urine test is best to detect Bence Jones proteins?

A

Immunoelectrophoresis is most specific and sensitive.

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23
Q

How is urine protein loss quantified?

A

Calculate the urine protein creatnine ratio. There are strips for this that work in the dog. Use the reagent strips to screen for urine and then calculate the UPC ratio.

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24
Q

Under what conditions may you get a false positive urine protein on the reagent strip?

A

IN a highly alkaline urine.

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25
Q

What other information is necessary when interpreting the UP:UC ratio?

A

An occult blood and urine sediment exam to distinguish renal from non renal proteinuria.

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26
Q

What is prerenal proteinuria?

A

Pre-renal proteinuria is a low-level proteinuria caused by an overabundant filtered load of low molecular weight proteins that overwhelm the reabsorptive capacity of the proximal tubule (overload proteinuria). Examples of this include the presence of hemoglobin, myoglobin, and immunoglobulin light-chain monomers and dimers (Bence Jones proteins from neoplastic plasma cells) in the urine.
- Shock, muscle exertion, fever, cardiac or CNS dz may also cause this in some cases.

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27
Q

In the absence of prerenal proteinuria, hemorrhage and inflammation what are the UP:UC normal values?

A

UP:UC ratio below 0.5 is considered normal.
0.5-1.0 is suspect.
> 1.0 = renal proteinuria

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28
Q

What are the four main causes of urogenital proteinuria?

A
  • Hemorrhage into the urinary tract (trauma, inflamm, neoplasia, urine occult blood is pos and you would see RBC onsediment; the dipstick protein is high d/t plasma derived albumin and it can be high).
  • Inflammation in the urinary tract (intermediate proteinuria)
  • Renal dz (+/- casts, glomerular dz causes high proteinuria and its albumin; Primary renal tubular dz cause moderate proteinuria)
  • Pre renal proteinuria (see previous question, usually mild proteinuria).
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29
Q

Which disease causes the most severe proteinuria? And which subtype of that disease is most severe?

A

Glomerular disease.

Amyloidosis and glomerulonephritis are the best examples and usually amyloidosis causes the most severe protienuria.

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30
Q

At what serum glucose level does glucosuria occur in the cat and dog?

A

Above 180 mg/dL in the dog and

280mg/dL in the cat

31
Q

What are the causes of Glucosuria when there is Normoglycemia?

A

This would indicate decreased tubular reabsorption of glucose:

  • Canine fanconi like syndrome or Basenji, Lab, defective renal tubular absorption
  • Renal tubular damage like from Gentamycin
  • Excitement in cats may cause glucosuria from transient hyperglycemia
32
Q

How do ketones interact with the glomerulus which ketones are tested for?

A
  • Freely filtered by the glomerulus and normally completely resorbed by the proximal tubules
  • Reagent strips detect acetone and acetoacetic acid but not Beta hydroxybutyrate (the major intermediate in ketosis).
33
Q

How do you interpret ketonuria?

A

It precedes detectable ketonemia and means that ketones are being incompletely resorbed by the renal tubule epithelial cells.
NOT an indicator or renal disease but rather suggestive of ketonemia and titrational acidosis and high anion gap - which may also be caused by lactic acidosis so you could test the urine for ketones to diff these two causes of high AG acidosis.

34
Q

Ketonuria specifically tells you what process is taking place and what are 5 ddx?

A

It tells you there is excessive degradation of fat and/or deficiency in carbohydrate metabolism / negative energy balance.

  • Ketosis of cattle (preg tox)
  • Pregnancy dz of Ewes (preg tox)
  • Diabetes mellitus (cells can’t get glucose)
  • Starvation (young animals)
  • Low carb high fat diets
35
Q

Which conjugated and unconjugated bilirubin enter the urine?

A
  • Conjugated is water soluble and can pass the glomerulus and readily enter the urine - it is NOT reabsorbed by the renal tubules. (in the dog some conj bili may be formed by the renal tubular epi cells from absorbed hemoglobin.
  • Unconjugated is bound to albumin and so it cannot pass the glomerulus.
36
Q

How do you interpret a result of Bilirubinuria?

