Urinary Tract Disease Flashcards

1
Q

Define: azotemia

A

abnormal increase in the concentration of non-protein nitrogenous wastes in blood

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2
Q

How much must GFR decrease before azotemia develops?

A

25%

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3
Q

How much of the nephron population must be non-function for renal failure to occur?

A

75%

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4
Q

What general signs are associated with renal disease?

A

o PU/PD, dehydration, melena/hematemesis/vomiting
o Anorexia / GI signs / weight loss (uremia causes GI ulceration)
o Pale mucous membranes (EPO not produced)
o Lethargy
o Blindness (angiotensin II —> vasoconstriction —> high BP)
o Distended abdomen

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5
Q

Define: uremia

A

the clinical signs and biochem abnormalities associated with critical loss of functional nephrons

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6
Q

Differentiate gross hematuria, occult hematuria, and pseudohematuria.

A

Gross (macroscopic) - sufficient blood to be apparent to the naked eye

Occult (microscopic) - present but not visible to the naked eye

Pseudo - red to brown urine w/o intact RBC, instead d/t hemoglobin, myoglobin, or chemicals

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7
Q

What is the gold standard measurement of GFR?

What indirect measurement is most commonly used?

A

Clearance of radioisotopes with renal scintigraphy

Serum creatinine

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8
Q

What are the 4 limitations of using creatinine as a measure of GFR?

A
  1. does not tell you why GFR has fallen
  2. does not discriminate between causes of azotemia, ARF/CRF, or reversible/irreversible renal failure
  3. severity of CS are not directly proportional to magnitude of increase
  4. cannot prognosticate magnitude of azotemia
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9
Q

What parameters (5) are evaluated on a urine dipstick?

A
Protein
pH
Blood
Glucose
Ketones
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10
Q

What is considered ‘normal’ SpGr of urine in the dog and cat?

A

Dog >1.030

Cat >1.035

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11
Q

What is assessed with fractional excretion of electrolytes?

Which electrolyte is most commonly analyzed?

A

Assessment of tubular dysfunction

Na-fractional excretion (compared to Cr) differentiates prerenal (1%) disease

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12
Q

How is proteinuria detected?
What are the parameters to diagnose proteinuria in cats and dogs?
What condition might give a false positive in this test?

A

UPC

Cats >0.4 (0.2-0.4 borderline)
Dogs >0.5 (0.2-0.5 borderline)

LUTD causes false positive

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13
Q

What are 5 main ddx for renomegaly?

A
  1. Neoplasia
  2. Renal inflammation
  3. Amyloidosis
  4. Hydronephrosis
  5. Portosystemic shunts
  6. Polycystic kidney disease
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14
Q

Which renal tumors are more common in dogs?

Describe the CS, Dx, Tx, and prognosis.

A

Adenocarcinoma
♣ CS: few early on (only affects one kidney), hematuria, weight loss, unilateral renomegaly, rarely azotemia, polycythemia (paraneoplastic), hypertrophic osteopathy (paraneoplastic)
♣ Dx: renal US with FNA
♣ Tx: nephrectomy
♣ Prog: MST 16 months with treatment, ~50% have metastases at diagnosis

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15
Q

Which renal tumors are more common in cats?

Describe the CS, Dx, Tx, and prognosis.

A

Lymphoma
♣ Usually affects both kidneys
♣ CS: renomegaly, weight loss, inappetence, PU/PD, renal azotemia, tends to spread to CNS
♣ Low to moderate association with FeLV infection
♣ Dx: renal US with FNA
♣ Tx: multi-agent chemotherapy (COP or CHOP), may resolve the azotemia
♣ Prog: 60% complete remission, MST 91 days with treatment

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16
Q

Is acute kidney injury considered reversible?

A

Yes

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17
Q

What parameters are assessed in IRIS staging of acute renal failure?

