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