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77 Cards in this Set

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  • Back
What are some signs of lower urinary tract dz?
inappropriate urination
lower urinary tract dz: ddx for dogs w/o obstruction
bacterial cystitis
prostatic dz
bladder trauma
lower urinary tract dz: ddx for cats w/o obstruction
idiopathic cystitis
bacterial cystitis
lower urinary tract dz: ddx for dogs w/ obstruction
reflex dyssynergia
muscle spasm
lower urinary tract dz: ddx for cats w/ obstruction
urethral plug
reflex dyssynergia
tx for initial episode of UTI

empirical selection (Clavamox, trimethoprim-sulfa, 1st gen. cephalosporins) or based on C/S: 10-14 days
tx for recurrent UTI
-correct predisposing factors: owner compliance, medical, surgical
-antibiotics: based on urine C/S
treat for 30-45 days (sometimes up to 60 days)

-repeat U/A +/- culture: sometime during middle of ABs, then 5-10 d. after stopping
-ideally, want 3 neg. cultures over 3 months
tx for urethral obstruction
if weak & depressed: start fluids & do cystocentesis
else, relieve obstruction by placing urethral catheter
flush bladder
rehydrate (diurese if azotemic)
if can't relieve obstruction:
if stable --> PU
else --> cystostomy catheter
tx for acute pyelonephritis or prostatitis
-correct predisposing factors: owner compliance, medical, surgical
-antibiotics: based on urine C/S
treat for 30-45 days (sometimes up to 60 days)

-repeat U/A +/- culture: sometime during middle of ABs, then 5-10 d. after stopping
-ideally, want 3 neg. cultures over 3 months
tx for feline interstitial cystitis (idiopathic cystitis)
-acute, non-obstructive FIC resolves w/in 5-7 days, regardless of tx
-no tx effective in preventing recurrence
-can give SQ fluids to dilute urine or NSAIDs for pain, inflammation; don’t need ABs
-switch to canned diet
-environmental enrichment
struvite uroliths

a. tx
b. prevention
-dissolve w/ diet: produces acidic urine, diuresis, restricted in P & Mg (s/d)
-eliminate bacterial UTI
-removal: sx or voiding UHP
-prevent & control UTIs
-encourage water consumption: consider canned diet
-maintain acidic urine, dec. dietary intake of calculogenic salts (c/d)
calcium oxalate uroliths

a. tx
b. prevention
a. surgical removal
-diet: moderate protein restriction, Ca, oxalate, sodium, restriction (u/d)
-maintain less concentrated urine
-potassium citrate if needed to keep urine pH up
-prevent CaOx crystalluria (vitamin B6, thiazide diuretics)
urate uroliths

a. tx
b. prevention
-dissolve w/ diet: dec. protein & purine content, produces alkaline urine (u/d)
-treat UTI
-u/d diet
-inc. water consumption +/- canned diet
- +/- allopurinol
cystine uroliths

a. tx
b. prevention
-dissolve w/ diet: dec. protein, promotes diuresis, alkalanizes urine (u/d)
-+/- 2-MPG: inc. solubility of cystine in urine
-surgical removal
-u/d diet
-+/- 2-MPG
silicate uroliths

a. tx
b. prevention
a. surgical removal
-prevent ingestion of plant proteins (u/d)
-inc. urine volume
-alkalinize urine
-discourage consumption of dirt or grass
neurogenic causes of incontinence
LMN injury
UMN injury
reflex dyssynergia
detrusor areflexia
non-neurogenic causes of incontinence
ectopic ureters
urethral obstruction
urethral sphincter mechanism incontinence (USMI)
detrusor hyperreflexia (urge incontinence)
LMN injury --> incontinence

a. signs
b. tx
a. distended bladder that is EASY to express, absent or diminished perineal reflexes
b. frequent bladder expression or catheterization
prevent urine scalding
UMN injury --> incontinence

a. signs
b. tx
a. distended bladder that is difficult or impossible to express --> paradoxical incontinence

b. phenoxybenzamine
catheterize bladder repeatedly
prevent urine scalding
reflex dyssynergia