A

Blood Cr concentration

Non-oliguric / oligoanuric

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18
Q

Describe the first (initial) phase of acute renal failure

A
  1. Initial (onset)
    - no clinical signs
    - usually triggered by an ischemic event
    - definable by a decrease in urine output or increase in creatinine
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19
Q

Describe the second (extension) phase of acute renal failure

A
  1. Extension
    - continued hypoxia and inflammation, damaging to PT and LOH
    - compromised Na/K pumps leads to cell swelling and death
    - increased cytosolic calcium
    - loss of brush border or apical and basal cell surfaces
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20
Q

Describe the third (maintenance) phase of acute renal failure

A
  1. Maintenance
    - 1-3 weeks duration
    - urine output may be increased or decreased
    - urine is ultrafiltrate
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21
Q

Describe the fourth (recovery) phase of acute renal failure

A
  1. Recovery
    - heralded by polyuria and extreme Na loss
    - may take months
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22
Q

What are the risk factors for ARF?

A
dehydration
hypovolemia
anesthesia
hypoxia
SIRS
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23
Q

What is normal urine output?

What is considered abnormal?

A

1-2 ml/kg/hour

Abnormal

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24
Q

What is normal CVP?

A

0-10 cmH2O

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25
Q

What fluid bollus should be given to patients at risk for ARF?

A

10-15 ml/kg crystalloids

2-5 ml/kg colloid

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26
Q

What 5 diagnostic parameters are indicators of ARF?

A
  1. Reduced urine output (abnormal 1%
  2. Renal tubular biomarkers
    o GGT(:Cr) present on the brush border in the tubule - increased GGT (compared to Cr) indicates tubular damage
    o N acetyl glutamate (NAG:Cr) found inside cells of proximal tubules - acute injury/swelling/rupture of cells indicates tubular damage
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27
Q

What fluid administration is appropriate to treat ARF?

A
  1. Correct shock: over 60 minutes, 15 minute interval boluses
    ♣ 60-90ml/kg (canine) / 45ml/kg (feline)
  2. Correct dehydration: over 6-12 hours, crystalloids (LRS, normosol R) or 0.9% NaCl (if hyperK+)
    ♣ % dehydration x 10 x BW = …mL
    ♣ Reduce sodium content once hydrated 0.45% NaCl + 2.5% dextrose
  3. Ongoing fluid requirements: maintenance usually around 60ml/kg/day, but in ARF urinary losses vary
    ♣ Insensible fluid loss = 22ml/kg/day
    ♣ Ongoing fluid losses = estimate vomiting, diarrhea, etc.
    ♣ Urinary losses = monitored directly (usually ~44ml/kg/day)
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28
Q

What is the shock dose of fluids in the dog and cat?

A

Dog 60-90ml/kg

Cat 45ml/kg

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29
Q

How are dehydration replacement fluids calculated?

A

% dehydration x 10 x BW = … mL

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30
Q

How much fluid is lost “insensibly”?

A

22ml/kg/day

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31
Q

How is mannitol used to treat oliguria?

When is it contraindicated?

A

Osmotic diuretic, increases circulatory volume

Contra: anuria, dehydration

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32
Q

How is furosemide used to treat oliguria?

When is it contraindicated?

A

Loop diuretic, inhibits Na/K/2Cl symporter in LOH and decreases Na/K/ATPase pump

Renoprotective d/t increased urine production without increased GFR

Contra: dehydration, lethargy, tachycardia, ototoxicity

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33
Q

How is dopamine used to treat oliguria?

When is it contraindicated?

A

May convert to non-oliguria
Only benefit as a pressor when ARF secondary to CO failure or severe hypertension

Contra: cats

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34
Q

How are Ca-channel blockers used to treat oliguria?

When is it contraindicated?

A

Pre-glomerular vasodilation

Renoprotective

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35
Q

What is extracorporeal renal replacement therapy (ERRT) and when is it indicated?

A

Artificial porous membrane with artificial hydrostatic and solute concentrations to prevent solute loss

Indications:
♣	Fluid overload with pulmonary edema
♣	Hyperkalemia
♣	Progressive azotemia
♣	Acute toxicity
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36
Q

What is the specific therapy for ARF caused by ethylene glycol?

A

4-methylpyrazole

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37
Q

What is the specific therapy for ARF caused by NSAIDs?

A

misoprostal

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38
Q

What is the specific therapy for ARF caused by leptospirosis?

A

penicillins and doxycycline

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39
Q

What is the specific therapy for ARF caused by pyelonephritis?

A

culture

fluoroquinolones or TMS (4-6 weeks)

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40
Q

What is the specific therapy for ARF caused by aminoglycoside toxicity?

