Exam 5 Flashcards
Urinary Tract Disorders Introduction Lecture
Clinical approach
CKD
AKI
UTI
Urolithiasis
FIC (Pandora Syndrome)
Urinary Incontinence
Urinary Tract neoplasia
PLN & Evaluation of Proteinuria
Clinical Approach
History
-Signalment
-Reproductive status
-Current complaint
-Environment
-Work status
-Past medical history: travel, other animals, exposure to infectious agents/toxins
-Vaccination
-Diet: be precise
-Cat litter boxes
-Previous surgery, trauma, response to meds, antibiotics, steroids.
Review of Body Systems
-Body discharge
-Skin problems
-Weight loss
-Lameness
History specific to urinary tract
-Character of urine
-Change in color
-Dark yellow: concentrated, Bilirubin
-Red: heme pigments
-Brown/black: heme pigments
-Green: drugs, infection, bile
-Colorless: dilute urine
-Water intake: polydipsia (increased intake), polyuria (increased volume), hematuria, straining.
Physical Exam
Laboratory Findings
Imaging
Biopsy
Complication factors that require management
-Dehydration
-Electrolyte and acid-base disturbances
-Infection in urinary tract
-Urinary tract obstruction
-Genital tract disease
Define and use medical terminology that describes specific clinical signs associated with the urinary tract
Character of Urination
-Character of urine
-Change in color
-Dark yellow: concentrated, Bilirubin
-Red: heme pigments
-Brown/black: heme pigments
-Green: drugs, infection, bile
-Colorless: dilute urine
-Water intake: polydipsia (increased intake), polyuria (increased volume), hematuria, straining.
Lower urinary tract problems
-Dysuria: painful or difficult urination, difficulty establishing stream
-Stranguria: straining to urinate
-Initial difficulty: functional or partial obstruction of urethra
-Decreased stream diameter: urethral obstruction or spasm
-Increased duration of urination: polyuria maybe
Pattern of Urination
-Pollakiuria: increased frequency of urination
-Change in urinary habits, location
-Periuria: urinating all over the place, inappropriate urination maybe due to incontinence
Urine Volume
-Anuria: no urination
-Oliguria: decreased urination
-Normal: 20-40 ml/kg/day dogs/cats
-Incontinence vs. polyuria
-Incontinence: constant, intermittent, awake vs. asleep
Identify pivotal problems from the history and physical exam that indicate urinary disease
History
Blood in Urine
-Beginning Stream: urethra, genital tract
-End of stream: bladder
-Throughout urination: bladder, upper urinary tract
-Unassociated with urination: urethra, prostate, genital
-Lower: painful
-Upper: painless
Thirst
-Normal: 40 ml/kg/day dogs, 20 ml/kg/day cats
-1 cup = 250 ml
Increased grooming or licking of perineum or prepuce?
Hair loss confined to caudal abdomen?
Exposure to NSAIDs? Steroids
Postural changes may indicate renal pain or urinary tract obstruction
Physical Exam
-Dehydration: Skin pinch estimate
-Body weight
-Urine specific gravity
-Overhydration: iatrogenic from fluid therapy. Peripheral edema/ascites due to nephrotic syndrome
Oral cavity
-Uremic ulcers
-Foul odor: necrosis
-Aliphactic amines odor: azotemia
-Tongue tip necrosis: dogs
-Fibrinoid necrosis of small vessels
MMs
-Moistness: estimate hydration, tachy gum 3-5% dehydration
-Pallor: anemia
Ocular Manifestations
-Hypertension: diffuse retinal edema, hemorrhage, detachment, blindness
Always check blood pressure when kidney disease
Abdominal Palpation
-Kidneys cats: 2-3 x L2 VD in length, mobile
-Kidneys dogs: 2.5 x L2 Vd length, immobile
Bladder Palpation
-Ureters: never palpable
-Bladder: palpable
-Thickness of wall bladder, intraluminal masses, intramural masses, extent of distension, stones
Rectal Examination
-Routine in dogs, rare in cats
-Prostate gland: normal in pelvic canal, symmetrical with median raphe, non-painful
-Pelvic urethra: difficult to palpate
-Trigone region of bladder
-Sublumbar internal iliac lymph node palpation
-Perineal Urethra male dogs: deep palpation from below anus to the Os penis
Genitalia - Male
-Prolapse penis
-Lesions, foreign bodies in fornix
-Os penis
-External urethral meatus
-Testes palpation symmetry and consistency
Genitalia Female
-Perineum and vulva
-Vaginoscopy is indicated
-Discharges, masses, foreign bodies, urethral papilla, cervix evaluation
Diagnostic Problem solving Strategies
-List all major problems identified
-History
-Laboratory testing
-Results of imaging
-Histopathology
-Try to determine common denominator for all listed problems
- Hx + PE + Lab + Imaging + Path
- Identify + List problems
- Identify MAJOR problems Pivot problem
- List Ddx DAMN ITCH
Urinary clinical pathology review
-Always collect and analyze urine same time as CBC and Biochemistry BEFORE FLUIDS and DRUGS
Integrate findings from signalment, environmental history, and specific diet history as part of the diagnostic process
Urinalysis
Indicated for UUT and LUT disease
-pH
-Glucosuria: stress in cats, diabetes mellitus, AKI
-Blood: red cells, hemoglobin, myoglobin
-Proteinuria: albumin, subjective, FP with alkalinuria, affected by S.G.
-Bilirubinuria
-Ketonuria
-Urobilinogen
-Nitrate
-S.G.
-Leukocytes
- Pre renal
- Renal
-Creatinine: byproduct of phosphocreatinine (muscle food)
-Proportional to kidney function, muscle mass, protein intake
-Estimator of GFR
-Exponential relationship of GFR to BUN & Creatinine - Post Renal
Test of choice is the UPC (urine protein creatinine ration)
Sediment
-Hematuria
-Pyuria
-Bactiuria
-Epethilal cells
-Casts
-Crystalluria
SDMA - Symmetric DiMethyl Arginine
Azotemia
SDMA
-Product of proteolysis
-Estimated by GFR only
Azotemia
-Dehydration? disruption of obstruction?
