Urology Flashcards
cause of AKI
renal ischemia or exposure to nephrotoxins (NSAIDs)
pre-renal cause of AKI
- Anything that causes decrease in effective blood volume
- Arterial occlusion or stenosis of renal artery
- Increase in: BUN, creatinine and high USG, fractional excretion of Na = low
- USG measurement:
o USG > 1.030 dogs or USG > 1.035 cats
renal cause of AKI
- Ischemic events: shock, decreased CO, trauma, hyper(o)thermia, transfusion, DIC, NSAIDs
- Primary renal disease: infection, immune mediated, neoplasia
- Secondary disease with renal manifestation: infection, SIRS, sepsis, MOF, DIC, pancreatitis, hepatorenal syndrome
- Nephrotoxins: exogenous toxins, drugs, exogenous toxins
post renal cause of AKI
- Urinary leakage within tissue
- Urinary obstruction and increased pressure
- Azotaemia + variable USG + rapidly reversible if drainage provided
pathogenesis of AKI
- loss of ability to excrete water
- loss of ability to maintain fluid
- electrolyte disturbances
- acid-base disorder
- blood pressure changes
- loss of endocrine function
- Azotaemia – increase in concentration of nitrogen-containing substances in the blood
- Uraemia – azotaemia + adverse clinical manifestation
signs of AKI
non specific) Usually <1 week of anorexia, lethargy, nausea and/or vomiting, diarrhoea, PUPD
- Dehydration generally good BCS, uremic halitosis, oral ulcers, unspecific abdo pain or renal pain, renal enlargement
- MM pallor
normal GFR
- GFR
o normal dogs: 3.5-4.5 ml/min/kg
o normal cats: 2.5-3.5 ml/min/kg
diagnosis of aKI
- abrupt serum creatinine and BUN (azotaemia)
- urea and creatinine are “surrogate plasma/serum markers of GFR”
- lab work – anaemia, stress response
- Xray, US, CT, MRI
- biomarkers
o more sensitive than creatinine
o faster and safer than GFR
o can detect KI earlier
o can distinguish AKI from CRF
treatment of AKI
If oliguric/anuric
- mannitol 0.25-1g/kg slow bolus
- loop diuretics: furosemide: boluses 2-6mg/kg IV
supportive therapy
- arterial hypertension: amlodipine
- GI complications: antiemetic (maropitant), PPI
- pain management
Renal replacement therapy
- indications: inadequate urine production, fluid overload, hyperkalaemia, progressive azotaemia
- methods:
o Intracorporeal (peritoneal dialysis: removes uremic toxins by diffusion from peritoneal cavity)
o extracorporeal
removes toxins from blood stream by diffusion and or convection: both need vascular access and anticoagulation
intermittent haemodialysis (IHD): rapid blood flow and rapid dialysate flow
continuous renal replacement therapy (CRRT): slow flow of dialysate
monitoring of AKI
- hydration, BP, PCV, total solids and central venous pressure
- cardiac monitoring (HR, ECG, US)
- Acid-base
- urine output: N 1-2ml/kg/h, casts
prognosis of AKI
oliguria/anuria that persists or develops during treatment is associated with a poor prognosis
definition of ureic syndrome
Clinical manifestation of cumulative metabolic derangements which ensue as the result of renal failure: clinical picture of endogenic intoxication
cause of uremic syndrome
chronic kidney disease (in association with prerenal, renal or postrenal causes for azotaemia)
signs of ureic syndrome
vomiting, lethargy, weight loss, dehydration, oral ulcers, melena
diagnosis of ureic syndrome
medical history, physical exam, urinalysis, CBC, biochemistry, abdominal Xray, urinary ultrasound
treatment of ureic syndrome
fluid, if uremic haemorrhagic gastritis (cimetidine, famotidine), renal replacement therapy
prognosis of ureic syndrome
depends on severity of renal damage
cause of urethral obstruction
formation of struvite or cysteine stones
pathogenesis of urethral obstruction
functional (eg reflex dyssynergia, urethral spasm) or autonomic (urolithiasis, granulomatous urethritis)
signs of urethral obstruction
stranguria, pain, nausea, anorexia, ataxia, reluctance to move, prepuce may be red/inflamed from licking, urinary bladder may be distended
diagnosis of urethral obstruction
radiography, US, CBC (azotaemia, hyperphosphatemia, metabolic acidosis, hyperkalaemia), urinalysis (show haematuria and crystals)
treatment of urethral obstruction
urinary catheterisation, cystotomy, midazolam to relax, ATB
prognosis of urethral osbtruction
good if noticed quick enough
differential urethral obstruction
blockage by neoplasia of tissue surrounding the urethra, include prostate hyperplasia, cysts
cause of haematuria
inflammation, trauma or neoplasia, strenuous exercise, heat stroke or renal infarcts
signs of haematuria
can be gross (macroscopic haematuria) or occult (microscopic haematuria)