A

ticarcillin IV

3rd gen penicillin, binds with gentamycin

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41
Q

What is the specific therapy for ARF caused by TMS toxicity?

A

urinary alkalinazation

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42
Q

How is hyperkalemia secondary to ARF managed?

A

insulin followed by dextrose

calcium gluconate

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43
Q

How is acidosis secondary to ARF managed?

A

HCO3 administration IV

calculated by base deficit x BW x 0.3

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44
Q

How is hypocalcemia secondary to ARF managed?

A

calcium gluconate 10%

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45
Q

How is hypercalcemia secondary to ARF managed?

A

diuresis / ERRT
furosemide / glucocorticoids
calcitonin
biphosphates

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46
Q

How is hyperphosphatemia secondary to ARF managed?

A

protein restriction diet

aluminum hydroxide/carbonate

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47
Q

Why is hypertension a complication of ARF?

How is hypertension secondary to ARF managed?

A

Secondary to RAAS activiation and fluid overload

amlodipine (Ca-channel blocker)
hydralazine (smooth muscle vasodilator)

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48
Q

How are GI symptoms secondary to ARF managed?

A

uremic gastropathy
-omeprazole, pantoprazole

prokinetics
-ondansteron, metoclopramide

antiemetics
-metoclopramide, maropitant

49
Q

What is the progression of chronic kidney disease, including when urine concentrating ability is impaired and when azotemia develops?

A
CKD
nephron disease and loss 
>66% loss =urine concentration impaired
>75% loss = azotemia
further progression, uremia
50
Q

Describe the (6) secondary effects of CKD and their etiologies.

A
  1. Failure of excretion of nitrogenous wastes –> uremia
  2. Failure of urine concentration –> PU/PD
  3. Failure to synthesize calcitriol –> hypoCa and renal secondary hyperPTH
  4. Failure to synthesize EPO –> anemia
  5. Failure to catabolize peptide hormones (eg. gastrin) –> uremic gastritis
  6. Production of renin to increase GFR –> systemic hypertension
51
Q

What is the general ‘clinical picture’ of a CKD patient?

A

PU/PD (+nocturia) and general NDR
Poor body condition
Pale mm
Small kidneys on palpation

52
Q

What is expected on urinalysis of a CKD patient?

A

Isosthenuria (1.008-1.030 in cats, 1.008-1.022 in dogs)
Possible concurrent UTI
Proteinuria

53
Q

What is expected on the biochemistry of a CKD patient? (5 components)

A
  1. Azotemia
  2. Hyperphosphatemia
    - may not be apparent in stage I and II d/t compensation to increase phosphate loss
  3. Hypokalemia
    - reduced intake and increased loss
  4. Calcium changes
    - iCa often low
    - hyperCa can occur secondary to renal failure or cause renal failure
    - high Ca and P = metastatic calcification
  5. Metabolic acidosis
    - reduced excretion of H+
54
Q

What is expected on hematology of a CKD patient?

What is the cause and what is the result of this abnormality?

A

Non-regenerative, normocytic, normochromic anemia

Cause (multifactorial):

  • EPO deficiency
  • decreased life span of RBC
  • effect of PTH on bone marrow
  • anemia of chronic dz
  • GI hemorrhage

Effect:
-lethargy, inappetance, hypoxia

55
Q

What factors affect how blood pressure is measured? (type of measurement, size of cuff)

A

Oscillometric - large patient
Doppler - small patient

cuff size 30-40% of circumference

56
Q

What are the general goals of management of CKD by IRIS staging?

A

Stage I: identify primary dz and start specific therapy

Stages II-III: renoprotective therapy to slow progression

Late stage III-IV: symptomatic

57
Q

How is pyelonephritis (UTIs) secondary to CKD treated?

A

Abx 4-6 weeks, must have renal excretion and UUT penetration

eg) amoxicillin, cephalosporins, TMS, fluoroquinolones

58
Q

How is dehydration secondary to CKD treated?

A

Control losses (vomiting/diarrhea)
Short term: fluids (IV/SQ)
Long term: oral/SQ fluids, feeding tube placement

59
Q

How is anorexia secondary to CKD treated?