A

It indicates obstruction of bili flow and regurg of conjugated bili into the blood and d/t the low renal threshold >
Bilirubinuria may be detected before bilirubinemia.
*- May be increased in hemoglobinuria and intravascular hemolysis.
A trace amt in the concentrated urine of dog is WNL but
Any degree of bilirubinuria is significant in cats

37
Q

How does hemoglobinuria occur?

A

It must be high enough to exceed the binding capacity of plasma haptoglobin and then split into dimers and then those dimers must exceed the capacity of the tubules to absorb them before they end up in the urine.

38
Q

*What are the three causes of a positive occult blood test and how do you differentiate them?

A
  • Hematuria (red cloudy urine that clears when spun and RBCs are seen in the sediment and there will be no other lab evidence of hemolytic dz or muscle dz)
  • Hemoglobinuria (red to brown urine that doesn’t clear when spun, NO rbc’s in the urine sediment; there is red discoloration of plasma, evidence of anemia, particularly the hemolytic type; If you add ammonium sulfate it will remove the color which DOES NOT occur with myoglobin).
  • Myoglobinuria (Red to brown urine that does not clear when spun, no rbcs on sediment, clear plasma - its NOT disocolored; clinical or other lab evidence of muscle dz.
39
Q

What are urine casts made of, how do they form and what do they indicate?

A

They are elongate structures made of Tamm-Horsfall protein (mucoprotein in the urine produced in the distal tubular epithelial cells.)
Casts are formed in the distal tubules where urine is more acidic - may dissolve in alkaline urine. Stuff present in the tubule when the cast formed are embedded in the cast.
They indicate some kind of tubular change but don’t correlate to severity of change.

40
Q

What are the types of casts and what is each made of(5)? Note which is most comon and which means the worst prognosis.

A

Classified by their major component.
Hyaline casts: Colorless, homogenous, semi transparent and difficult to detect, mostly made of Tamm Horsfall protein.
*Granular casts: Most common type, made of mucoprotein, plasma protein, degenerate cells.
Cellular casts: Epithelial cells desquamated from the renal tubules. WBC casts > Mean renal inflammation RBC casts > Mean renal hemorrhage and inflammation.
*Waxy casts: Wide and non granular, sharp broken or square ends and notched edges and evolve from degenerating cellular and granular casts; formed in large collecting tubules and indicate chronic tubular lesions, severe urine stasis and poor prognosis.
Fatty casts: Fat globules derived from degenerating tubular epithelial cells, most commonly observed in cats.

41
Q

Name four parasites that may be observed in urine samples?

A

Stephanurus dentatus
Dioctophyma renale
Capillaria plica
Microfilaria of Dirofilaria immitis

42
Q

Fungi and other organisms besides bacteria that may be found in urine?

A

Yeasts are contaminants but.
Aspergillus terreus has been documented in GSDs
Algae like Prototheca sp. with disseminated algal infection.

43
Q

What are the 9 types of crystals found in urine (5 are important)?

A

*Ammonium biurate (hyperammonemia, portosystemic shunt, yellow to brown thornapples)
Amorphous urates or phosphates (ill defined, think birds)
Bilirubin (yellow, twigs or antlers)
Calcium carbonate (dumbell shaped with spokes, equine urine)
*Calcium oxalate (monohydrates, spindle shaped or picket fence appearance, think ethylene glycol tox; the dihydrates are normal and are octahedrons or enveloped shaped).
Cholesterol crystals (cell bk down, may indicate renal dz, parallelogram with notched corner)
*Cysine cyrstals (hexagonal, indicate altered protein metabolism in dogs like congenital cystinuria of dogs)
*Triple phosphate (struvite, Mg Ammon Phos, coffin lids, 3-6 sided, not a big deal, alkaline urine, infection)
*Uric acid crystals (parallelograms with rounded corners, rhomboids or rosettes; normal finding in dalmatian dogs).

44
Q

What are the thornapple crystals and what are they associate with?

A

Ammonium biruate and theyh are associated with portosystemic shunts and other liver dz with hyperammonemia.

45
Q

What are spindle shaped picket fence crystals and what are they associate with?

A

Calcium oxalate monohyhdrate and they area ssocaited with ethylene glycol toxicity or other oxalate poisoning.

46
Q

Which type of crystal is seen with altered protein metabolism in dogs?