Urine SG
>1.030 = pre-renal dogs. Rehydrate and verify azotemia resolution
>1.035 = pre-renal cats
Post renal: variable. Correct obstruction/disruption. Provide fluid therapy and verify if it resolves
Renal: 1.008-1.012. Rule out suspects, fluid therapy only if symptomatic
Conditions affecting USG
Drugs
-Diuretics
-Corticosteroids
Endocrine
-Hypoadrenocorticism
-Hyperadrenocorticism
-Ketoacidosis
-Hyperthryroidism
Other
-Hypercalcemia: hepatic disease (PSS and severe hepatitis)
-Pyometra
-Urinary obstruction
Characterize hematuria as to the timing observed within the act of urination and its clinical relevance
History
Blood in Urine
-Beginning Stream: urethra, genital tract
-End of stream: bladder
-Throughout urination: bladder, upper urinary tract
-Unassociated with urination: urethra, prostate, genital
-Lower: painful
-Upper: painless
Determine the significance of abnormalities detected during palpation of the kidneys and urinary bladder (size, shape, irregularities, masses, pain, location)
Use the DAMN ITCH approach to list some essential differential diagnoses for the identified clinical problem
Chronic Kidney Disease Lecture
Glomerulonephritis & Tubulointestitial Nephritis
Glomerulonephritis accounts for 30-50% canine CKD
-Sharpei: renal amyloidosis
-Shih Tzu: renal dysplasia
-Amyloidosis, renal dysplasia, chronic pyelonephritis, polycystic kidney disease, neoplasia, chronic partial obstruction, incomplete resolution of AKI, vasculitis, infarction.
-Severity of tubule-interstitial damage predicts decrease in renal function
Tubulointerstitial Nephritis
-Cats 70% of CKD
-Cats 15% Glomerulonephritis
-Chronic pyelonephritis
-PKD
-Renal dysplasia
-Ureterolithiasis
-Amyloid
-AKI resolution
-Vasculitis
-Infarction
-Neoplasia
Diagnose CKD in a dog, cat using results from history, PE, urinalysis, serum biochemistry, UPC, and renal imaging
CKD = progressive disease ongoing at least 1-3 months
Inexorable progression once nephron loss
-Critical mass of nephron mass loss tipping point for auto-progression; variable by species
Hyperinfiltration - single nephrons
-Tubulointerstitial inflammation and fibrosis
-MIneralization
-Bad guys: PTH, Pi, RAAS
C/S
-PU/PD
-Anorexia (Hyporexia)
-Weight loss
-Vomiting
-Halitosis
-Dysphagia
-Oral discomfort
-Weakness
-Altered consciousness
-Depression
-Seizures
-Bleeding problems
Any inflammation/infection can go to the glomerulus Teeth infection 2.7 x increased risk when periodontal disease present
PE findings
-Dehydration
-Small, irregular, or asymmetrical kidneys
-Normal kidneys, large rare
-Renal pain uncommon
Azotemic, hypertension 20-90% cats, 31% dogs
-Take BP first
Inadequate urine concentration
<1.030 dogs
<1.035 cats
Urinalysis
-USG
-Protein
-Blood dipstrip
-Sediment
-RBC, WBC, Bacteria
-Cats
Azotemia + sub maximally concentrated urine = Kidney disease
Dehydration + sub maximally concentrated urine = kidney disease
Ddx: prior fluid therapy, diuretic drug, Addison’s disease, diabetes insipidus, central, diabetes nephrogenic, hypercalcemia, hypokalemia.
Renal Imaging
-Radiographs
-Ultrasound
-CT
-MRI
-Size, shape, symmetry, lesions, echo texture
Diagnose first, then staging
Stage a CKD in a dog or cat using IRIS CKD guidelines regarding serum creatinine, UPC, and systemic blood pressure
Diagnose CKD first, then Stage
Stage I
-Non-azotemic
<1.4 dogs serum creatinine
<1.6 cats serum creatinine
>/= 0.3 mg increase in hydrated stable patient
-Trending SMDA
-Sub maximal urine concentration
-Renal proteinuria
-Cylindruria
-Abnormal imaging
-Abnormal kidney palpation
-Systemic hypertension
-Increased SDMA
Stage II
1.4-2.8 dogs serum creatinine
1.6-2.8 cats serum creatinine
-Mild renal azotemia
Stage III
2.9-5.0 dogs and cats serum creatinine
-Moderate renal azotemia
Stage IV
>5.0 serum creatinine
-Severe renal azotemia
IRIS Sub-stages
- Proteinuria: degree (UPC)
- Systemic hypertension: magnitude
UPC Ration
<0.2 cats and dogs = Nonproteinuric
0.2-0.5 dogs = Borderline proteinuric
0.2-0.4 cats = bordeline proteinuric
> 0.5 dogs = Proteinuric
0.4 cats = Proteinuric
Systolic Blood Pressure (mmHg)
Hypertension is one of the most important players in disease progression
<140 minimal risk to kidney
140-159 low risk to kidney
160-179 moderate risk to kidney
>180 High risk to kidney
Control systemic hypertension
-ACE inhibitors
-Angiotensin receptor blockade
-Renoprotection: omega fatty acids, spironolactone
-Anti-thrombin anti-platelet activation therapy
-Immunosuppressives
Develop a treatment plan for CKD dog or cat that is designed to limit progression of CKD. Include targeted phosphorous control as central piece of this plan
Treatment
- Treat underlying cause of CKD when possible
- Treat signs, symptoms, complications
Compensated treatment
-In hospital
-ECC management
-ECFV, electrolytes, acid-base
Compensated at home
Prevention/Slowing Progression: Lever arms
-Diet
-Phosphorous restriction: Total body (Pi binders) Single most powerful treatment
-RASS: inhibition, ACE-I & ARB
-Proteinuria
-Hypertension
-Calcitriol
-EPO
-Recognize and treat infection
Fluid Rx - Dehydration
-Minimal dehydration: water feeding tube or SQ fluids
-Moderate dehydration: IV fluids
Dietary Management
-Decreased phosphorus: extends life of kidney, extend life and quality (High Phosphorus = mineralization of kidney)
-Intestinal Pi (phosphorus) binders
-Decreased sodium
+/- Protein
-Increased potassium
-Increased water intake
Serum Phosphorus IRIS Goals of therapy
3-4 mg/dl normal
Stage III: <5.5 mg/dl Ok
Stage IV: < 6.0 mg/dl
Stage I: <4.5 mg/dl better
Stage II: <5.0 mg/dl
Intestinal Phosphate Binders
-Aluminum salts
-Hydroxide/Carbonate
-Calcium salts
-Carbonate Acetate
-Sevelamer HCL
-Lanthanum salts, iron salts
All work better when given with food or near food intake time
Potassium CKD & Acid-Base in CKD
Uremia GI signs
Hyperkalemia - Rare
Hypokalemia - Common
Cats hypokalemia
-Anorexia
-Vomiting
-Weakness
-Low USG
-New renal lesions
IV Potassium
Do not exceed 0.5 mega/Kg/hr
Acid-Base
-CKD: decreased nephron mass leads to
-Impaired ability to reabsorb HCO3- and excrete H+
Metabolic acidosis common
Tx
-Avoid acidifying diets
-Calcium carbonate, potassium citrate, sodium bicarbonate good
-Omeprazole, Famotidine: acid suppression
GI signs of UREMIA
-Nausea
-vomiting
-Anorexia
-Hematemesis
-Melena
Tx
-Antiemetics: Maropitant (NK1 antagonist), Ondansetron (5-HT3 antagonist), Metoclopramide (D2 antagonist).
