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ACVP Phase II - Clinical Pathology > Stockham & Scott Chapter 8 Urinalysis TAMU > Flashcards

Stockham & Scott Chapter 8 Urinalysis TAMU Flashcards

1
Q

1. What comprises the glomerular filtration barrier?

A
  1. Capillary endothelium, basement membrane, podocytes with foot processes
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2
Q
  1. What factors influence the ability of a substance to pass through the filtration barrier?
A
  1. Molecular size(<2.5nm=100% passage; >3.4nm=almost 0% passage) & electric charge (+>neutral>negative)
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3
Q
  1. In what species may a small amount of albumin be found in the urine?
A
  1. Canine
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4
Q
  1. What is the ideal solute for measuring GFR?
A
  1. Inulin, iohexol, and mannitol–these pass freely, are not protein bound, and neither secreted nor resorbed by renal tubules. Creatinine–very little is secreted and it meets other criteria
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5
Q
  1. What stimulates proximal tubular resorption of Na, Cl, and water?
A
  1. Angiotensin II
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6
Q
  1. What is sodium cotransported with in the proximal tubules?
A
  1. Glucose, amino acids, and phosphates
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7
Q
  1. What establishes the concentration gradient for sodium resorption in the proximal tubules?
A
  1. Na–K ATPase pump (basolateral membrane)
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8
Q
  1. What stimulates/inhibits the Na–K–Cl cotransporter in the thick ascending loop of Henle?
A
  1. ADH (minor role) simulates/Furosemide diuretics inhibit.
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9
Q
  1. What is the net function of the nephron?
A
  1. Excrete urea, creatinine, K, H, NH4, and PO4 and conserve Na, Cl, HCO3, Ca, Mg, glucose, amino acids, and H20.
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10
Q
  1. What is the major action of ADH?
A
  1. Promote resorption of H20 and urea
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11
Q
  1. What are the major actions of aldosterone?
A
  1. Conserve Na, Cl and excrete K and H
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12
Q
  1. What promotes Mg and Ca resorption?
A
  1. PTH
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13
Q
  1. What percentages of Na, Cl, and HCO3 are resorbed in the proximal tubules?
A

Na=75%, Cl=75%, HCO3=90%

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14
Q
  1. How does aldosterone promote Na resorption?
A
  1. Opening Na channels & enhancing Na–K–ATPase in the basolateral membrane
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15
Q
  1. What do thiazide diuretics block?
A
  1. Na–Cl cotransporter in the distal tubule
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16
Q
  1. What is the action of ANP in the distal nephron?
A
  1. Reduces Na resorption during volume expansion by reducing open Na channels via guanylate cyclase pathway
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17
Q
  1. How is Cl resorbed in the ascending loop?
A
  1. Na–K–2Cl cotransporter
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18
Q
  1. How is HCO3 conserved in the proximal tubules?
A
  1. Indirectly, via Na–H antiporter and is dependent on Na resorption. H+HCO3––>H2CO3––>CO2+H2O––>proximal tubular cells––>H(secreted)+HCO3––>peritubular fluid via Na–3HCO3 cotransporter.
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19
Q
  1. Where does the majority of K secretion occur?
A
  1. Principal cells of collecting tubules & is promoted by aldosterone.
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20
Q
  1. What promotes secretion of H from Type A intercalated cells?
A
  1. Aldosterone and acidemia
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21
Q

21.How is PO4 resorbed from the proximal tubule?

A
  1. Na–PO4 cotransporter. Stimulated by hypophosphatemia and insulin and diminished by hyperphosphatemia and increased PTH activity.
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22
Q
  1. What stimulates Mg resorption in the thick ascending loop>
A
  1. ADH, PTH, glucagon, calcitonin, Beta–adrenergic agonists
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23
Q
  1. How is glucose resorbed in the proximal tubule?
A
  1. Na–glucose cotransport system.
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24
Q
  1. How do large proteins enter tubular cells?
A
  1. Endocytosis
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25
Q
  1. How are amino acids resorbed?
A
  1. Carriers specific for seven amino acid groups.
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26
Q
  1. What constitutes the majority of the interstitial solute for establishment of hypertonic medulla necessary for renal concentrating ability?
A
  1. Urea
27
Q
  1. What are causes of decreased urea nitrogen in serum/plasma?
A
  1. Hepatic insufficiency, PSS, diabetes insipidus, urea cycle enzyme deficiencies (reported in 2 dogs and 1 dairy cow and people=Citrullinemia=argininosuccinate synthetase deficiency).
28
Q
  1. What species may have normal or low phosphorous in the face of azotemia?
A
  1. Horses–due to decreased conservation of PO4 or to extra renal excretion of PO4 & cattle–renal excretion is a minor contributor compared to saliva and rumen.
29
Q
  1. In what types of renal dz are abnormal K and pH most commonly seen?
A
  1. Oliguric or anuric renal failure in either acute or terminal chronic state.
30
Q
  1. What are the typical electrolytes in azotemic cattle?
A
  1. Hypokalemia, alkalosis, hypochloremia, hyponatremia
31
Q
  1. What is the major route of amylase and lipase excretion/inactivation in the dog?
A
  1. Kidney
32
Q
  1. What is the refractive index of a solution?
A
  1. The ratio of the speed of light in a vacuum to the speed of light in the solution
33
Q
  1. Marked proteinuria and glucoseuria with do what to the USG?
A
  1. Overestimate the concentration of solutes (increase the USG). Each gram of protein/dL adds 0.003–0.005 to USG and each gram of glucose/dL adds 0.004 to 0.005 to the USG.
34
Q
  1. What are causes of impaired concentrating ability?
A
  1. ADH deficiency (central DI), lack of response to ADH (nephrogenic DI), solute overload, medullary washout (loop diuretics, prolong hyponatremia/hypochloremia, decreased urea production, prolonged diuresis)
35
Q
  1. What are causes of the following USG parameters?
A
  1. What are causes of the following USG parameters?
36
Q

a. USG >1.030 in an oliguric dog, >1.035 in oliguric cat, > 1.025 in oliguric horse/cow?