PUPD, stranguria, inability to urinate, vocalising in litterbox, bruising on the skin, bleeding from nose/gums, bloody vomit or faeces
diagnosis of haemturia
- history and physical exam
- CBC, biochemistry and urinalysis (maybe test for leptospirosis)
- urine culture is UTI suspected
- abdominal X-ray/ US
treatment of haematuria
depending on cause, UTI (ATB), kidney/bladder stones (therapeutic diet)
disorders of micturition definition
inappropriate passage of urine
cause of disorders of micturition
congenital abnormalities or acquired disorders
urinary incontinence
- involuntary escape of urine during the storage phase
- distended/small/normal urinary bladder
- palpation of UB: size, wall thickness, possibility of expression
- causes:
o urethral sphincter mechanism incompetence
o anatomic abnormality in the termination of the urethra
o inability of bladder to expand in capacity
o spasms of the bladder
o nerve damage - Paradoxal: induced by bladder or urethral obstruction – some urine is leaking around the blockage
- overflow: bladder cannot contract but will fit until urine flows passively
urinary retention
- apparent reduction in the frequency of urination
- occurs temporarily in partial obstruction
- spasm of external sphincter
- inability to adopt normal posture for urination
- Gross distension of bladder
diagnosis of disorders of micturition
history
physical exam
x-ray
treatment of disorders of micturition
NSAIDs
cause of PUPD
multifactorial, corticosteroids, diuretics
pathogenesis of PUPD
typically occur simultaneously, PD usually occurs as a response of PU
signs of PUPD
water consumption greater than 80-100ml/kg/day and urine production greater than 40-50ml/kg/day
diagnosis of PUPD
- owner can measure animals (dog) urine intake at home
- routine urinalysis
- USG (normal values in dog 1.050-1.076 and in cat 1.047-1.087), (>1.040 = dehydration)
- CBC, biochemistry, serum thyroxine (cats)
- renal US
- measurement of serum symmetric dimethylarginine (SDMA), or estimation of GFR
differentials of PUPD
kidneys disease, DM, hyperadrenocorticism, hypoadrenocortism, hepatic disease, hypercalcaemia, bacterial cystitis, pyelonephritis etc
normal intake for dogs and cats
dogs 60-90mL/kg/day,
cats 45mL/kg/day
normal urine production
dogs and cats is 26-44mL/kg/day
when is is PD
water intake >100ml/kg/day
when is it PU
urine output >50ml/kg/day
cause of proteinuria
renal proteinuria: glomerular capillary wall lesions, tubular lesions, both
signs of proteinuria
discoloured urine (prerenal proteinuria), polyuria, stranguria, discoloured urine – pink/red (postrenal proteinuria), acute dyspnoea, hypothermic, often no clinical signs
diagnosis of proteinuria
semiquantitative methods: dipstick colorimetric test, sulfosalicylic turbidimetric test, interpreted in light of USG and urine sediment, urinalysis
treatment of proteinuria
eliminating the underlying cause, if glomerular proteinuria can be managed using renal diet
definition of azotemia
increased concentrations of urea and creatinine in the blood
cause of azotemia
reduced GFR, uroabdomen, increased absorption of nonprotein nitrogenous compounds, increased protein catabolism
signs of azotemia
depression, lethargy, poor coat quality, poor appetite, and nausea, ataxia, stupor, PUPD, uremic
diagnosis of azotemia
biochemistry, USG, urinalysis, CBC, Total T4
treatment of azotemia
IV therapy, gastric protectants (sucralfate), specific treatment for underlying cause
predisposition of renomegaly
more common in cats
cause of renomegaly
edema, acute inflammation, diffusely infiltrating neoplasia, unilateral compensatory hypertrophy, trauma, perirenal cysts, hydronephrosis, haematoma, polycystic kidney disease
pathogenesis of renomegaly
can be unilateral or bilateral enlargement by symmetric or asymmetric, can be acute / chronic in onset
- acute Renomegaly is uncommon – when occurs, presentation is acute abdomen
- chronic Renomegaly is moderate - severe but occasionally mild
- unilateral renal enlargement occurs because of compensatory hypertrophy in animals with a solitary kidney or with severe end-stage disease in contralateral kidney
signs of renomegaly
lethargy, anorexia, vomiting, diarrhoea, weight loss, oral ulcers, dehydration, discoloured urine, pale MM, halitosis, abdominal pain, one/both kidney palpable, PUPD
diagnosis of renomegaly
- physical exam or by abdominal imaging
o C: 2.5-3 x length of L2
o D: 2.5-3.5x length of L2 - renal excretory function, quantification of proteinuria, bladder/urethral function, bacterial antibiotic sensitivity testing, diagnostic imaging
- US
treatment of renomegaly
- treating underlying cause
- IV fluids