-Histamine-2 Blockers: Famotidine (Pepcid)
-Proton-Pump Blockers: Omeprazole
Managing Appetite
-Common early sign of CKD
-Appetite stimulant drugs: Mirtazapine, Cyproheptadine, Diazepam (Valium), Oxazepam, Capromorelin (FDA approved in dogs).
-Esophagostomy tube
Describe how RAAS inactivation (ACE-I or ARB) can provide reno protection in CKD
Angiotensin II Hemodynamic effect
-Vasoconstriction
-Glomerular arterioles
-Preferential effect = efferent arteriole
Intraglomerular capillary pressure increased
Super Nephrons
-Increased GFR
-Fixed and dilated afferent arteriole
ACE-Inhibitor & Glomerulus
-After load reduction
-Decreased AG-II effects
-“Popping off” glomerular pressures
-Same concept as for the heart
-Enalapril
-Benazepril
ARB
-Telmisartan (FDA approved) hypertension drug
-Losartan
Ibesartan
ACE-I and ARBs
Benefits
-Reduced proteinuria
-Lower blood pressure
-anti-inflammatory
-anti-fibrotic
Risks
-Hypotension
-Progressive azotemia
-Hyperkalemia
-Vomiting, diarrhea, anorexia
-Start low-dose and up titrate
-Close monitoring of clinical, biochemical, and blood pressure parameters
-Single agent vs. multimodal therapy
CKD Hypertension & Rx
-Stroke
-Left ventricular hypertrophy
-Murmurs
-Gallop rhythm
-CHF
1st Choice if Proteinuric - ACE-I
-Enalapril or Benazepril
1st Choice with Cats - Calcium Channel blockers
-Amlodipine
-Beta blockers if tachycardia
Alpha Blockers
-If 1st and 2nd choice not effective
Hydralazine
-Adjunctive
Best Balanced Anti-Hypertensive
-ACE-I + Calcium channel blockers
Renal Proteinuria Trigger for Treatment Intervention - Control
-Decreased dietary intake
-ACE inhibitors
-Azotemic UPC >0.4-0.5
-Non azotemia UPC >2
Renal 2nd Hyperparathyroidism
Effects of HPTH on Heart
-Hypertension
-Arrythmias
-LV hypertrophy
-Heart failure
Describe calcitriol can provide reno protection in CKD
Pathogenesis
-Decreased calcitriol = Increased phosphorus
-Decreased ionized calcium = parathyroid gland hyperplasia
-High PTH is toxic = increased phosphorus retention
-High cellular calcium is BAD = Kidney damage
Calcitriol
-PTH suppression
-Blocks synthesis of the PTH molecule in gland by preventing transcription of the PTH gene
-Immune system, anti-proliferative, anti-tumor and other effects
Daily dosing
-2.5 ng/kg/day
-When phosphorus <6mg/dl and Ca x P <70
-Renal secondary hyperparathyroidism can develop prior to azotemia in cats even in the absence of hyperphosphatemia and hypocalcemia
-HPTH & hyperphosphotemia occur frequently in digs with naturally occurring CKD, even at early stages. Monitor this parameter
Management
-Dietary phosphate restriction
-Intestinal Phosphate binders
-Vitamin D sterols: CALCITRIOL effective in prolonging survival
Anemia CKD
-Decreased erythropoiesis
-Decreased RBC survival and increased RBC loss
-Non-regenerative
-Normocytic, normochromic
-Hypoproliferative
Tx
-Transfusion
-Darbepoetin
Acute Kidney Injury Lecture
Diagnose AKI in dog or cat using results from history, PE, urinalysis, serum biochemistry, renal imaging
-Abrupt renal function decline
-Recent onset of azotemia
-Inability to regulate solute/water
-Decreased renal synthetic and metabolic functions
Potentially reversible
-Important to consider: pre-renal, intrinsic (primary) renal, post-renal
-Injury not a specific diagnosis
Causes of Nephritis/Nephrosis
-Lepto
-Ischemia
-Nephrotoxicity
Post Renal
-Obstruction: penile urethra most common in cats
-Unilateral
-Bilateral
-Uroperitoneum
Cats & Radiographs
ALL need it
-Nephroliths
-Ureteroliths
-Big kidney little kidney syndrome
Stage AKI grade using IRIS AKI guidelines regarding serum creatinine, volume replacement responsiveness, and urine output while on treatment
Pre-Renal Volume Responsive AKI = Stage I
IRIS Grading same as for CKD Staging
Increased S-creat = prediction of outcome
Hemodymanic AKI
-Volume responsive
-Transient Azotemia
-Pre-renal AKI: low volume, low pressure
-Usually rapidly reversal
-Can progress to intrinsic AKI
Azotemia Acute Pre-renal
-Decreased perfusion of the kidney
-Retention of Nitrogenous waste
-It can be on top of primary renal, post renal.