a. signs
b. tx
-male dogs
-distended bladder that is DIFFICULT to express, yet catheter passes easily
-initiation of urine stream is normal but stream is abruptly interrupted
-may dribble urine as walks after urination
-+/- catheterization
detrusor areflexia

a. signs
b. tx
a. atonic bladder d/t urethral obstruction, UMN lesion, reflex dyssynergia
b. catheterization
ectopic ureters

a. signs
b. tx
young females
continuously dribble urine
b. surgery
urethral obstruction --> incontinence

a. signs
b. tx
a. dribbling urine, straining to urinate w/o producing urine, restlessness, abdominal pain
b. relieve obstruction
+/- phenoxybenzamine, diazepam

a. signs
b. tx
a. older spayed females
incontinence most pronounced when animal is asleep or relaxed
detrusor hyperreflexia

a. signs
b. tx
a. pollakiuria, dysuria-stranguria, hematuria, intermittent dribbling, esp. when walking or after urination
b. tx primary disorder (ex. ABs for bacterial UTI)
Define renal dz.
morphologic or functional lesions of kidney(s)
Define renal failure.
accumulation of nitrogenous wastes & alterations in water, electrolyte & acid-base balance d/t ↓ functional renal mass
Define renal insufficiency.
loss of functional nephron mass b’twn 66.6% & 75%

animal can no longed produce concentrated urine, but is not yet azotemic
causes of:

a. ↑ BUN
b. ↓ BUN
a. ↑ production: high protein diets, upper GI hemorrhage, ↓ excretion

b. ↓ production: liver failure, low protein diets; ↑ excretion: diuresis (↓ tubular reabsorption)
causes of:

a. ↑ creatinine
b. ↓ creatinine
a. ↓ excretion; false ↑ can occur w/ diabetic ketoacidosis b/c acetoacetate contributes to measured creatinine independent of renal fn

b. ↓ production: rarely occurs w/ loss of muscle mass
causes of pre-renal azotemia
-↓ delivery of blood to kidneys: CHF
-↓ effective arterial volume
*intravascular volume loss or shift to ECF: hemorrhage, severe burns, pancreatitis, Addison’s, shock
*extravascular fluid loss: vomiting, diarrhea
*↑ vascular capacity: sepsis
-↑ protein catabolism: mild ↑ in BUN, normal creatinine (animal NOT uremic): GI hemorrhage, fever, burns, starvation, infection, azathioprine, exogenous corticosteroids, tetracyclines
-high protein diet: affects BUN only
dx of pre-renal azotemia based on...
concentrated urine: dogs > 1.030, cats > 1.035

urine sediment is inactive

resolves quickly (24-48 hrs) w/ appropriate tx of underlying cause
causes of post-renal azotemia
obstruction to urine outflow: calculi, stricture, foreign body, tumor

urinary tract rupture
dx of post-renal azotemia based on...
hx: signs of uremia; dysuria, hematuria, paradoxical incontinence, fluctuations in urine volume (if outflow obstruction)

-signs of uremia
-outflow obstruction: markedly distended bladder, inability to pass urinary catheter, renomegaly if hydronephrosis is present
-urinary tract rupture: bladder may be small or not palpable, abdominal fluid, abdominal pain

urine sediment: crystalluria, hematuria, pyuria

+/- hyperkalemia

in case of urinary tract rupture, abdominal fluid creatinine > serum creatinine
What tests are used to estimate GFR?
plasma clearance of iohexol
endog. creatinine clearance
exog. creatinine clearance
plasma clearance of creatinine
radioisotope studies
What tests measure renal tubular fn?
urine SG & osmolality
fractional clearance of electrolytes
ammonia challenge tests
Under what circumstances should renal bx be considered?
ARF, when appropriate medical management is ongoing & renal function deteriorates or oligoanuria is present
-consider bx to establish etiologic dx, facilitate prognostication

protein losing nephropathy (glomerular dz) when:
-no identifiable predisposing dz is present
-proteinuria persists several mos. after tx of potential predisposing dz
-owner interested in treating 1º dz & differentiation of type of glomerular dz becomes important
dx of renal azotemia based on...
confirmed by:
-azotemia + isosthenuria or minimally concentrated urine
-pre-renal & post-renal causes eliminated

supported by:
-hx & PE findings
-glucosuria w/o hyperglycemia
-moderate to severe proteinuria of renal origin
-moderate to severe cylinduria
-alkalinuria w/ concurrent systemic acidosis
-non-regenerative anemia
What is expected in acute vs. chronic renal failure?

