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RUSVM SAM II > Introduction to Urology (Rolph) > Flashcards

Introduction to Urology (Rolph) Flashcards

1
Q

Name some (or all) the functions of the kidneys.

A
  • Excretes waste
  • Retrieves filtered particles
  • Maintains acid/base balance
  • Regulates BP
  • Monitors/modifies oxygenation (erythropoietin production)
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2
Q

What 3 activities regulate fluid-electrolyte balance and where are they carried out?

A

Carried out by the nephron

  1. Glomerular filtration
  2. Tubular secretion
  3. Tubular reabsoprtion
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3
Q

What percent of cardiac output do the kidneys recieve?

A

25%

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4
Q

What does the high, constant renal blood flow allow for?

A
  • High = metabolic requirements and to maintain GFR
  • Constant = Excretion and homeostasis
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5
Q

What percentage of oxygen do the kidneys consume?

A

~8%

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6
Q

What are some conditions associated with decreased renal blood flow?

A
  • Volume depletion
  • Heart failure (abnormal circulation)
  • Hypotension (long-term kidney effects)
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7
Q

What condition is associated with increased renal blood flow?

A

Hypertension

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8
Q

What is the kidney’s role in controlling blood pressure?

A

Insert image, page 8

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9
Q

Where is antidiuretic hormone released from and what does it cause?

A

Released from posterior pituitary

  • Drop in blood pressure
  • Decreased blood volume
  • Beta-adrengergic stimulation
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10
Q

What are the ADH receptors and their effects?

A
  • V1 receptors → promotes vasoconstriction
  • V2 receptors → increased H2O reabsorption
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11
Q

Name the components of the nephron and label them.

A

Insert image, page 10

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12
Q

Where is angiotensin II (ang II) generated and what does it interact with?

A
  • Produced in afferent arteriole
  • Interacts w/ AT1 receptors on cellular components of nephron
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13
Q

Define renal disease.

A

Presence of morphological or functional lesions in one or both kidneys, regardless of extent

  • Renal disease ≠ azotemia
  • Renal disease ≠ renal failure
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14
Q

Define azotemia.

A

Abnormal increased in the blood concentration of non-protein nitrogenous wastes (NPN, i.e. urea and creatinine)

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15
Q

What are the types and causes of azotemia?

A
  • Pre-renal (perfusion): volume depletion, hypotension
  • Renal: Parenchymal disease, infection, cysts, infalmmation, neoplasia, toxin
  • Post-renal: obstruction or rupture of lower urinary tract
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16
Q

What is renal failure?

A

Clinical syndrome that occurs when kidneys are no longer able to maintain:

  • Regulatory function
  • Excretory function
  • Endocrine function
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17
Q

What biochemical changes can occur with renal failure?

A
  • Retention of nitrogenous solutes
  • Fluid, electrolyte, and acid-base derangements
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18
Q

When does renal failure occur relating to nephron population?

A

Renal failure occurs when > 75% of the nephron population is non-functional

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19
Q

The function of what is used to assess renal function?

A

Glomerular function

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20
Q

The glomerular filtration rate is (directly/indirectly) related to renal functional mass.

A

Directly

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21
Q

What are the accurate technqiues to assess renal function?

A
  • Clearance of radioisotopes w/ renal scintigraphy (best, most accurate)
  • Iohexal/inulin/creatinine clearance tests
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22
Q

What are the indirect methods for assessing renal function?

A
  • Serum urea levels
  • Sreum creatinine levels
  • Cystatin C
  • SDMA (Symmetrical dimethylarginine)
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23
Q

What are some characteristics of urea (synthesis, excretion, concentration)?

A
  • Synthesized in the liver
  • Excreted by the kidneys
  • Urea concentration in renal medulla helps maintain solute gradient
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24
Q

What are urea serum levels affected by?

A
  • Species/age
  • Liver function
  • Dietary protein content
  • Endogenous protein catabolism
  • Renal function
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25
Q

What are the limitations of urea?

A

Subject to passive reabsoprtion in tubules

  • Exacerbated by slower tubular flow rates → volume depletion
  • Urea clearance not relaible estimate of GFR
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26
Q

What can lead to false positives in urea?

A
  • GIT bleeding
  • Intravascular hemolysis
  • High protein diets
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27
Q

What is creatinine and its characteristics?