A

Appetite stimulants:
cyproheptadine (cats)
mirtazapine (cats and dogs)

60
Q

At what IRIS stage of CKD is a renal diet indicated for dogs / cats?

A

Dogs - stage III

Cats - stage II

61
Q

How is anemia secondary to CKD treated?

What treatment should NOT be used?

A

EPO therapy (rHuEPO or darbopoeitin-alpha) indicated for symptomatic animals with PCV

62
Q

How is hypertension secondary to CKD treated in dogs / cats?

A

Dogs: ACE inhibitors (benazepril)
Cats: Ca channel blockers (amlodipine)

Angiotensin receptor blocker (Telmisartan) also licensed for reduction of proteinuria associated with CKS in cats

63
Q

What is ‘acute on chronic’ kidney disease?

How is it managed?

A

CKD + inciting cause of AKD

Identify and treat underlying cause

Treat dehydration and optimize GFR with IV fluids

Monitor urea, Cr, P, and electrolytes

64
Q

What is the prognosis for dogs / cats with CKD?

A

Dogs: up to 1-2 years
Cats:
-IRIS stage II MST 2 years
-IRIS stage IV MST 1 month

65
Q

What are the 3 component of a glomerulus?

A
  1. Juxtaglomerular cells: release renin
  2. Mesangial cells: endothelial cells holding capillary beds together
  3. Bowman’s capsule: parietal layer of epithelial cells + podocytes surrounding capillary beds
66
Q

What are the causes of proteinuria?

A

Physiological - strenuous exercise, seizures, fever, stress

Pre-renal - abnormal concentrations of proteins presented to kidney

Renal - defected renal function or inflammation (glomerular/tubular)

Post-renal - inflammation of the ureter, bladder, urethra, or prostate

67
Q

What is the first diagnostic test that will pick up proteinuria?

A

Urine dipstick

68
Q

Which protein is the urine dipstick most sensitive to?

What can give false negatives and positives?

A

Albumin

False positive:
alkaline urine
contamination

False negative:
acidic urine
Bence-Jones proteins (multiple myeloma)

69
Q

How is proteinuria quantified?

What value is considered proteinuria in dogs /cats?

A

24-hr urine protein measurement (gold standard, but rarely done)

UPC (can only evaluate if urine sediment negative)

Dogs: >0.5
Cats: >0.4

70
Q

What UPC values generally indicate PLNs (glomerular pathology)?

71
Q

What is the main pathology in glomerulonephritis?

A

Immune complexes deposited in the glomeruli

72
Q

What are the 4 etiologies for glomerulonephritis?

A
  1. Chronic antigenic stimulation (inflammation, infection, neoplasia)
  2. Idiopathic
  3. Familial
    - X-linked hereditary PLN of Samoyeds
    - Alport syndrome of cocker spaniels
  4. Amyloid depositis
73
Q

(In addition to history, PE, and MDB) What is involved in the workup for glomerulonephritis?
(4 components)

A
  1. Systolic blood pressure
    - low protein, edema
    - high protein, end-organ damage
  2. 4Dx (Borrelia, Dirofilaria, Ehrlichia, Leishmania)
  3. Screen for neoplasia
  4. Hypercoagulability test
    - thromboelastography (direct)
    - PLT, antithrombin, fibrin, d-dimers (indirect)
74
Q

What is nephrotic syndrome?

A

Kidney disease characterized by edema and loss of protein from the plasma into urine d/t increased glomerular permeability

  1. Proteinuria
  2. Hypoalbuminemia
  3. Ascites
  4. Hypercholesterolemia
    Often systemic hypertension
75
Q

How is glomerulonephritis treated?

What considerations should be made regarding the tx?

A

Immunosuppresive therapy

  1. Mycophenolate (DOC)
  2. Glucocorticoids

Indicated when proteinuria is confirmed to be glomerular in origin and a biopsy confirms ICGN

Contraindicated with pancreatitis, bone marrow suppression, DM

76
Q

How is hypercoagulability secondary to glomerulonephritis treated?

A

Aspirin

Clopidogrel

77
Q

What are the 4 outcomes possible with urethral obstruction?