A

a. Nonrenal process leading to decreased renal perfusion

37
Q

b. USG <1.030 in dehydrated dog, <1.035 in dehydrated cat, < 1.020 in horse/cow?

A

b. renal concentrating defect

38
Q

c. USG=1.020–1.035 in polyuric animal

A

c. Diabetes mellitus (osmotic diuresis), partial diabetes insipidus, hypoadrenalcorticism, renal failure

39
Q

d. USG=1.007–1.013 in oliguric animal or polyuric animal

A

d. renal failure or end–stage renal dz. if azotemic, solute diuresis, decreased tubular response to ADH.

40
Q

e. USG=1.001–1.015 in polyuric nonazotemic animal

A

e. central DI, nephrogenic DI, Cushing’s, hypercalcemia, Addison’s, Pyometra, liver failure, Hypokalemia, hypoparathyroidism, feline hyperthyroidism, Psychogenic polydipsia, Thyroiditis

41
Q
  1. What is renal glucosuria?
A
  1. Normoglycemic glucosuria. Causes=acquired–renal tubular toxicosis or ischemia & congenital–Fanconi syndrome and pure renal glucosuria (basenji, Norwegian elkhound, Shetland sheepdog).
42
Q
  1. What form of bilirubin may be found in the urine?
A
  1. Conjugated bilirubin (unconjugated bilirubin may be seen in canine urine because of the normal presence of small amounts of albumin.
43
Q
  1. What number of leukocytes & erythrocytes may be found in urine?
A
  1. <5/hpf
44
Q

39.What are Tamm–Horsefall proteins?

A
  1. Mucoproteins secreted by epithelial cells of the loops of Henle, distal tubules, and collecting ducts that are thought to comprise the matrix of casts.
45
Q
  1. What types of casts may be seen in healthy animals?
A
  1. Hyaline or fine granular (<2/lpf), but a shower of casts may occur after physical activity
46
Q

41.What is cylindruria?

A
  1. Casts in the urine.
47
Q
  1. Name the common situation in which the follow casts are seen.
A
  1. Name the common situation in which the follow casts are seen.
48
Q

a. Hyaline

A

a. healthy animals and glomerular proteinurias. Form from conglutination of Tamm–Horsefall proteins

49
Q

b. Granular, cellular, or fatty

A

b. active tubular degeneration or necrosis. A few granular casts may be seen in healthy animals. Form when cellular debris or cells are trapped in Tamm–Horsefall mucoprotein

50
Q

c. Leukocyte or erythrocyte casts

A

c. inflammation or hemorrhage,

51
Q

d. Waxy casts

A

d. Uncommon and primarily in chronic renal disease. Form from the deterioration and solidification of granular casts.

52
Q

e. Hemoglobin and myoglobin casts

A

e. hemoglobinuria and myoglobinuria

53
Q

For urinary crystals see plate 6 in Stockham text.

A

For urinary crystals see plate 6 in Stockham text.

54
Q
  1. What are the values for protein:creatinine ratios in dogs?
A
  1. <0.5=healthy dogs; 0.5–1.0=borderline value
55
Q
  1. What are the causes of increased protein:creatinine ratios?
A
  1. Proteinuria due to overflow/prerenal, glomerular injury, tubular injury, inflammation, hemorrhage
56
Q
  1. What is prerenal/overflow proteinuria?
A
  1. A pathologic state that causes increased plasma concentration of a small protein that passes through the glomerular filtration barrier (paraproteins, hemoglobin, myoglobin, postcolostrum)
57
Q
  1. What ketones are detected by reagent strips?
A
  1. Acetoacetate (mostly) and acetone (less reactive), beta–hydroxybuterate is not detected by the reagent strip system (Bayer). While beta–hydroxybuterate is a ketone body it lack the chemical structure of ketones and is not detected in the reaction.
58
Q
  1. Why may prolonged ketonuria (excretion of acetoacetate or hydroxybuterate) cause hyponatremia or hypokalemia?
A
  1. Both ketones are anions and renal excretion obligates excretion of cations (Na or K) in conjunction with ketone excretion.
59
Q
  1. What are causes of an increased fractional excretion?
A
  1. Increased tubular secretion of analyte, decreased tubular resorption of analyte, increased plasma analyte concentration––>increased filtered load, decreased creatinine excretion
60
Q
  1. What are causes of decreased fractional excretion?
A
  1. Decreased tubular secretion, increased tubular resorption, decreased filtered load.
61
Q
  1. What does the fractional excretion of sodium do in cases of renal failure? In cases of prerenal azotemia?
A
  1. Renal failure=increased F.E. & decreased in prerenal azotemia.
62
Q
  1. What does increased fractional excretion of GGT mean?
A
  1. Indicates active renal tubular damage or necrosis.
63
Q
  1. What are the causes of an animal that does not demonstrate the ability to concentrate urine in the face of an abrupt water deprivation test?
A
  1. Medullary washout, nephrogenic DI, central DI

ACVP Phase II - Clinical Pathology (14 decks)

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