C/S
-Dehydration
-Hypotension
-Anesthesia, ACE-I; NSAIDs history
-Shock
-Decreased CO
Dx
-Highly concentrated urine
-USG >1.030, often >1.040
-Urinalysis normal
-Hayline casts possible
-Rapidly resolves if corrected volume issues ECFV
-Increased urine volume
-Improved Renal function
If oliguria or poor renal function persists, suspect primary renal failure
Pathophysiology AIRF
-Nephrotoxins: Ethylene glycol (cytotoxic metabolites), antimicrobials (Aminoglycosides: Amphotericin, cephaloridine, sulfonamides, tetracyclines, Amikacin, Gentemacin). Cancer chemotherapeutics, Cholecalciferol rodenticide, heavy metals, radio contrast agents IV, fluorinated inhalant anesthesia Lilly - cats Raisins/grape - dogs, melamine + cyanotic acidic tainted food (crystal-associated nephropathy)
-Acute tubular necrosis or injury
-Acute Ischemic Renal failure: can take a long time in maintenance before resolution 1-3 weeks. Removal of inciting cause will not right away result in return of normal renal function
-Recovery phase: Normal BUN/Creatinine. Complete recovery may not be possible with great injury
-Partial improvement: can lead to CKD. Some nephron drop-out = inevitable
NSAIDs
-Any impairs renal auto regulation: Banamine, Ibuprofen, naproxicin, aspirin, carprofen, meloxicam, robenacoxib
-Do not directly damage the kidney
-Block renal vasodilatory response
-AIRF
-Renal injury occur if mediators of vasoconstriction activated by perception of volume depletion
Describe the phases of AKI and how they can develop following exposure to a major ischemic or nephrotic insult
Diagnosis of Azotemic AKI
History
-Uremia in general
-Not specific for AIRF
-Anorexia
-Depression
-Lethargy
-Vomiting/diarrhea
-Recent onset
-Recent PU/PD
PE
-Dehydration
-Overhydration: post fluid Rx
-Bradycardia, arrhythmia, hyperkalemia
-Normal to large kidneys
-No evidence of LUT obstruction
-Renal pain
Urinalysis & Lab findings
-USG 1.007-1.017
-Glucosuria, normoglycemia
-Proteinuria, hematuria
-Sediment: calcium oxalate or “hyppurate-like” crystals, ethylene glycol poisoning
-Rapid increase BUN, serum creatinine, and serum phosphorus
-Serum Potassium: sometimes >5.5 mEq/L
-Severe decreased renal excretory function
+/- Oliguria
-Metabolic acidosis
-Azotemia
Describe how use of NSAID can create AKI under certain circumstances
Urine Production Category - AKI
While on IVF
Anuria <0.05 ml/kg/hr
Oliguria <1ml/kg/hr
Polyuria relative 1-2 ml/kg/hr
Normal - No IVF
5-10 ml/kg/day = 0.2-0.4 ml/kg/hr
Develop an IV fluid treatment plan for an azotemic AKI dog or cat. Focus on the volume of fluid to be given initially and how this prescription should be carefully adjusted
Treatment
- Remove underlying cause
- Fluids
- Drugs
- Dialysis
- Prevention
Ethylene Glycol
-Fomepizole 4-mythylpyrazole
-Less CNS depression than Ethyl alcohol
-Ethyl alcohol diluted to 20%
Prognosis Dogs
<3 hrs excellent
5-8 hrs good to grave
>24 hours Grave
Prognosis Cats
>3hrs grave
Leptospirosis
-Doxycycline
-Penicillins K
AIRF Maintenance phase 1-3 weeks therapy
-IV fluids
-Calculate ins and outs
Too many fluids = kidneys die, interstitial edema, new paradigm
-Too many fluids: acute pulmonary edema
- Rapidly correct dehydration
- Replace urine loss (20 ml/kg/day)
- No weight gain after 1st 12 hours: consider curtail volume prescription. Avoid visceral edema
Systemic Hypertension
-Caused in part by fluid administration
-Amlodipine: Ca channel blocker, fast, effective
AKI Drug Rx: none proven beneficial. Prevention is key
Oliguric Phase Tx
-Furosemide: loop diuretics
-Dopamine: renal vasodilation when <5ug/kg/min. If >5ug/kg/min = vasoconstriction (adrenergic receptors)
-Mannitol: osmotic diuretic, contraindicated in volume overload
-Diltiazem: Ca channel blocker, reversal of renal vasoconstriction, pre-glomerular vasodilation, natriuresis independent of GFR. Prevent intracellular calcium accumulation. Used in Lepto AIRF 1.76x faster decrease in creatinine
Hyperkalemia
-Severe >8.0 mEq/L = death soon
-Tx: Calcium gluconate, Sodium bicarbonate, Dextrose injection, insulin.