A

​Biproduct of conversion of creatine to creatine phosphate

  • Producted at a constant rate
  • Dependant on muscle mass (grayhounds vs. puppies)
  • Influenced less by diet
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28
Q

How is creatinine excreted?

A

Unchanged by the kidneys

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29
Q

How are serum creatinine concentrations affected?

A
  • Increased: reduced renal clearance
  • Decreased: reduced muscle mass, significantly in elderly or pateitns w/ cachexia
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30
Q

What are the limitations of creatinine testing?

A
  • Does not tell you why the GFR has decreased
  • Doesn’t discriminate between:
    • Causes of azotemia
    • Acute vs. chronic renal failure
    • Reversible or irreversible renal failure
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31
Q

Severity of clinical signs of azotemia are (directly/indirectly/not directly) proportional to magnitude of creatinine increase.

A

Not directly

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32
Q

What is cystatin-C and its characteristics?

A

Small polypeptide protease inhibitor produced by all cells with a nucleus

  • Freely filtered by glomeruli
  • Doesn’t undergo tubular secretion
  • Produced at constant rate in all tissues
  • Excretion not dependent on age, sex, diet, or muscle mass (debated)
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33
Q

What is the accuracy of cystatin-C versus creatinine and what may be detected early?

A

Possibly more accurate than creatinine

  • May detect early changes in GFR
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34
Q

What is cystatin-C potentiall affected by?

A
  • Neoplasia
  • Levels of C-Reactive Protein
  • Thyroid dysfunction
  • Glucocorticoid administration
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35
Q

What is SDMA and its characteristics?

A

Methylated form of amino acid arginine (produced in every cell and released into body’s circulation during protein degradation)

  • Excreted almost exclusively by kidneys
  • Correlates highly w/ GFR by inulin (r = 0.85)
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36
Q

How accurate is SDMA testing compared to creatinine?

A

Increased

  • 17 months earlier in cats
  • 9 months earlier in dogs

when there’s 40% decline in GFR

  • useful in cases w/ normal creatinine
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37
Q

What can alter SDMA levels?

A

Emergeing evidence suggests diseases like hyperthyroidism alter SDMA levels

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38
Q

When collecting urine for an urinalysis, what are the options?

A
  • Free flow
  • Catheterization
  • Cystocentesis
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39
Q

What are the advantages and disadvantages of each urine collection method?

A
  1. Free flow
    • Contamination potential
    • Non-invasive (used to r/o infection/check for glycosuria)
  2. Catheterization
    • Contamination potential
    • Difficult in female dogs, all cats
  3. Cystocentsis
    • Best method for culture
    • Blind vs. ultrasound guided
    • Can lead to slight increase in RBC urine content
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40
Q

How is a cystocentesis performed?

A
  • Ultrasound-guided or blind
  • Positioning: lateral, dorsal, standing (cats) or “turned sheep” (dogs)
  • Locate and stabilize bladder (DON’T SQUEEZE)
  • Wet the site w/ alcohol
  • Stabilize bladder w/ 1 hand
  • Hold syringe so you can aspirate w/o changing position
  • Confidently insert needle into bladder at 45 degree angle
  • Slowly aspirate until you have adequate volume of urine
    • If you don’t get urine, completely remove needle from abdomen
  • Once sample is obtained, release hand stabilizing bladder, THEN remove needle from abdomen
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41
Q

What are the main things to assess with a urinalysis and what’s used?

A
  • Color/clarity
  • Concentration
  • Dipstick
  • Sediment
  • Culture and sensitivity
  • Urine Protein to Creatinine Ratio
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42
Q

How is the concentration assessed in a urinalysis?

A
  • Osmolality
  • Estimated by USG
    • Hand-held vs. digital
    • Hyperosmolar substances alter USG
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43
Q

What is the “normal” range of urine concentration in dogs and cats?

A
  • Dogs: 1.030-1.065
  • Cats: 1.035-1.090
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44
Q

Why is the “normal” urine concentration range of cats problematic?

A

Upper limit is too high for most in-house refractometers to detect

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45
Q

What are the ranges for hyposthenuria and isosthenuria?

A
  • Hyposthenuria: < 1.009
  • Isosthenuria: 1.010-1.015
  • Hypersthenuria doesn’t really exist b/c it’s basically normal
46
Q

What’re normal and abnormal water intake levels?

A

40-60 mL/kg/day

  • Depends on diet and species
  • > 100 mL/kg/day = polydipsia
47
Q

What’s the dipstick’s main purposes, when is it not useful, and what affects it?