definition of Chronic kidney disease
structural and/or functional abnormalities of one/both kidneys that have been continuously present for 3 months or longer, irreversible and incurable
cause of chronic kidney disease
Hereditary and congenital (renal hypoplasia, polycystic kidneys, familial nephropathy), acquired (neoplasia, amyloidosis, nephritis, glomerular), idiopathic (hyperglycaemia, hypokalaemia, toxins, kidney stones)
stages of chronic kidney disesase
1 – reduced GFR to 30%, other functions preserved
2. Further decrease of GFR to 15%
* Reduced excretion leading to azotaemia
* Reduced urine concentration
* Anaemia due to reduced erythropoietin
* Hypertriglyceridemia due to reduced lipoprotein lipase activity
3 – severe anaemia, severe arterial hypertension, disorders of cardiovascular, digestive and nervous system
4 – significantly reduced GFR to <5%, terminal uraemia leading to uremic syndrome
signs of chronic kidney disease
PUPD, weight loss, inappetence, vomiting, diarrhoea, lethargy/depression, messy hair coat, blindness, dehydration, pale MM, teeth problems
diagnosis of chronic kidney disease
CBC (non regenerative anaemia which can be masked by dehydration so look at haematocrit with total protein concentration), Biochem, urine analysis + urine protein, BP, X-ray and US, kidney biopsy, USG, UPCR, creatinine, BP, rectal examination (evaluate for evidence of melena or haematochezia which may indicate uremic ulcers)
treatment of chronic kidney diseasde
specific therapy, preventive, slowing the progression of CKD, dietary management, access to fresh water all the time, fluid therapy, calcitriol, H2 receptor blockers (famotidine)
prognosis of chronic kidney disease
may live from months to years
what are markers of renal fucntion
urea and creatinine
extra renal factors affecting urea
- Growth: dehydration, postprandial, GI bleeding, high protein intake, catabolic conditions
- Drop: liver disease, low protein intake, non-renal polyuria
extra renal factors affecting creatinine
- Growth: animals with strong musculature, high protein intake, postprandial, extreme exercises
- Drop: extremely weak musculature
UTI
- occurs in approx. 14% of dogs during their lifetime
- spayed females, older dogs (7-8yr)
- UTI is less common in cats 1-3%
- female, old age, decreased BCD
- signs: stranguria, pollakiuria, inappropriate urination, dysuria, haematuria
predisposition of sporadic bacterial cystitis
intact male dogs: rare, animals have fewer than 3 episodes of cystitis in 12 months
cause of sporadic bacterial cystitis
urinary tract abnormalities, systemic diseases, Corynebacterium urealyticum, clostridium
pathogenesis of sporadic bacterial cystitis
complicated bacterial cystitis implies underlying comorbidity
signs of sporadic bacterial cystitis
discomfort of caudal abdomen, small and thickened bladder, stranguria, haematuria, pollakiuria, peruria, dysuria
diagnosis of sporadic bacteria cystitis
- urinalysis: cystocentesis, ideal urine specimens should be palpated within 30 minutes of collection, or they should be refrigerated and processed within 24 hr
- clinical signs
- bladder palpation
- quantitative aerobic bacterial culture (by cystocentesis)
- CBC, Biochem, imaging not usually warranted
treatment of sporadic bacterial cystitis
- analgesics
- duration of ATB 7-10 days (amoxicillin, trimethoprim-sulphonamides)
- second time ATB (nitrofurantoin)
prognosis of sporadic bacteria cystitis
good
predisposition of recurrent bacterial cystitis
diagnosis of 3 or more episodes of clinical bacterial cystitis in 12 months or 2 or more episodes in 6 months, may result from relapsing or persistent infection or reinfection
cause of recurrent bacterail cystitis
same as sporadic, deep seated infection, or resistant to chosen antimicrobial
pathogenesis of recurrent bacterial cystitis
relapsing infection, reinfection, refractory infection or persistent infections
signs of recurrent bacterial cystitis
urethra more prominent or more severely thickened (same as sporadic)
diagnosis of recurrent bacterial cystitis
urinalysis, CBC, Biochem panel, US, cystourethrography, excretory urography
- not only urine bacterial culture, but diagnostic workup to evaluate the animal for predisposing factors, such as anatomical or structural defects
treatment of recurrent bacterial cystitis
- analgesics
- duration of ATB: 4 weeks for persistent and potentially relapsing infections (3-4 days for reinfection)
prevention of recurrent bacterial cystitis
prophylactic antimicrobial therapy isn’t recommended
predisposition of urolithiasis