-Dx: ECG Atrial Standstill, Sino-ventricular rhythm. Calcium Gluconate protective
Metabolic Acidosis
-Variable
-Tx: Sodium bicarbonate IV for most
Phosphorus Control
-Phosphate binders in gut, added to enteral feeding
GI signs
-Maropitant
-Omeprazole
-Famotidine
Nutrition
-Appetite stimulants
-Esophageal tube
-
Provide prognosis for azotemic AKI, based this on history, PE, UA, serum biochemistry, blood gases, urine output during therapy and whether there is access to dialysis or not
Ethylene Glycol
-Fomepizole 4-mythylpyrazole
-Less CNS depression than Ethyl alcohol
-Ethyl alcohol diluted to 20%
Prognosis Dogs
<3 hrs excellent
5-8 hrs good to grave
>24 hours Grave
Prognosis Cats
>3hrs grave
Hyperkalemia
-Severe >8.0 mEq/L = death soon
Dialysis
-Peritoneal and hemodialysis
-Not a last ditch therapy
-Refer early and before over hydrated
-Becoming more available $$$
Prognosis
-Magnitude of azotemia
-Oliguria or anuria
-Electrolytes: hyperkalemia
-Acidosis
-Anemia
Most likely cause of death during maintenance phase
-Hyperkalemia
-Metabolic acidosis
-Severe Azotemia
Overhydration and pulmonary edema
PREVENTION
Urinary Tract Infection Lecture
Diagnose UTI in the cat/dog with certainty based on qualitative urine culture reported in cpu/ml (cystocentesis, urinary catheter, and voided urine samples)
Lower UTI
-Associated C/S not specific to any particular Lower urinary tract disease
LUTD
C/S
-Hematuria
-Stranguria/Dysuria
-Inappropriate urination
-Decreased volume of urine: obstruction to urethra
-Most asymptomatic bacteriuria. Lower irritative voiding, upper may have fever, renal pain, PU/PD, uremia
Cystitis
-Inflammation of the bladder
Urethritis
-May coexist with cystitis
UTI
-Bacterial colonization
-Superficial luminal surfaces
-Deeper within the parenchyma or both
-Gram negative E. coli most common
-25% gram positive, 75% gram negative
Uncomplicated UTI
-1 isolate (bacteria)
-2 isolates (bacteria)
-Ascending infection most commonly, bowel flora, females >males, distance to anus shorter in females, short wide urethra
-Normal host defenses in urine: High osmolality, highly acidic, ammonia content, all inhibit bacterial growth
-Hydrokinetic Wash out when voiding, protective mechanism for bladder, also some antibacterial secretions
-Host defenses abrogation = often UTI establish
Urinalysis UTI
-Most important screening
-Increased leukocytes
-Pyuria and bacteria
-Hematuria and proteinuria suggestive but non specific
-pH increase due to urease production bacteria
-Gram stain urine sediment
Urine Culture
-Cystocentesis highly preferred Gold standard
-Quantitative culture = colonies forming units per ml - cfu/ml
Most UTI >100,000 cfu/ml some labs 30,000 cfu/ml
-Convention >1,000 cfu/ml = UTI some skin contamination possible
Key Points
-Catheterized female can result >100,000 cfu/ml making diagnosis impossible
-Midstream voided urine samples not satisfactory due to contamination
Imaging
-No visible lesions for uncomplicated UTI
Tx General principles
-Eradication of infection
-Avoiding development of resistance
Clinical UTI should be treated with antibiotics, Asymptomatic depends
UTI Duration of Treatment
7-14 days for uncomplicated, 7 days per ISCAID
30-60 days for Upper UTI
30 days for sexually intact males
Describe two ways that antibiotics can reach the site of infection during UTI and how this relates to MIC
Minimum Inhibitory Concentration (mg/ml)
In vitro
-Amoxicillin 59%
-Cephalexin 66%
-Enrofloxacin 74%
-Trimethorpim sulfamethoxazole 86 %
Higher in uncomplicated vs. complicated
-Uncomplicated susceptibility <90% for PO administration
Getting the drug to the bug
-Urine concentration antibiotics: aim to achieve 4-7 times MIC at site of infection
-Can = 10-100 times that of blood
-Time: above MIC dependent
-Maximal concentration: above MIC dependent
Amoxicillin with Clavulanate
-Poor prostate penetration, not for intact dogs
-Good against E. coli
-Alternative to Sulfa-TMP
1st Generation Cephalosporins
-Not a good choice
-E. colu resistance
Trimethoprim/Ormetoprim Sulfa
-Side effects: IMHA, ITP, keratosis conjunctivitis sick
Fluoroquinolones
-Kidney friendly
-Chose when other agents fail
-Concentration dependent above MIC
-High tissue concentration
-Excellent GI absorption
-Ciprofloxacin, enrofloxacin, Cefovecin not USA
Aminoglycosides
-Reserve for highly resistant bacteria
-Nephrotoxic
-Gentamicin
Urolithiasis Lecture
Describe how urinary stone can form emphasizing urinary saturation concepts, presence of promoters or absence of inhibitors
Urolith types
-Infection related: Struvite & Calcium phosphate
-Metabolic: Struvite, calcium phosphate, oxalate, urate, xanthine, cystine, silicate
-Both
Stone Growth
-Crystalloid supersaturation/precipitation
-Absence of critical inhibitor: crystal poison lacking
-Nidus for precipitation
-Growth on another lattice: epitaxy
Formation
-pH
-Time
-Temperature
-Promoters
-Inhibitors
Most frequent type of stone
Struvite, Oxolate
60% small breed dogs
History - Kidney
-Flank pain
-No pain
-Painless hematuria
-Signs of infection
-Signs of renal failure
History - Ureter
-No signs, especially cats
-Flank pain (acute urethral obstruction)
-Signs of post-renal azotemia (bilateral obstruction)
History - Bladder
-No signs
-Dysuria
-Increased frequency
-Hematuria
-Sensitivity varies by individual
History - Urethra
-Signs of obstruction
-Signs of post-renal azotemia
-Dysuria
-Increased frequency
-Hematuria
PE findings
-Thickened bladder wall
-Palpable stones in bladder
Do not rely on palpation to determine if stones are present
-Rectal exam stone palpable if urethra obstruction
-Large distended bladder
Design a treatment plan to induce medical dissolution of struvite stones in the dog, cat
Medical Dissolution calculolytic Diets DOG
-Highly acidifying
-Severe decrease in protein
-Decrease urea generation
-Decrease precursor minerals: Mg, Pi, Ca
-Promote diuresis, increase Na, Cl
-Diet 1-3 months, then maintain for 1 month
Medical Dissolution calculolytic Diets CAT
-Can not protein restrict
-Mean 13 days for S/D, 27 days for C/D multicore diet
-Struvite Stones should be gone within 4 weeks
-No antibiotic needed in most cases
Diet Modifications Struvite Prophylaxis
-Urinary acidification (pH 6.0-6.5)
-Magnesium restriction
-Increase water intake
-Decrease urine SG
-Monitor dogs for UTI
-Prevention diets
Describe a treatment program designed to limit recurrent calcium oxalate urolithiasis
Increasing frequency in dogs and cats
Dogs
-Second most common type
-Acid or neutral pH urine
-Hypercalcemia can predispose
-Older male dogs»_space; females 8-9 years old
-Small/miniature breeds: Min Schnauzer, Min poodle, Yorkshire terrier, etc.