A
  • Designed for humans → problem w/ veterinary medicine
  • Not useful parameters: SG, nitrite, urolbilinogen, WBC
  • Affected by: icterus, drugs (e.g. vitamin C, oxyglobin), urine temperature
48
Q

When is bilirubinuria normal?

A

NORMAL dogs have bilirubinuria, NOT cats

49
Q

What is the urine pH, and what’s normal range for dogs and cats?

A

H+ ion concentration of urine

  • Normal dog and cat range: 6-7 (6.5)
50
Q

How is pH related to diet?

A
  • High protein = acid pH
  • High vegetable content = alkaline pH
  • pH tends to ride after a meal (‘alkaline tide’)
51
Q

What can pH be associated with?

A
  • Crystals
  • Calculi
52
Q

What conditions are associated w/ alkaline urine?

A
  • Respiratory alkalosis
  • Urinary tract infection
  • Urine retention
  • Alkaline tide
  • Tubular disorder
53
Q

What conditions are associated w/ acidic urine?

A
  • Respiratory acidosis
  • Severe vomiting
  • Ketoacidosis
  • Ethylene glycol toxicity
  • Azotemia
54
Q

How common is proteinuria?

A

Normally, minimal protein found in urine

  • Range from: 1+ to 4+
55
Q

What are the different etiologies for proteinuria?

A
  • Inflammation and infectious
  • Gross hematuria
  • Chronic renal failure
  • Protein-losing nephropathies
    • GN, nephrotic syndrome, amyloidosis
    • [Multiple myeloma (Benz Jones proteins)]
56
Q

How is urine protein:creatinine ratio used?

A

Quantify the amount of protein present

57
Q

What is the reference range for urine protein:creatinine ratio in dogs and cats?

A
  • Dogs: <0.5
  • Cats: <0.4
58
Q

What are some conditions that increase protein/cause proteinuria?

A
  • Infections
  • Inflammation
  • HAC
59
Q

Is glucosuria normal or abnormal?

A

Glucose should NOT be present in normal urine

60
Q

How does glucosuria affect the USG?

A

Glucosuria elevates the USG

61
Q

What’s the renal threshold of glucose in dogs and cats?

A
  • Dogs: 10-12 mmol/L
  • Cats: 10-16 mmol/L
62
Q

When assessing glucosuria, what should you check for?

A
  • Ketones (ketonuria)
  • Blood glucose levels
63
Q

What conditions can cause glucosuria?

A
  • Diabetes mellitus
  • Hyperglycemia (stress induced)
  • Renal tubular diseases (i.e. Fanconi syndrome)
  • Infections (pyelonephritis, leptospirosis)
  • Drugs (alpha-2 adrenoceptor agonists, Gentamycin, Chlorambucil [cats], Tetracycline exposure)
  • Toxicixities (copper storage hepratopathy, ethylene glycol, lead, grapes, raisins, lilies)
  • False + on dipstick associated w/ amoxicillin, cephalexin, enrofloxacin exposure
64
Q

Is ketonuria normal?

A

NO

  • Ketones should not be present in normal urine
65
Q

What ketone(s) does a dipstick measure and what are the sensitivities and specificities, if applicable?

A

Dipsticks measure

  • Acetoacetate
  • Plasma ketones (100% sensitivity, 88% specificity)
  • Urine ketones (82% sensitivity, 95% specificity)
66
Q

What ketone is mainly produced in dogs and cats, and how is that measured?

A

Beta-hydroxybutyrate

  • Can convert ot acetoaxetate w/ H2O2 (measure w/ dipstick)
67
Q

What are the differentials for ketonuria?

A
  • Diabetes mellitus w/ DKA
  • High fat diets?
  • Starvation?
  • Drugs (N-acetylcysteine, Captopril, Penicillamine)
68
Q

Is bilirubinuria normal?

A
  • Normal in dogs (conjugate bilirubin in kidneys)
  • Abnormal in cats (renal threshold x9 of dogs)
69
Q

What are the causes of bilirubinuria?

A
  • Liver disease
  • Cholestasis
  • Bile duct obstruction
  • Hemolytic diseases
  • Infections (Leptospirosis, FIP)
70
Q

What are the characteristics of urobilogen?

