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77 Cards in this Set
- Front
- Back
What are some signs of lower urinary tract dz?
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dysuria
stranguria pollakiuria inappropriate urination hematuria |
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lower urinary tract dz: ddx for dogs w/o obstruction
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bacterial cystitis
cystoliths prostatic dz neoplasia bladder trauma |
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lower urinary tract dz: ddx for cats w/o obstruction
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idiopathic cystitis
cystoliths bacterial cystitis neoplasia |
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lower urinary tract dz: ddx for dogs w/ obstruction
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uroliths
neoplasia FB stricture trauma reflex dyssynergia muscle spasm |
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lower urinary tract dz: ddx for cats w/ obstruction
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urethral plug
urolith neoplasia stricture spasm reflex dyssynergia |
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tx for initial episode of UTI
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antibiotics
empirical selection (Clavamox, trimethoprim-sulfa, 1st gen. cephalosporins) or based on C/S: 10-14 days |
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tx for recurrent UTI
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-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 |
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tx for urethral obstruction
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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 |
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tx for acute pyelonephritis or prostatitis
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-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 |
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tx for feline interstitial cystitis (idiopathic cystitis)
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-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 -amitryptyline |
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struvite uroliths
a. tx b. prevention |
a.
-dissolve w/ diet: produces acidic urine, diuresis, restricted in P & Mg (s/d) -eliminate bacterial UTI -removal: sx or voiding UHP b. -prevent & control UTIs -encourage water consumption: consider canned diet -maintain acidic urine, dec. dietary intake of calculogenic salts (c/d) |
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calcium oxalate uroliths
a. tx b. prevention |
a. surgical removal
b. -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) |
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urate uroliths
a. tx b. prevention |
a.
-dissolve w/ diet: dec. protein & purine content, produces alkaline urine (u/d) -allopurinol -treat UTI -removal b. -u/d diet -inc. water consumption +/- canned diet - +/- allopurinol |
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cystine uroliths
a. tx b. prevention |
a.
-dissolve w/ diet: dec. protein, promotes diuresis, alkalanizes urine (u/d) -+/- 2-MPG: inc. solubility of cystine in urine -surgical removal b. -u/d diet -+/- 2-MPG |
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silicate uroliths
a. tx b. prevention |
a. surgical removal
b. -prevent ingestion of plant proteins (u/d) -inc. urine volume -alkalinize urine -discourage consumption of dirt or grass |
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neurogenic causes of incontinence
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LMN injury
UMN injury reflex dyssynergia detrusor areflexia |
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non-neurogenic causes of incontinence
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ectopic ureters
urethral obstruction urethral sphincter mechanism incontinence (USMI) detrusor hyperreflexia (urge incontinence) |
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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 bethanecol prevent urine scalding |
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UMN injury --> incontinence
a. signs b. tx |
a. distended bladder that is difficult or impossible to express --> paradoxical incontinence
b. phenoxybenzamine diazepam catheterize bladder repeatedly prevent urine scalding |
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reflex dyssynergia
a. signs b. tx |
a.
-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 b. -+/- catheterization phenoxybenzamine diazepam |
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detrusor areflexia
a. signs b. tx |
a. atonic bladder d/t urethral obstruction, UMN lesion, reflex dyssynergia
b. catheterization bethanecol |
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ectopic ureters
a. signs b. tx |
a.
young females continuously dribble urine b. surgery |
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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 |
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USMI
a. signs b. tx |
a. older spayed females
incontinence most pronounced when animal is asleep or relaxed b. DES, PPA |
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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) |
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Define renal dz.
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morphologic or functional lesions of kidney(s)
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Define renal failure.
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accumulation of nitrogenous wastes & alterations in water, electrolyte & acid-base balance d/t ↓ functional renal mass
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Define renal insufficiency.
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loss of functional nephron mass b’twn 66.6% & 75%
animal can no longed produce concentrated urine, but is not yet azotemic |
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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) |
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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 |
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causes of pre-renal azotemia
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-↓ 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 |
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dx of pre-renal azotemia based on...
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concentrated urine: dogs > 1.030, cats > 1.035
urine sediment is inactive resolves quickly (24-48 hrs) w/ appropriate tx of underlying cause |
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causes of post-renal azotemia
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obstruction to urine outflow: calculi, stricture, foreign body, tumor
urinary tract rupture |
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dx of post-renal azotemia based on...
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hx: signs of uremia; dysuria, hematuria, paradoxical incontinence, fluctuations in urine volume (if outflow obstruction)
PE -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 |
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What tests are used to estimate GFR?