-Risk factors: chronic hypercalcemia
-Hyperadrnocorticism
Cats
-Least likely breeds: Siamese, Abyssinian, Mixed breed, Birman
-Diets helpful for Struvite = Increased risk for Calcium oxalate in a sensitive animal
Hypercalciuria
-Resorptive bone
-Hyperabsorptive - intestine
-Renal leak
Treatment
-Medical calculolytic protocols DO NOT WORK
-Prophylactic NOT EFFECTIVE
-Avoid vitamin C
-Diet change
-Chlorothiazine: Increases renal tubular calcium reabsorption. Recurrent cases only
-Potassium Citrate = more soluble than calcium oxalate
-Promote water intake, canned diets
-Urine pH >6.5
-Add Citrate if needed
-Mild alkalinizing diet, veterinary diets for renal failure patients “O” neutral pH
Goals
-Reduce calcium excretion
-Reduce calcium urinary concentration
-Reduce urinary calcium availability
Recurrence Rates
-25-48%
-Slow growing
-3-4 months
-6 months until large enough to obstruct
Miniature Schauzers 3x at risk
Retrieval of Small Uroliths
- Catheter Aspiration
- Voiding Urohydropropulsion
General Principles
-Relieve urinary tract obstruction
-Correct fluid, electrolyte, and acid-base imbalances
-Non-surgical retrieval
-Surgical retrieval if necessary
-Lithotripsy
-Medical dissolution
-Struvite, urate, cystine
-Preventative therapy
-Increase water intake
-Add water to dry food, change to canned food
-Induce polyuria, decrease USG
-Increase voiding opportunities
-Treat UTI
Stone Prevention COCO
C: clear
O: odorless
C: colorless
O: Often
Feline Interstitial Cystitis Lecture
63% Idiopathic
Diagnose FIC by excluding all other causes of LUT signs
Rule Out
-Urolithiasis
-Behavioral
-UTI
-Neoplasia
Pandora Syndrome: it is more than just the bladder
-Bladder is the target organ
-Clinical signs in other organs present
-Hear disease, arrhythmia, gallop rhythm.
-GI vomiting, diarrhea, dyschezia.
-Lung asthma
C/S
-Intermittent hematuria
-Stranguria
-Pollakiuria
-Urinating outside the box
Urinalysis, PE findings, Histopathology
-Idiopathic Cystitis
-Thick bladder palpable
-Increased bladder vascularity
Stress Response System - Pivotal feature of FIC
-Increased activation of sympathetic system
-Dysregulation of SRS
-Unrestrained outflow of CATECHOLAMINES
-Chronic “wear and tear”
-Upregulation of pro inflammatory genes
Explain how the cat’s perception of stress initiates and maintains FIC through the process of neurogenic inflammation
See previous card
-The brain is the central organ of stress response
-Physiological and behavioral response to what is potentially or actually harmful
-Loud stimuli response
-Acoustic startle reflex in cats
Develop a treatment plan for FIC that emphasizes MEMO (multi-modal environmental modifications) stress reduction, and enrichment
Spontaneously resolve (85%)
-5-7 days or earlier
>50% recurrence within 12 months
Acute Episode
-Analgesics: BUPRENORPHINE 5-7 days
-NSAIDs? renal risk
-Antispasmodics: Acepromazine 3-5 days
-Tranquilizer
Water increase intake
-Diet: canned food = decreased osmolality USG 1.030 vs. 1.050, increased voiding pattern
-Food puzzle trays good
MEMO
-Detailed questionnaire, environmental, behavioral
-Drugs
-Pheromones
-TCA- Amitryptyline
-Clomipramine
-GAG: Glucosaminoglycans
-Improve husbandry
-Enriched environment
-Decrease magnitude of stress
-Behavioral Cat and human
-Environmental
The client is the treatment
Litter Box
Litterbox hygiene/husbandry PIVOTAL
Rule 1+1
-Size: bigger is better
-No scented
-Litter texture
-Depth of liter
-No hoods
-Location
-Access
Environment
-Cats are not pack animals
-They are not antisocial
-They are independent
-Resting areas
-Toys
Antibiotics: NO
NSAIDs: NO
Outside: preferably NO
GAG (glycosaminoglycans): YES, sometimes, no proof it works
Pheromones: YES
Recognize that FIC is part of a greater systemic process called PANDORA SYNDROME
Urinary Incontinence Lecture
Identify the cause of urinary incontinence in a particular patient, distinguishing between congenital and acquired diseases
Involuntary Passage of Urine
-Results from high bladder pressure, low urethral pressure or combinations
-Or anatomical defects, urethral or sphincter mechanism
Diagnosis urinary incontinence
-Observations
-PE
-History, where, when, urinary habits
-Rectal/vaginal PE
-Anal tone: tells you if Sacral reflex are is intact or not
-Bulbocavernosus reflex
-Bladder size at time of episode
-Caudal neurologic exam
History is key
Urinary bladder residual volume is Key
-Urinary incontinence: when resting or sleeping, unaware of leakage?
-Pollakiuria: small, frequent volumes
-PU/PD large volumes
-Inappropriate: in your shoes
Bladder Residual Volume
- Storage disorders
Small residual volume
-Primary sphincter mechanism incontinence
-Ectopic ureters
-Detrusor hyper contractility
-PU/PD resulting from inability to hold urine
-Inflammation/infectious: weakening sphincter
-Both exacerbate problem - Emptying disorders
Large residual volumes
Functional
-Detrusor-urethral dyssynergia
-Urethrospasm
-Detrusor atony
-Neurogenic upper motor neuron bladder
Obstructive/Mechanical
-Neoplasia
-Calculi
-Stricture
Minimum Data Base
-CBC/Chem
-Urine culture
-Neurologic exam
-Imaging to exclude calculi, stricture, pelvic bladder, ectopic ureters
Describe multiple factors that can contribute to the pathophysiology of PSMI including estrogen, FSH, LH, body weight, age at neuter, breed
Primary Sphincter Mechanism Incompetence
-Spay incontinence 12-18 months post op
-Urethral pressure continues to decrease with advancing age
-Hormone responsive incontinence, estrogen, testosterone
-Seen in some castrated males
The most common and important acquired cause of incontinence in dogs
Pathophysiology
-Failure of urethral sphincter to function adequately
-Dogs >20kg more at risk
-Breeds: Boxer, doberman, Gian schnauzer, Old English sheepdog
Urethral Smooth Muscle
-Alpha adrenergic stimulation provides 60% urethral tone
-Receptors may have decreased in number or responsiveness to stimulation
Spayed Females
-Decreased estrogen = increased FSH = Increased LH
-Estrogen: sensitizes smooth muscle of proximal urethra to the effects of catecholamines, increasing urethral tone
-Aging: may affect collagenous support tissue
-Abnormal positioning of the bladder and/or urethra can contribute to functional failure
-Obesity exacerbates
-Vestibulo-vaginal structural abnormalities are associated
C/S
-Sleeping incontinence
-Recumbent, no urgency
-May dribble before OHE and then it increases after OHE
Breeds
-Dobermans
-Soft coated wheaten terrier
-Greater swiss mountain dog
Dx
-Exclusion
-History of leaking when recumbent or sleeping
-Minimum database
-Rule our other causes, calculi, masses, pelvic bladder, bacterial infection, ectopic ureters
-Neurologic exam
-Imaging
Develop a treatment plan for PSMI with either estrogens or PPA, including monitoring for possible adverse drug effects. Describe the mechanism of action for these drugs
Goal: tighten urethra, increase pressure, cause smooth muscle cells to contract
Medical management
-Alpha agonist (PPA) in both males and females
-Estrogen in females
-Testosterone only in males
-Combination hormone and alpha agonist synergistic
Alpha adrenergic agonists
-Phenylpropanolamine
-Stimulate proximal urethra alpha receptor and cause norepinephrine release = increase urethral closure function
-70-90% effective, TID most effective
-Monitor systemic blood pressure 0, 1, 3, 6 months, Twice yearly
Epinephrine
-Adverse effects: restlessness, anorexia, tachycardia, hyper excitability, aggression, tremors, GI upset.