A
  • May normally be present inurine
  • Urine strip may be inaccurate
  • Intermittent excretion
  • Source: bilirubin conversion in gut
71
Q

How is urobilogen as an indicator of bile duct obstruction?

A

Poor indicator

72
Q

What are the different types of hematuria?

A
  • Gross (macroscopic)
  • Occult (microscopic)
  • Pseudohematuria
73
Q

What are the differences between the types of hematuria?

A
  • Gross (macroscopic)
    • Sufficient blood to be seen w/ naked eye
    • Urine may appear brownish-red
    • Will increase UPC
  • Occult (microscopic)
    • Hematuria present but NOT visible to naked eye
  • Pseudohematuria
    • Red-brownish urine W/O intact RBCs
74
Q

What can cause pesudohematuria?

A
  • Hemoglobinuria
  • Myoglobinuria
  • Chemicals
75
Q

What are some causes of hematuria in general?

A
  • Systemic disorders (homeostatic defects)
  • Renal (neoplasia, calculi, truama, infarction, cysts, glomerulonephritis, infection)
  • Bladder, ureter, urethra (bacterial infection, calculi, trauma, neoplasia, polyps, cyclophosphamide therapy, feline idiopathic cystitis)
  • Genital tract (prostatic disease, estrus, infection, neoplasia, trauma)
76
Q

What should be investigated when hematuria is involved?

A
  • Determine site of hematuria
  • History
  • Clinical Examination
  • Bloods
  • Full urinanalysis including urine culture
  • Imaging
  • Cytoscopy
  • Vaginoscopu
  • Cytology (vaginal cytology, prostatic wash)
77
Q

What’s important in the history regarding hematuria?

A
  • Bleeding noted from other sites?
  • Trauma?
  • Exposure to anticoagulant rodenticides?
  • Timing of occurrence of blood (throughout urination or only at end)?
  • Color of mucous membranes, urine, etc.
78
Q

What’s important to check in the clinical examination when hematuria is involved?

A
  • Other hemorrhage sites?
  • Examine feces?
  • Palpate kidneys and bladder
  • Digital rectal examination
  • Check blood pressure
79
Q

What blood testing should be performed with hematuria?

A
  • Hematology, blood smear
  • Biochemistry
  • Clotting times
80
Q

What imaging should be performed when investigating hematuria and what should be looked at?

A
  • Ultrasound kidney, bladder, prostate
  • Double contrast pneumocystogram w/ retrograde urethrogram (bladder, urethra)
81
Q

What’s the process of examining urine sediment?

A
  1. If dilute, centrifuge urine at low speed (2-3000 rpm) before examination
    1. Discard supernatant, leaving 0.2-0.5 mL in tube
    2. Resuspend last few drops in supernatant (aspirate w/ pipette)
  2. Place drop onto slide (± add drop of sedi-stain)
  3. Add coverslip (optional)
  4. Use subdued microscope lighting (condenser must be lowered nad iris diaphragam partically closed for optimal viewing/conspicuous constituents)
82
Q

Where do casts seen in sediment examinations form?

A

DCT and ducts

83
Q

What are hyaline casts and when are they formed?

A

Composed of solidified Tamm-Horsfall mucoprotein

  • Low urine flow states
  • Concentrated urine
  • Acidic environments
84
Q

How are granular casts developed?

A

Can develop either from

  • Breakdown of cellular casts OR
  • Inclusion of aggregates of plasma proteins (e.g. albumin or immunoglobulin light chains)
85
Q

What are waxy casts and when are they seen?

A
  • Considered final stage of cellular cast degeneration
  • Usually seen in tubular injury (common w/ chronic renal disease, renal amyloidosis)
86
Q

What are fatty casts and when are they seen?

A

Hyaline casts w/ fat globule inclusions formed by the breakdown of lipid-rich epithelial cells

  • Tubular degeneration
  • Nephrotic syndrome
  • Hypothyroidism
87
Q

What’s important about crystalluria and its presence?

A
  • Some crystals (struvite, calcium oxalate) can occur in normal urine and can precipiate rapidly as it cools or evaporates on a slide
  • Important not to overinterpret significance when seen in low numbers or when there’s no evidence of stone formation or secondary infection
88
Q

Name the different types of crystals and if they’re concerning or not.

A

Insert images

89
Q

What imaging techniques can be used to image the urinary tract?

A
  • Ultrasonography
  • Radiography/CT
90
Q

When should ultrasonography be used to image the urinary tract?