A
  1. Acute unilateral (clinically silent)
  2. Acute bilateral (uncommon, emergency)
  3. Big kidney-little kidney (past obstruction causing one kidney to become fibrotic, subsequent obstruction of contralateral)
  4. Bilateral CKD + ureteral obstruction (most guarded prognosis)
78
Q

What signalment is associated with ureteral obstruction?

A

Cats > 7 years

79
Q

What clinical signs are associated with ureteral obstruction?

A

Acute uremia
Anorexia, depression
Vomiting
Oligo/anuria

80
Q

What diagnostic tests can be used in ureteral obstruction cases?

A

Rads (don’t confuse with normal renal pelvic calcification)
US (hydronephrosis)
CT

81
Q

How is ureteral obstruction managed (4 options)

A
  1. Medical (20-30% resolve within 3-4 days)
    - fluids and pain management
    - mannitol for oliguria
    - prazosin and amitryptilline (ureteral relaxants)
  2. Lithotripsy (excellent in dogs, poor for cats)
  3. Ureteral stents (standard of care!)
  4. SUB
82
Q

What are 3 etiologies for urethral obstruction?

A
  1. Idiopathic cystitis/urethritis
  2. Cystic calculi
  3. Decreased luminal diameter (stricture, idiopathic urethritis, urethrospasm)
83
Q

How is urethral obstruction diagnosed?

A
  1. Enlarged bladder (esp. male cats)
  2. Signs of forced urination
  3. Difficulty in manually expressing urine
  4. Resistance during passage of urethral catheter
84
Q

What initial stabilization and testing should be done with urethral obstruction?

A
Heat
Fluids
ECG (hyperK common)
BUN/Cr, lytes, acid/base
Therapeutic cystocentesis
85
Q

How is hyperkalemia treated in an emergency?

4 options

A
  1. Shock rate fluids
  2. Calcium gluconate for cardioprotection
  3. IV insulin
  4. Bicarbonate (not required unless severely acidotic)
86
Q

How is urethral obstruction managed?

A

Preparation:

  • anesthetize
  • cytocentesis
  • penile extrusion
  • catheterization
  1. Retrograde flushing
  2. Penile/rectal massage
87
Q

What clinical signs are associated with non-obstructive LUT disease?

A

Dysuria, pollakiuria, periuria, stranguria, pigmenturia
Incomplete voiding
Urinary incontinence

88
Q

What does yellow/orange urine indicate?

Red urine?

A

Yellow/orange: bilirubin

Red: hematuria, hemoglobin, myoglobin

89
Q

DDx for hematuria (source of blood)

A

Renal
LUT
Reproductive (prostatic, vaginal, uterine)
Systemic dz (bleeding disorder, hypertension, hyperviscocity)

90
Q

What two bacterial types are most commonly found in UTIs?

A

E. coli, gram+ cocci

91
Q

How are uncomplicated UTIs treated?

A

Amoxicillin, cephalosporins, TMS
10-14 days

HDSD of enrofloxacin

92
Q

What is a reinfection UTI and how is it treated?

A

New or different organism found >7 days after tx course

Nitrofurantoin good choice

  • bedtime admin at 30-50% original dose
  • culture q4 weeks during tx -q1 month for 3 months after tx
  • q3 months for 1 year
93
Q

What is a superinfection?

A

New or different organism found at day 7 after beginning tx

94
Q

What is a relapse infection?

A

Same organism found 7 days after tx course

95
Q

T/F, crystalluria = urolithiasis

A

False, it may indicate urolithiasis or may simply indicate urine has been supersaturated

96
Q

What signalment and predisposing factors are associated with struvite crystals?

A

Schnauzer, Lassa apso, cocker spaniel, shit tzu, bisson friesse

Dogs: UTIs with urease-producing bacteria and high urine pH
Cats: alkalinizing agents in diet

97
Q

How are struvite crystals treated?

A

Dietary (Hills s/d) to acidify

98
Q

What signalment and predisposing factors are associated with calcium oxalate crystals?

A

Schnauzer, Lassa apso, mini poodle, yorkies, shit tzu, bisson friesse

Male dogs
Obesity
Acidic urine
Hyperparathyroid (hyperCa in urine)

99
Q

How are CaOx crystals treated and prevented?

A

Tx: surgical
Px: Diet (Hills U/d) with potassium citrate
Thiazide diuretics (hydrochlorothiazide)
Potassium citrate

100
Q

What breeds are associated with cysteine crystals?