-Hypertension
-Caution with cardiac or renal disease
Estrogen (DES, diethylstilbestrol)
-Enhance the number and responsiveness of the alpha adrenergic receptors in proximal urethra
-65% response fully, 20-25% partially
-Dose per dog, not body weight
-Maintins normal urethral submucosal blood flow, maturation and collagen synthesis
-Low dose protocols to avoid anemia, thrombocytopenia.
-Adverse effects: vulvar or mammary swelling, attractiveness to males, lethargy, vomiting, diarrhea. Bone marrow suppression with overdose
should not be used in intact females, males, cats
Estradiol cycloproprionate should not be used
Recognize when to refer to as specialist and what options are available when adrenergic or estrogen treatments have failed to adequately restore continence in dogs with PSMI
Urethral Bulking
-Candidates: when failed medical therapy or can not tolerate side effects or oral medication
-3 submucosal urethral protrusions to touch in center of lumen
Artificial urethral sphincter: Hydraulic occluder
-Used for PSMI unresponsive to medical therapy or failed ectopic ureter repair
-Occluders medical grade silicone
-90% effective and safe
-Potential complications: obstruction due to fibrosis, lack of efficacy
Surgical Management
Colposuspension
Cytosurethropexy
Urethropexy
Prostatopexy
Males PSMI (Primary sphincter mechanism incompetence)
Tx
Testosterone
-Methyltestosterone. Should not be used in patients with prostatic carcinoma, caution with renal, cardiac or hepatic disease. May decrease insulin needs in diabetic patients
-Testosterone cypionate effective and safe option
Emptying Disorders
Detrusor-urethral dyssynergia
-Functional urethral obstruction
-“Reflex dyssynergia”
-Urethral sphincter relaxes during onset of detrusor contraction and urination
-Normal neurologic exam
-Unclear pathophysiology
-Middle aged, large giant breeds, males»_space; females
Large residual volume after conscious void
Dx
-Ruling out mechanical obstruction
-Easy passage of urinary catheter
-Large residual volume
-Interrupted urination pattern
-Ultrasound
-Contrast urethrography and or urethroscopy
Tx
-Reduce smooth muscle sphincter tone
-Reduce skeletal muscle sphincter tone
-Address anxiety if present
-Prevent bladder over-distension
-Teach owner to catheterize dog
Meds
-Alpha adrenergic blockage
-Phenoxybenzamine
-Prazosin
-Tamsulosin: side effect hypotension
Striated muscle involvement
-Benzodiazepine: diazepam
-Acepromazine
-Methocarbamol
-Dantrolene and baclofen
Associated Bladder Atony
-Bethanechol (parasympathomimetic)
-Cisapride or Metoclopramide (dopaminergic)
Monitor for bacterial cystitis
Prognosis: usually good
-May need anxiolytic
-Life long therapy
Urethrospasm
-Functional urethral obstruction
-Address similar to Detrusor-Urethral dyssynergy
-Alpha adrenergic blockage
-Skeletal muscle relaxation
Detrusor atony
-Results from neurogenic or myogenic causes
Tx
-Goal: detrusor muscle contraction
-Bethanechol (parasympathomimetic)
-Metoclopramide or Cisapride (dopaminergic)
-Keep bladder empty: catheter, manual expression
Neurogenic upper motor neuron bladder
-Suprasacral spinal cord lesions
-Brain stem lesions
-Cerebellar lesions
Urinary Neoplasia Lecture
Definitively diagnose and stage TCC as the most common tumor of the bladder and urethra
Transitional Cell Carcinoma or Urothelial Carcinoma
-9 years
-No sex predilection
-Collies, Scottish terriers, Beagles, America Eskimo, Airedales
-Lawns and gardens treated with herbicides and or insecticides
-Consumption of yellow-orange vegetables association
Staging Bladder TCC
T1 Carcinoma in situ
T2 Infiltration of sub epithelial
T3 Invasion of muscular layers
T4 Tumor fixed to adjacent
History and C/S
-Lower urinary tract signs
-Urgency
+/- Palpable mass
-Incontinence
-Stranguria
-Hematuria
-Pyuria +/-
-Urine culture often positive
-Malignant epithelial cell in 30% sediment
Lab findings
25-50% positive culture at diagnosis
-Avoid cystocentesis due to tumor seeding concerns
Dx
Biopsy, urinary catheter aspiration/traumatic, Gold Standard
-Free catch UA 30% dogs ID tumor cells
-Urine sediment wet mount - Rafts
-Urine Cytoprep dry mount - cellular detail
-Traumatic catheterization, blind or ULS guided. Chunk of TCC often retrieved into catheter
-Biopsy through cystoscope at surgery
Do NOT FNA = tumor seeding
-Imaging: Bladder mass lesions
-Radiographs metastasis: sublumbar LN, then lungs and bones
TCC presumptive diagnosis
-Rafts of epithelium
-Cellular Atypia
-Reactive epithelium = confusing
Develop a treatment plan for TCC of the bladder depending on how advanced the condition is
66% occur in Trigone region
>50% metastasized at presentation
Locally invasive, prone to transplantation - seeding
Treatment
-Surgery only if not in the trigone area
-Chemotherapy
-Photodynamic therapy
-Radiation therapy
-Immunotherapy
-Tube cystotomy or permanent urethral scenting
Piroxicam or other NSAIDs great therapy
Surgery
-Complete resection = 12 months survival
-Incomplete resection = 4 months survival
Bladder TCC Prognosis
-Poor if hydronephrosis, hydrometer, Azotemia, Metastatic disease.