Calcium oxalate (N America, asia, Europe), Struvite (S America, Africa, Australia), males = calcium oxalate, females = struvite
- tends to be middle-older cats (7 years)
cause of urolithiasis
mostly from UTIs (bacteria creates ureases)
pathogenesis of urolithiasis
dogs: almost all struvite calculi are infection-induced. Cats: most struvite calculi are sterile, if evidence of bacterial cystitis = antimicrobial drugs
signs of urolithiasis
bacterial urine cultures
Signs: bladder and urethral uroliths can often be palpated during abdo or rectal examination, full bladder/thickened, inflamed bladder wall may obscure small uroliths, haematuria
diagnosis of urolithiasis
in male dogs with dysuria, urethra should be palpated subcutaneously from ischial arch to os penis, US or plain/contrast enhanced radiography
- elevated BUN and serum creatinine concentrations
treatment of urolithiasis
medical dissolution or urohydropropulsion, basket retrieval, laser lithotripsy, percutaneous cystolithotomy, cystotomy
prognosis of urlothiasis
12-month survival rate after medical treatment is around 66%
predisposition of feline urethral obstruction
10-20% of wats with LUTS, cats: crystalline-matrix urethral plugs and uroliths, most common struvite and calcium oxalate
cause of feline urethral obstruction
physical obstructions (urethral plugs, urinary stones, strictures or tumours)
pathogenesis of feline urethral obstruction
abnormalities in the structure and/or function of the urinary tract caused by impairment of the normal flow of urine and resulting in local and systemic effects of that impairment
signs of feline urethral obstruction
large/non-existent bladder (+/pain), bradycardia, hypothermia, prolonged CRT, pale MM, hyperpnea, halitosis, tip of penis (dark purple to almost black and swollen)
with complete obstruction, uraemia usually occurs within 24hours. dysuria, haematuria, pollakiuria, inability to pass urine, pain
consequence of feline urethral obstruction
Detrusor atony, urethral injury, urethral and bladder mucosal damage, UTI, urethral and/or bladder rupture
diagnosis of feline urethral obstruction
- Survey abdo x-ray (contrast urethrocystography), abdominal US
- blood: CBC, biochemistry, blood gases and electrolytes
- urine: urinalysis and urine culture
- cystocentesis: yes/no
treatment of feline urethral obstruction
Emergency stabilisation
- depressed patients: oxygen and IV catheter
- fluid therapy
o estimate degree of shock and dehydration (isotonic replacement)
- hyperkalaemia
o ECG alterations: P-R interval, S-T segment and T waves, 3rd degree heart block
- metabolic acidosis
o often present in acute urethral obstruction
- hypocalcaemia
o if present should be treated with Ca-gluconate
Relieving the urethral obstruction
- butorphanol, morphine, propofol, ketamine, diazepam or acepromazine
- cystocentesis: G 22, decompress the bladder and get samples
o pull in caudal-dorsal direction straightening the urethra , flushing with sterile solution
prognosis of feline urethral obstrucion
1/3 re-obstruct again, clinical signs recur in ½, 20% euthanasia
- perineal urethrostomy: stricture formation, urine leakage, recurrent bacterial UTI
complications of feline urethral obstruction
bacterial infections, micturition dysfunction, post obstructive diuresis, intrinsic renal failure
predisposition of feline idiopathic cystitis (FIC)
~5% cats older than 1yr have: bladder/ UT problems, overweight, M>F 2- 7 years, multi cat household, nervous and fearful, diet, increased in: persian, manx, Himalayan, decreased: siamese
cause of FIC
neuroendocrine abnormalities
pathogenesis of FIC
it’s a problem that involves the bladder, isn’t directly a bladder problem.
- changes in sensory nerve function (increase in substance P immunoreactivity)
- abnormalities in dorsal root ganglion and of the central stress response system activation of sympathetic system acute increase in epithelial permeability and increased levels of catecholamine circulation
signs of FIC
periuria, dysria, stranguria, haematuria, vomiting, diarrhoea, inappetence, fever, lethargy, decreased generally activity, somnolence, decreased social interaction, painlike behaviours
diagnosis of FIC
X-ray, contrast (cystogram, urethrogram), US abdomen, urinalysis, cystoscopy
treatment of FIC
- MEMO (multimodal environmental modification)
o offer more litter boxes, organised time for play, different food - feline facial pheromone
o Feliway + valerian, analgesia (buprenorphine, acepromazine) - supplements and therapeutic food for stress
- pharmacologic therapy
o amitriptyline and clomipramine, NSAID, GAG
prognosis of FIC
normal life if management is correct and carried out