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plasma clearance of iohexol
endog. creatinine clearance exog. creatinine clearance plasma clearance of creatinine radioisotope studies |
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What tests measure renal tubular fn?
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urine SG & osmolality
fractional clearance of electrolytes ammonia challenge tests |
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Under what circumstances should renal bx be considered?
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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 |
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dx of renal azotemia based on...
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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 |
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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 |
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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) c. volume depletion (hypovolemia, severe dehydration, hemorrhage) dec. effective arterial volume --> hypotension (sepsis, pancreatitis) DIC d. bacterial pyelonephritis, lepto |
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What are some risk factors for developing ARF?
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older animals
pre-existing renal dz dehydration, ↓ renal perfusion diuretics, nephrotoxic drugs used concurrently |
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What are the therapeutic goals for tx of ARF?
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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 |
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What are the Cr values & proposed treatment regimens for stages 1-4 of chronic kidney dz?
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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 |
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What are the therapeutic goals for tx of CRF?
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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 |
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What are the 4 factors known to slow the progression of CRF?
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-feed renal diet
-↓ magnitude of proteinuria -monitor & manage systemic hypertension (BP > 170 --> ↑ rate of progression) manage renal 2º hyperparathyroidism |
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How would you approach conversion of oliguria to non-oliguria in ARF patients?
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-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 *euthanasia |
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When & how would you tx acid-base disturbances assoc. w/ renal failure?
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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 |
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hyperkalemia
a. clinical signs b. tx |
a. weakness, cardiac arrhythmias, EKG changes, ileus, & vomiting
b. 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) |
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hypokalemia
a. clinical signs b. tx |
a.
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 b. potassium gluconate PO potassium citrate PO: manages hypokalemia AND acidosis |
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tx of hyperphosphatemia
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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) |
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What are the important factors in dietary management of CRF?
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-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) |
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anemia
a. clinical signs b. tx |
a. weakness, lethargy, anorexia, cold intolerance
b. 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 |
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tx of GI distress d/t uremia
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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 |
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hypertension
a. results if uncontrolled b. tx |
a. ocular abnormalities (incl. blindness), CV changes, cerebrovascular hemorrhage, progressive ↓ in renal function, ↑ morbidity
b. 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 |
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causes of pre-glomerular proteinuria
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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 |
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causes of post-glomerular proteinuria
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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 |
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causes of glomeruluar proteinuria
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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 |
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qualitative tests to detect proteinuria
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urine dipstick
bumin test |
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quantitative tests to detect proteinuria
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24 hr. urine protein content
urine protein:creatinine ratio microalbuminemia urine protein electrophoresis |
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What is the diagnostic approach to proteinuria?
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-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 |
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When would you suspect glomerular proteinuria vs. tubular proteinuria?
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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 |
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What are some historical & PE findings of glomerular dz?
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most commonly asymptomatic
edema/ascites evidence of predisposing dz thromboembolic dz systemic hypertension uremia: occassionally |
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Before considering a renal bx for protein losing nephropathy, what should you do?
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CONDUCT A COMPLETE SEARCH FOR NINs! (found in ~50% of cases)
Non-infectious inflammatory dz Infectious dz Neoplastic dz |
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What are the 4 components of nephrotic syndrome?
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hypoalbuminemia
proteinuria hypercholesterolemia edema |
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What are the main points of clinical management of proteinuria?
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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 |
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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 |
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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) |
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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 c. 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 d. congenital: thiazide diuretics acquired: tx underlying cause |
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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 |
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What are some iatrogenic causes of PU/PD?
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diuretics, glucocorticoids (dogs only), phenobarb
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When would a water deprivation test be considered?
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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) |
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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 |
a.
animal dehydrates rapidly (3-6 hrs) & does NOT produce concentrated urine responds to vasopressin by concentrating urine b. animal dehydrates rapidly (3-6 hrs) & does NOT produce concentrated urine does NOT respond to vasopressin c. 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 |
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ddx for glucosuria
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assoc. w/ hyperglycemia: DM, epi response (cats), acute pancreatic necrosis, dextrose administration
primary renal glucosuria renal tubular dysfunction (congenital or acquired) |
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primary renal glucosuria
a. cause b. effects c. dx |
a. 1º defect in glucose reabsorption
b. -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 |
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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 |
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What are some causes of acquired renal tubular dysfunction?
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aminoglycosides
pyelonephritis (~1/3 of these dogs will have glucosuria) chronic hypocalcemia copper storage dz lead toxicosis other tubular toxins |
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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 |