a. duration of signs
b. BCS
c. palpation of kidneys
d. PCV
e. urine sediment
f. acid/base status
a. ARF: short, CRF: long
b. ARF: good, CRF: poor
c. ARF: normal to large, CRF: small & irregular
d. ARF: normal to inc., CRF: anemia
e. ARF: active, CRF: inactive
f. ARF: severe acidosis, CRF: less severe acidosis
What are some common causes of ARF in the following categories?

a. nephrotoxins
b. metabolic derangements
c. ischemia
d. infection/inflammation
a. ethylene glycol, aminoglycosides, amphotericin B
b. hypercalcemia, hypokalemia (cats)
volume depletion (hypovolemia, severe dehydration, hemorrhage)
dec. effective arterial volume --> hypotension (sepsis, pancreatitis)
d. bacterial pyelonephritis, lepto
What are some risk factors for developing ARF?
older animals
pre-existing renal dz
dehydration, ↓ renal perfusion
diuretics, nephrotoxic drugs used concurrently
What are the therapeutic goals for tx of ARF?
prevent further damage to kidneys
-remove inciting cause
-remove pre-renal & post-renal factors

production of diuresis: ↑ amt. of urine being produced
-acute injury kidney often results in ↓ urine output
-polyuric patients have better px

sustain patient’s life during recovery phase
What are the Cr values & proposed treatment regimens for stages 1-4 of chronic kidney dz?
stages 1-2: normal to mild azotemia
-stage 1: Cr < 1.4 (dog), < 1.6 (cat)
-stage 2: Cr < 2.0 (dog), < 2.8 (cat)
-stage 1 may have PU/PD, proteinuria
-evaluate & provide specific tx of 1º dz

stage 3: moderate azotemia (Cr < 5.0 (dog & cat))
-include therapy to delay progression

stage 4: severe azotemia (Cr > 5.0 (dog & cat))
-include tx for uremic signs
What are the therapeutic goals for tx of CRF?
alleviate clinical signs

dec. rate of progression
-eliminate obvious factors causing acute deterioration
-implement factors known to slow progression

work w/in owner's comfort zone
What are the 4 factors known to slow the progression of CRF?
-feed renal diet
-↓ magnitude of proteinuria
-monitor & manage systemic hypertension (BP > 170 --> ↑ rate of progression)
manage renal 2º hyperparathyroidism
How would you approach conversion of oliguria to non-oliguria in ARF patients?
-1st step: fluid diuresis to restore volume: replace w/in 6 hrs w/ replacement fluids
-if fluids alone don’t work --> diuretics (furosemide, mannitol)
if diuretics don’t work --> dopamine: used to combat reductions in renal blood flow that may contribute to pathogenesis of ARF; synergistic w/ furosemide; need continuous ECG monitoring
-if unable to convert:
*referral: hemodialysis, peritoneal dialysis
When & how would you tx acid-base disturbances assoc. w/ renal failure?
tx when pH < 7.20 or TCO2 < 12

ARF: sodium bicarbonate IV

stage 4 CRF
-sodium bicarbonate PO
-potassium citrate PO: may be used in hypokalemic cats

a. clinical signs
b. tx
a. weakness, cardiac arrhythmias, EKG changes, ileus, & vomiting
serum K = 6-8 mEq/L: fluid diuresis

serum K > 8 mEq/L or arrhythmias
-sodium bicarbonate
-insulin & dextrose: drives K into cells
-calcium gluconate: protects heart (used in emergency situations)

a. clinical signs
b. tx
hypokalemia can be cause or effect of CRF: excess K lost in urine
causes progression of renal failure: reversible ↓ in GFR
causes anorexia, vomiting, generalized weakness
muscle K becomes depleted --> ventroflexion of neck
potassium gluconate PO
potassium citrate PO: manages hypokalemia AND acidosis
tx of hyperphosphatemia
feed P restricted diet (renal diet): usually enough to control hyperphosphatemia in cats