A

Cystine crystals, ie like incongenital cystinuria in dogs.

47
Q

Which crystals do dalmatian dogs get and they are rosettrams.es or rhomboids.

A

Uric acid crystals > Dalmatians where they are considered normal in this breed and look like lemon drops or parallelogram

48
Q

Renal failure is based on what hypothesis or principal?

A

After substantial loss of nephrons based on the intact nephron hypothesis where decline in renal function is the result of a decreased number of functioning nephrons rather than decreased function of individual nephrons.

49
Q

What does uremia refer to and what are some common clinical signs?

A

A complex of clinical signs observed in renal failure and less commonly with pre and post renal azotemia. If clinical signs are absent in an azotemic animal, its not uremic.
Clin Signs: GI hemorrhage, ulcerative stomatitis etc.

50
Q

Under what conditions would you do a urine concentration test (s/a water deprivation)?

A

PU/PD in an animal lacking azotemia, dehydration and biochemical evidence of dz. OR Random urine samples from a non azotemic animal with a low or isosthenuric urine SG.
You wouldn’t do the test if the animal was dehydrated, azotemic or if there was some other reason for the PUPD documented.

51
Q

What USG is considered adequate in a water deprivation test?

A

> 1.030 in the dog
1.035 in the cat
1.025 in horse and cow

52
Q

What are the four possible causes of an abnormal urine concentration test?

A
  • Renal dz
  • Pituitary diabetes insipidus
  • Nephrogenic diabetes insipidus
  • Dzs that cause polyuria and medullary washout
53
Q

How does renal dz cause abnormal urine concentration test?

A

2/3 of nephrons are non functional to get decreased concentrating ability.
Impaired concentrating ability usually precedes elevations in BUN/Crea (but in the cat or any spp with primary glomerular dz azotemia may occur simultaneously or precede concentration abnormalities..

54
Q

What is pituitary diabetes insipidus?

A

Pitutary dz&raquo_space; A lack of ADH secretion - tubules are normal but aren’t being stim’d to resorb water. USG is 1.001-1.007 cause the tubules can still absorb solute and the animals respond to exogenous ADH by concentrating urine.

55
Q

What is nephrogenic diabetes insipidus?

A

Renal tubules refractory to ADH stimulation.
Could be primary tubular defect or secondary to other biochem abnormalities like Cushings, hypercalcemia and endotoxemia.

56
Q

Where does BUN come from?

A

Ingested and absorbed from the LI in small quantities but majority from liver via the urea cycle where urea is made from ammonia (from protein metabolism).

57
Q

How does kidney urea excretion work?

A

Kidney is the most important route of urea excretion and its passively filtered at the glomerulus ( the blood content is the same as in the filtrate).
Increased BUN means decreased glomerular filtration.

58
Q

*What happens to urea in the kidney once its resorbed and enters tubules? What about under the influence of ADH?

A

It passively diffuses with water from the tubule into the blood and the rate of resorption is inversely related to the rate of urine flow through the tubules SO
less urine flow means more urea resorbed (like in dehydration or obstruction).
Under the control of ADH (like in thirst or dehydration), the Urea flows from the collecting duct to the interstitium and comprises part of the medullary concentration gradient.

59
Q

What are the bodies other sources of UREA secretion?

A

Saliva, GI tract and sweat. (GI tract is futile in monogastrics cause its converted to ammonia and goes right back to the liver)

60
Q

How does urea excretion occur in ruminants and how is it governed?

A

Governed by nitrogen intake; if N deficient or anorexic almost all urea excreted via the GI tract and not kidneys so BUN may be normal in cases of severe renal dz.
Urea excreted into rumen is degraded by flora to ammonia which is used to make amino acids for protein production.

61
Q

When in renal dz does renal azotemia occur?

A

Three fourths of the nephrons are non functional, GFR is significantly decreased and there is insufficient excretion of urea and creatnine. And once azotemia is present, the BUN concentration approximately doubles each time remaining functional renal mass is halved.

62
Q

*Which usually comes first, azotemia or concentrating abnormalities?
What are the exceptions to this rule?