A

Australian cattle dogs, Daschnunds, Newfoundlands, bulldogs

101
Q

How are cysteine crystals treated?

A
Alkalinize urine (Hills u/d)
Thiol drugs to bind cysteine
102
Q

What signalment and predisposing factors are associated with urate crystals?

A

dalmatians, black Russian terrier, bulldog

Hepatic dz
Genetic tubular defects
Male dogs
Acidic urine

103
Q

How are urate crystals treated?

A

Tx hepatic dz
Hills u/d
Xanthin oxidase inhibitors for Dalmatians (allopurinol)

104
Q

What are the risk factors for FLUTD?

A
Age 2-6 years
Litter box use
Dry cat food
Inactivity and obesity
Stress
Spring / winter
105
Q

What are the clinical signs of FLUTD?

A

Hematuria, stranguria, pollakiuria, inappropriate urination
Palpable large firm bladder
Inability to urinate or periuria

106
Q

What is expected in a FLUTD urinalysis?

A

Protein, blood, crystals

Negative bacterial culture

107
Q

How is FLUTD treated?

A

Environmental enrichment
Dislodge obstructions
Opioids as needed

108
Q

What types of neoplasia are found in the LUT?

A

TCC (most common)
-Scotties predisposed

Leiomyoma/sarcoma
SCC
Adenocarcinoma
Fibrosarcoma
Hemangiosarcoma
109
Q

What treatment is indicated for TCCs?

A

Surgical if small and does not involve trigone

Chemo (mitoxane +/- piroxicam)
Photodymanic therapy
Urine diversion

110
Q

Describe the urinary cycle

A

Passive phase of filling (reservoir)
o Innervated by L1-4 (hypogastric)
♣ Activate beta-receptors to allow stretching
♣ Activates a1-receptors of the trigone and proximal urethra
♣ Blocks PSNS outflow

Active phase (voiding)
o Reflex: stretch receptors pelvic n. spinal cord brain stem PSNS outflow (pelvic n. S1-3)
o Contraction of muscle fibers of bladder wall
o Inhibition of pudendal n. decreased urethral sphincter tone
♣ Can be overridden by the cerebrum

111
Q

How does UMN disease cause micturition disorders?

How is this dx and tx?

A

Detrusor areflexia with sphincter hyperreflexia

Dx: bladder difficult to express
Tx: baclofen (antispasmotic)

112
Q

How does LMN disease cause micturition disorders?

How is this dx and tx?

A

Detrusor areflexia and sphincter areflexia

Dx: bladder easily expressed, constant leakage

Tx: bethanecol + manual expression

113
Q

How does detrusor-sphincter reflex dyssergia cause micturition disorders?
How is it tx?

A

Initiation of detrusor contraction causes urethral sphincter spasms

Tx: alpha-adrenergic blockers (phenoxybenzamine)

114
Q

How does detrusor atony cause micturition disorders?

How is this dx and tx?

A

Occurs d/t overfill (obstruction)

Dx: large flaccid bladder, normal neuro exam

Tx: manual expression, will resolve 7-10 days

115
Q

How does detrusor instability/hyperreflexia cause micturition disorders?
How is this dx and tx?

A

Contraction during storage of urine or low compliance of detrusor m.

Dx: cystometrography
Tx: anticholinergic drugs (oxybutynin, dyclomine)

116
Q

What disease causes 85% of incontinence cases?

A

Urinary Sphincter Mechanism Incompetence (SMI)

Intravesicular pressure (within bladder) > urethral pressure

117
Q

Describe the two etiological theories for urinary SMI

A

Pressure transmission theory
-when urethral neck not in abdominal cavity it is not subjected to the same pressures as the intra-abdominal bladder

Hammock theory
-anatomical structures maintaining the position of the bladder and urethra are abnormal

118
Q

How is urinary SMI diagnosed?

A

Urethral pressure profiles (if available)

CS, signalment, r/o other causes

119
Q

How is urinary SMI treated?

A

alpha-1 agonists (ephedrine, PPE)

Estriol - increases striated m. in sphincter

Collagen injection at cranial urethra

Surgical: artificial urethral sphincter placement