phosphate binders: dogs usually end up needing these
-aluminum hydroxide
-calcium carbonate (Tums), calcium acetate, Epakitin: all contain Ca (don’t use if P is really high, or P x Ca may cause mineralization)

renal 2º hyperparathyroidism
-calcitrol: active form of vitamin D; provides negative feedback to PTH (may be needed in dogs (& some cats) w/ CRF & renal 2º hyperparathyroidism)
What are the important factors in dietary management of CRF?
-protein of high biologic value: amt. depends on degree of azotemia
-phosphorous restricted, moderate sodium restriction
-enhanced potassium (cats), water soluble vitamins, omega-3 fatty acids
-↑ caloric density
-↑ fiber content?

young dogs & cats: use geriatric diet (not as protein restricted)

a. clinical signs
b. tx
a. weakness, lethargy, anorexia, cold intolerance
PCV < 20-25% may warrant tx
-ARF patients: whole blood transfusions
-CRF patients: erythropoietin (human recombinant product), darbepoietin (new)
*can be costly
*can exacerbate hypertension
*must give w/ Fe
*clinically relevant Abs develop in ~1/3 of patients
*animals feel & eat better, have more energy
tx of GI distress d/t uremia
dietary protein restriction

H2 blockers (cimetidine, ranitidine, famotidine): used 1st b/c of low cost; can become resistant: make more receptors

proton pump inhibitors (omeprazole, esomeprazole)

anti-emetics used PRN during ARF or acute exacerbation of CRF

a. results if uncontrolled
b. tx
a. ocular abnormalities (incl. blindness), CV changes, cerebrovascular hemorrhage, progressive ↓ in renal function, ↑ morbidity
should be treated if sustained pressure > 170-180 mm Hg
-salt restricted diet
-ACE inhibitors (enalapril, benazapril): 1st choice; added benefit of reducing proteinuria; expect only 15% ↓ in BP; protects kidneys against Ca channel blocker
-Ca channel blockers (amlodipine): if ACE inhibition alone is ineffective
causes of pre-glomerular proteinuria
functional: uncommon in vet med
-mild, transient: abates when cause is corrected
-may progress to overt proteinuria
-strenuous exercise, seizures, fever, extreme heat or cold, stress, venous congestion (heart failure)

overload: uncommon
-tubular resorptive capacity for certain proteins exceed by high serum concentration
-ex. Bence Jones proteinuria (Ab fragments: myeloma), hemoglobinuria, myoglobinuria

hemorrhage or inflammation of ureter, bladder, urethra, prostate, prepuce, or vagina
causes of post-glomerular proteinuria
tubular proteinuria: ex. Fanconi’s syndrome
-failure of proximal tubule to resorb small molecular weight proteins
-distal nephron incapable of compensation
-USG would be isosthenuric or minimally concentrated
causes of glomeruluar proteinuria
destruction of normal filtration barrier

causes: amyloidosis, glomerulonephritis (membranoproliferative, proliferative, crescentric), membranous glomerulopathy, lupus nephritis, hereditary nephritis, minimal change glomerulopathy, focal segmental glomerulosclerosis

usually characterized by persistent proteinuria: higher amt. than w/ tubular proteinuria
qualitative tests to detect proteinuria
urine dipstick
bumin test
quantitative tests to detect proteinuria
24 hr. urine protein content
urine protein:creatinine ratio
urine protein electrophoresis
What is the diagnostic approach to proteinuria?
-evaluate urine sediment for hematuria & pyuria
-repeat screening test if urine sediment is WNL

if negative, consider:
-response to tx of post-glomerular dz
-functional proteinuria
-false positive: common

if positive, pursue quantitative assessment to R/O:
-glomerular proteinuria
-tubular proteinuria -overload proteinuria
When would you suspect glomerular proteinuria vs. tubular proteinuria?
glomerular: hypoalbuminemia, concurrent systemic infectious, inflammatory or neoplastic dz present, patient has renal azotemia but is not isosthenuric

tubular: normal serum albumin, glucosuria, inappropriate alkalinuria
What are some historical & PE findings of glomerular dz?
most commonly asymptomatic
evidence of predisposing dz
thromboembolic dz
systemic hypertension
uremia: occassionally
Before considering a renal bx for protein losing nephropathy, what should you do?
CONDUCT A COMPLETE SEARCH FOR NINs! (found in ~50% of cases)