A
  • Observing renal size and general morphology including mineralization
  • Assess bladder wall (possibly ureters)
    • 70% sensitive for cystolith identification
  • Assess prostate
91
Q

When should radiography/CT be used to image the urinary tract?

A
  • Assess renal size and location
  • Assess bladder and urethrea (double contrast pneumocystogram and retrograde urethrogram)
  • IVU can be performed (better on CT) to assess urine flow (care re nephrotoxicity)
92
Q

What’s important regarding renal biopsies?

A
  • Rarely indicated (won’t change tx or prognosis)
  • FNA inaccurate, but may be useful in suspected lymphoma
  • Try-cut or Surgical Biopsy preferred (may require EM if wanting to investigate closely)
93
Q

What are some etiologies of renomegaly?

A
  • Hydronephrosis (ureteral obstruction)
  • Neoplasia
  • Renal inflammation (acute nephropathy, acute phyelonephritis, FIP granulomas, leptospirosis)
  • Amyloidosis
  • Polycystic kidney disease
  • Portosystemic shunts
  • Acromegaly
94
Q

What’s the occurrence of renal neoplasia and the different types with associated conditions?

A
  • Relatively uncommon in dogs (less so in cats)
  • Primary
    • Renal adenocarcinoma
    • Renal lymphoma
    • Renal sarcoma
    • Nephroblastoma (very rare)
  • Metastatic renal neoplasia (rare; e.g. hemangiosarcoma)
  • Occasiona benign renal tumors (rare)
95
Q

What’s the occurence of renal carcinoma?

A

More common in dogs than cats

96
Q

What are some signs of renal carcinoma?

A
  • Few clinical signs in early stages
  • Hematuria and weight loss
  • Unilateral (usually) renomegaly
  • Rarely causes renal azotemia
  • Can cause polycythemia as paraneoplastic syndrome
  • Can cause hypertrophic osteopathy as paraneoplastic syndrome
97
Q

What is the polycythemia as a paraneoplastic syndrome in renal carcinoma due to and what can it cause?

A
  • Due to erythropoietin production by tumor or due to renal hypoxia
  • Can cause neurological signs
98
Q

How do you diagnose renal carcinoma?

A

Ultrasound-guided biopsy

99
Q

What percentage of renal carcinoma patients have metastases at diagnosis?

A

50%

100
Q

How do you treat renal carcinoma?

A
  • Ensure sufficient function in contralateral kidney (IVU)
  • Nephrectomy (remove all of part of kidney)
101
Q

What’s the prognosis of renal carcinoma?

A

MST (dogs): 16 months w/ tx

102
Q

Renal lymphoma is (more/less) common in cats then dogs and (may/may not) affect both kidneys.

A
  • More common in cats than dogs
  • May affect both kidneys
103
Q

How does renal lymphoma present?

A
  • Renomegaly
  • Weight loss
  • Inappetence
  • PU/PD
  • Commonly causes renal azotemia
104
Q

Where does renal lymphoma usually spread?

A

Tendency to spread to CNS OR nose

105
Q

How do you diagnose renal lymphoma?

A
  • Renal ultrasound
  • FNAs of kidneys
106
Q

What’s the treatment for renal lymphoma?

A
  • Multi-agent chemotherapy (COP or CHOP)
  • Azotemia may resolve w/ tx
107
Q

What’s the prognosis of renal lymphoma?

A
  • ~60% go into complete remission (cats)
  • MST (cats): 91 days w/ tx
108
Q

How is polycystic kidney disease shared and who’s affected?

A

Affects Persian and Persian cross cats

  • Autosomal dominant gene
  • Mutation in PKD-1 gene
  • Occasional cases of PKD in cats/dogs W/O PKD-1 gene mutation
109
Q

How can the spread of polycystic kidney disease be slowed?

A
  • Genetic testing available
  • Breeding program (lead to marked reduction in prevalence)
110
Q

What’s the diagnostic sign of polycystic kidney disease and how is it seen?

A
  • Multiple cysts form in both kidneys
  • Increase in size and # over time
  • Seen on ultrasound
111
Q

What’s a negative implication of polycystic kidney disease?

A

Can cause renal failure in adulthood

112
Q

What other breeds are affected by inherited polycystic kidney disease?

A
  • Bull terriers
  • Cairn terriers
  • WHWT

RUSVM SAM II (4 decks)

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