A

Azotemia usually follows concentrating abnormalities. The decreased GFR causes the azotemia and the tubules cannot concentration urine.
EXCEPTIONS: Cats may be an exception to this.
*Animals with primary glomerular dz may develop azotemia before concentrating abnormalities are evident b/c tubular dz follows glomerular dz in the usual course of renal dz (d/t blood flow etc.)

63
Q

Whats the relationship between BUN and renal dz or failure in large animals?

A

Moderately increased in renal dz in the horse d/t intestinal excretion of urea (so very high levels of BUN likely prerenal).
In the ruminant BUN doesn’t increase proportionally to Crea d/t excretion of urea via the rumen.

64
Q

Standard clinical signs of post renal azotemia:

A

Oliguria and Anuria

65
Q

Where does creatinine come from and what is it influenced by?

A

Mostly endogenously from conversion of creatine that stores energy in muscle as phosphocreatine and its created at a relatively constant rate..
- Influenced by muscle mass and disease. (may decrease with muscle wasting or increase with rhabdomyolysis).

66
Q

How does creatinine diffuse compared to BUN and how is this useful?

A

It diffuses slower than urea so takes longer to equilibrate.
- If there is a ruptured urinary bladder the creatnine in the bladder would be much higher than in the serum and it persists longer than urea so its more useful when dxing ruptured urinary bladder.

67
Q

How is creatnine excreted (compare to BUN)?

A

Freely filtered by the glomerulus and tubule reabsorption DOES NOT occur so its a more accurate measure of GFR than BUN

68
Q

So increased Crea means what?

A
  • Decreased GFR just like renal dz (so 3/4 of renal function must be lost before abnormalities show up.)
  • Better than BUN in cow and horse cause there is little GI secretion
  • Ketones may interfere and cause false high values in serum
69
Q

What is a way to measure GFR?

A
  • Endogenous creatinine clearance (cause its filtered at a constant rate and not resorbed in the tubules) (calculated using urine creatnine and serum creatnine with a given volume over a given time).
70
Q

Other miscellaneous changes besides BUN/Crea that occur in renal dz?

A
  • Progressive nonregenerative anemia
  • Hyperphosphatemia (always follows BUN/Crea)
  • Hyperkalemia (when oliguria or anuria is associated with acidosis in renal failure).
  • Hypokalemia (in polyuric renal failure in cat and cow, not horse)
  • Metabolic / Titrational acidosis (inc AG d/t uremic acids)
  • Hypercalcemia in horses with renal dz d/t kidney being the major excretory route of Ca++; occasionally in dogs
  • Hypocalcemia in cows and sometimes in dogs and cats (probably d/t hyperphosphatemia)
  • Hypoproteinemia d/t proteinuria if primary glomerular dz.
  • Elevated fibrinogen (bovine renal failure, very high)
  • Amylase and lipase may be elevated d/t renal failure in the dog (they are excreted in the kidney)
71
Q

What constitutes nephrotic syndrome?

A

Tetrad of proteinuria (albuminuria), hypoproteinemia (hypoalbuminemia), edema and hypercholesterolemia. It occurs d/t glomerular dz.

72
Q

What is the acid base status in cows with renal dz and why?

Under what conditions would you get paradoxic aciduria?

A

Normal or Metabolic alkalosis. d/t
Rumen atony and HCl sequestration (prevents acidosis); BUT the AG will be high d/t salts of uremic acids.
When you have alkalosis, hypochloremia, and hypokalemia together. The Hypochloremia is d/t HCl sequestration in the rumen with fluid and so there is dehydration, which stims aldosterone release which stims Na resorption in the distal tubule, which is normally exchanged for K+, but K+ is low d/t alkalemia (its all intracellular) so the kidney exchanges H+ for Na+ in the tubule and you get aciduria. Also, Na is generally absorbed with bicarb whe Cl is low (sodium bicarbonate) so pulling bicarb out of the fluid may also contribute to tubular acidosis and aciduria.

73
Q

What are causes of prerenal azotemia?

A
  • Increased protein catabolism.
  • High protein diet
  • Decreased renal perfusion (reduces GFR > azotemia and decreased urine flow increases tubular urea absorption so it may be marked; Crea also increased).
  • USG is usually high unless the animal is Addisonian

Clin Path (14 decks)

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