Non-infectious inflammatory dz
Infectious dz
Neoplastic dz
What are the 4 components of nephrotic syndrome?
What are the main points of clinical management of proteinuria?
feed a renal diet
free access to water
limit stress
control edema: Na restricted diet, diuretics (spironolactone, furosemide), exercise
inhibit platelet function (when serum albumin < 2-2.5): low dose aspirin
control hypertension: ACE inhibitors +/- amlodipine
+/- fluid therapy if edematous or uremic: colloids
primary polydipsia

a. USG
b. ddx
c. tx
a. variable
b. hepatic failure (commonly seen w/ PSS), hypothalamic lesion, psychogenic (often have other behavior issues)
c. gradual restriction of water intake, tx other behavior issues
central diabetes insipidus

a. cause
b. USG
c. ddx
d. tx
a. lack of ADH: complete or partial
b. hyposthenuric
c. idiopathic, trauma, neoplasia, pituitary malformation, inflammation
d. give DDAVP (synthetic ADH)
nephrogenic diabetes insipidus

a. cause
b. USG
c. ddx
d. tx (acquired vs. congenital)
a. lacks of response of distal tubule & collecting duct to ADH: complete or partial
b. hyposthenuric
congenital: rare
acquired: most common cause of PU/PD (most partial)
-dogs: Cushing's, pyelonephritis
-cats: hypokalemia, hyperthyroidism
-also Addison’s, hepatic failure, pyometra, hypercalcemia, acromegaly, renal insufficiency/failure
congenital: thiazide diuretics
acquired: tx underlying cause
osmotic diuresis

a. cause
b. USG
c. ddx
a. too much solute going thru tubules --> osmotic overload
b. usually isosthenuric
c. DM, 1º renal glucosuria, renal insufficiency/failure, post-obstructive diuresis
What are some iatrogenic causes of PU/PD?
diuretics, glucocorticoids (dogs only), phenobarb
When would a water deprivation test be considered?
when dx for PU/PD not established by hx, PE, repeat USG, quantification of water intake, CBC/Chem, etc.
AND renal insufficiency has been ruled out (w/ iohexol clearance test to estimate GFR)
What are the expected results of a water deprivation tests w/

a. central DI
b. nephrogenic DI
c. Cushing's or psyschogenic PD
d. normal animal
animal dehydrates rapidly (3-6 hrs) & does NOT produce concentrated urine
responds to vasopressin by concentrating urine
animal dehydrates rapidly (3-6 hrs) & does NOT produce concentrated urine
does NOT respond to vasopressin
concentrate urine to range of minimal conc.
10-50% inc. concentration in response to vasopressin
d. animal dehydrates slowly (~40 hrs), then produces concentrated urine
ddx for glucosuria
assoc. w/ hyperglycemia: DM, epi response (cats), acute pancreatic necrosis, dextrose administration

primary renal glucosuria

renal tubular dysfunction (congenital or acquired)
primary renal glucosuria

a. cause
b. effects
c. dx
a. 1º defect in glucose reabsorption
-affected dogs may be asymptomatic
-PU/PD d/t ↑ osmotic load in tubules
-recurrent bacterial cystitis: glucose is substrate for bacterial growth
c. glucose present in all urine samples, fasting BG < 120 mg/dl
Fanconi's syndrome

a. breed most commonly affected
b. cause
c. effects
a. Basenjis
b. assoc. w/ multiple transport abnormalities
c. initially, only abnormal U/A, but slowly progresses to CRF
What are some causes of acquired renal tubular dysfunction?
pyelonephritis (~1/3 of these dogs will have glucosuria)
chronic hypocalcemia
copper storage dz
lead toxicosis
other tubular toxins
What type of urethrostomy is generally performed in:

a. dogs?
b. cats?
c. why performed?
a. scrotal
b. perineal
c. permanent urethral obstruction w/ stones or fibrosis