-Survival poor: overall 16% alive 1 year after diagnosis
-50% metastatic disease development to lung and bone
Urethral Tumors
-Rare in dogs
-Extremely rare in cats
Females»_space; males
Small breeds
C/S
-Bladder obstruction
-Rectal exam = mass palpable
Ddx
-Urethral stricture
-Proliferative urethritis
Renal Carcinoma
Primary Renal Neoplasia
- German shepherd predisposed
- Mean age 9 yo
C/S
-Abdominal mass
-Weight loss
-Hematuria
-Classic triad
-Often no c/s
-Highly invasive
-Poorly response to chemotherapy
-Pareneoplastic syndromes
Imaging Ultrasound
-Nephroblastoma
-Adenoma/Papilloma
-Sarcoma
-Fibroma
-Lymphoma
Lab findings
-Polycythemia
-Paraneoplastic
Tx
-Surgery
-Median survival 8 months
Recognize the value of UPC and microalbuminuria measurement over dip strip pad reaction for accurate proteinuria detection
Dipstrip
-Mostly Albumin
-Nuance interpretation with USG
-Lower limit 30 mg/dl
-Over diagnosed and under diagnosed
-False positives: alkaline urine, concentrated urine, prolonged contact with pad.
-False negatives: dilute urine, acidic urine, Bence-Jones proteinuria
Urine protein creatinine ratio (UPC)
- Albumin + Globulins = mg/dl
- mg/dl Creatinine
- Urinary Creatinine = constant steady state
-Proportional change urinary creatinine concentration or dilution
<0.2 = normal
>/= 0.5 abnormal in dogs
>/= 0.4 abnormal in cats
>0.2 <0.3 = primary glomerular disease, not always black and white
Amyloid 22.5 (11-47)
Glomerulonephritis 5.73
Glomerulosclerosis 2.89
Individual overlap
-3 Pool urine samples preferable within 24-36 hours
-Microscopic hematuria can interfere
-WBC can interfere (urine culture before UPC)
Microscopic hematuria
-ELISA species specific measures albumin
-Urine standardized to USG of 1.010
Value of Microalbuminuria
-Negative = great, barrier is working well
-Positive = worrisome, breakdown of barrier function, many possible causes
-Normal 0
-1-2 Micro Albuminuria
-30 macro Albuminuria, UPC >0.5
Antigen Hunt
Titers
-Borrelia (lyme)
-Ehrlichia
-Rocky mountain spotted fever
-Anaplasma
-Babesia
-Heartworm
-Brucella
-Lepto
Nephrotic Syndrome
Proteinuria - Severe
Hypoalbuminemia
Hypercholesterolemia
Edema/Ascites
More guarded prognosis than general PLN
Determine when Proteinuria is renal origin or not
Pre-Renal
-Causes: metabolic, neoplastic, hypertension, endocrine (cushing’s), early primary renal disease. Systemic inflammatory/infectious
-Hypertension
-Hyperthermia
-Hemoglobinemia –uria
-Myoglobinemia –uria
-Paraproteinemia – Bence Jones Proteins
Glomerulus and Tubules are normal
Intra-Renal
-Filtration - Glomerular
-Glomerular barrier function impaired
-Albuminuria (proteins from plasma “leaking”)
-Tubular reabsorption, degradation, necrosis, interstitial inflammation
Most common Glomerulonephritis
-Amyloidosis, glomerulosclerosis
Post-Renal
-Rule out: UTI, urolithiasis, neoplasia, trauma, iatrogenic, cells/plasma proteins
Diagnose the causes of renal proteinuria (GN, amyloidosis, glomerulosclerosis)
Glomerulonephritis
-48% immune complex GN
Glomerulosclerosis
Amyloidosis
-Breeds: Shar pei, Beagle, English foxhound, Abyssinian cat.
Familial Glomerulopathy
Decide when renal proteinuria should be treated on magnitude of UPC and if CKD is present or not
Conmsequences of Renal Proteinuria
-Epethilum into myofibroblast leading to fibrosis
-Tubular interstitial damage and fibrosis
-Damage to renal tubules by other molecules e.g., Free fatty acids
Glomerular Disease = Hypertension
-84% of dogs are hypertensive
-Check BP
-Treat
Tx
-ACE-I ~10mmHg reduction
-Calcium channel blocker: Amlodipine more effective than ACE-I to lower BP ~40 mmHg reduction
Protein Losing Nephrotic Syndrome Hypercoagulable State
Thromboembolic events may be the main reason for presentation
-Multifactorial
-Low albumin
-Loss of anti-thrombin
-Thromboembolism
-Pulmonary, others
Tx
-Aspirin
-Clopidogrel
Edema Control
-Furosemide
-Spironolactone
-As needed, avoid dehydration
Design a treatment plan to lessen renal proteinuria - diet and drugs
Design a diagnostic approach to identify predisposing chronic infectious/inflammatory conditions that can lead to GN or glomerular amyloidosis
Infectious/Inflammatory
-Lyme Nephritis
-Borrelia may or not may be present
-Most dogs with lyme are asymptomatic
-Breeds: Labrador, Golden
>0.5 UPC = follow closely
0.2-0.5 grey zone
-Measure BP
-Tx: Doxycycline, 30-45 days
-Immunosuppression if renal biopsy supports immune mediated IFA + complexes
EM deposits
Immunosuppression
-Mycophenolate - first choice
-Cyclophosphamide
-Chlorambucil
-Steroids alone not advised
Amylodosis
-B-pleated sheets subunit protein form
-Congo red Dx
Tx
-Colchicine administer prior to amyloidosis to prevent deposition. Share pei Fever
-DMSO: anti inflammatory effect, solubilize deposits??
-Nothing to prevent or slow progression
-Poor prognosis to grave
Shar pei dogs
-Recurrent acute self limiting fever and tibiotarsal joint swelling history
-Severe liver involvement may cause icterus or hemoabdomen due to liver rupture
