Renal CVT Flashcards

Question

What is the mechanism of PU/PD in Chronic renal failure?

Answer 1

Secondary NDI | Osmotic diuresis

Answer 2

Secondary NDI | Osmotic diuresis

Answer 3

Secondary NDI Osmotic diuresis Downregulation of aquaporin-2

Answer 4

Secondary NDI | Downregulation of aquaporin-2

Answer 5

Secondary NDI | Decreased renal medullary tonicity with loss of osmotic gradient

Answer 6

Secondary NDI Bacterial endotoxin reduced tubular sensitivity to ADH Damaged countercurrent mechanism

Answer 7

Secondary NDI | Bacterial endotoxin reduced tubular sensitivity to ADH

Answer 8

Secondary NDI Loss of medullary hypertonicity (medullary washout) Impaired hormone metabolism +/- psychogenic component

Answer 9

Secondary NDI Loss of medullary hypertonicity (medullary washout) Impaired GFR +/- psychogenic component

Answer 10

Secondary NDI Impaired tubular response to ADH Central = Impaired release of ADH Psychogenic polydipsia

Answer 11

Secondary NDI | Loss of medullary hypertonicity (medullary washout)

Answer 12

Secondary NDI Loss of medullary hypertonicity (medullary washout) +/- Psychogenic component

Answer 13

Secondary NDI Osmotic diuresis due to diabetes mellitus Interference with action of ADH? Partial CDI (some patients)

Answer 14

Secondary NDI | Excessive catecholamines

Answer 15

Secondary NDI Imapired tubular response to ADH +/- impaired release of ADH = CDI

Answer 16

Secondary NDI | Interferes with action of ADH on renal tubule

Answer 17

Secondary NDI Downregulation of aquaporin-2 Loss of medullary hyperonicity (medullary washout)

Answer 18

Secondary NDI | Loss of medullary hyperonicity (medullary washout)

Answer 19

Secondary NDI | Impaired tubular response to ADH

Answer 20

Secondary NDI Action of atrial natriuretic peptide Impaired release of ADH = CDI

Answer 21

Secondary NDI | Unknown!! But renal failure is not the cause in all cases!!

Answer 22

1. Ion overstauration in urine 2. Urine volume 3. Urine pH 4. Temperature 5. Inhibitors or promotors of crystal formation

Answer 23

Tamm-Horsfall proteins and nephrocalcin

Answer 24

Staph and Proteus (urease producing bacteria)

Answer 25

Yes, examples with 50% of patients with CaOx uroliths

Answer 26

Can be normal in concentrated dog urine | ALWAYS abnormal in cats!

Answer 27

Calcium oxalte monohydrate

Answer 28

1. Diet 2. Potassium cirtate (alkalizing urine and citrate inhibits CaOx formation) 3. Thiazide diuretics (humans)

Answer 29

○ Cysteine is usually filtered at the glomerulus and resorbed at the proximal tubule, so cysteine crystalluria can occur with defects in resorption at proximal renal tubule

Answer 30

1. Alkalize urine | 2. Break disulfide bond with d-penicillamine or 2-MPG (2-mercaptopropionylglycine)

Answer 31

Dalmatians and English Bulldogs

Answer 32

1. Alkaline urine 2. Feeding diet low in protein 3. Allopurinol (xanthine oxidase inhibitor)

Answer 33

xanthine oxidase inhibitor: Competitively inhibits the conversion of xanthine to uric acid

Answer 34

Cavalier King Charles Spaniel | Adminstration of allopurinol for uric acid crystals (Dalmatians/English Bulldogs)

Answer 35

Albumin: >30 mg/dl

Answer 36

sulfasalicylic acid test Detects albumin, globulins, and Bence Jones proteins > 5 mg/dl

Answer 37

• Proteinuria = positive test results on three or more occasions 2 weeks or more apart

Answer 38

• UPC of 0.4 (cats) and 0.5 (dogs) correspond with albumin of 30 mg/dl

Answer 39

• Normal UPC: < 0.2-0.3 (cats/dogs)

Answer 40

• Dogs: neoplasia, infection, polyarthritis, hepatitis, HAC, IMHA, systemic hypertension

Answer 41

• Cats: Viral infections, neoplasia, IM disease, polyarthritis, systemic hypertension

Answer 42

• Treatment when UPC >1.0 ○ Low protein diet, n-3 fatty acid supplementation (in renal diets), low dose aspirin, ACEi (Enalapril 0.5-1.0 mg/kg/day PO)

Answer 43

• In azotemic animals: treatment when UPC > 0.5 | ○ Renal diet (n-3 fatty acids), ACEi

Answer 44

NINs (neoplastic, infectious, noninfectious inflammatory) causes of glomerular disease

Answer 45

• Immune-mediate disease that if associated with deposition of immune complexes within glomerulus ○ Subendothelial, subepithelial, and/or mesangial ○ Complexes may be circulating and passively get trapped OR may form ""in situ"" when antibody binds to normal glomerular antigen or soluble antigen is localized here

Answer 46

Membranoproliferative GN = 20-60%

Answer 47

IgG mainly

Answer 48

Treat NINs and antiplatlet drug

Answer 49

Unknown - studies lacking

Answer 50

(Membranous GN) • Results form IgG deposits on the subepithelial aspect of GBM Result in complement-mediated injury to podocytes and diffuse foot process effacement

Answer 51

Membranous Nephropathy | In dogs, accounts for 10-45%

Answer 52

Possible immunosuppression, depends on stage of dz (1-4)

Answer 53

Progresses slowly, animals can liver out normal lives

Answer 54

• Accounted for 2-16% of dog lesions, expect proteinuria and renal failure, mediated by immune-complex deposition Characterized by mesangial cell hyperplasia and increased mesangial matrix

Answer 55

IgA (IgA Nephropathy)

Answer 56

Excessive IgA complexes can be formed by enteric disease or decreased clearance of IgA complexes in association with liver disease

Answer 57

§ Familial form = Glomerular (only 64%) and medullary amyloid deposition (ischemia, chronic interstitial fibrosis, papillary necrosis, and nephron loss) □ Shar Peis as few as 25-43% had proteinuria noted! More likely to present azotemic than proteinuria

Answer 58

• Breeds: Beagles, English foxhounds, collies, and walker hounds

Answer 59

• Nonspecific, End-stage response to glomerular injury or decreased functional renal mass • Seen on light microscopy as mesangial cell hyperplasia and mesangial expansions of the glomerulus ○ Hyalinosis, adhesions in tuft of Bowman's capsule

Answer 60

GN with no lesions on LM, but on EM Diffuse foot process effacement Severe proteinuria and nephrotic syndrome Uncommon in dogs Humans respond to steroids

Answer 61

* Inherited defects in structure of type IV (basement membrane) collagen * EM: Irregular GBM splitting (Unique to this disease)

Answer 62

○ Dogs: Up to 50% | ○ Cats: Up to 90%

Answer 63

BUN is highly influenced by tubular reabsoprtion

Answer 64

early in CKD large drops in GRF produce small increases in creatinine, and the reverse later in disease; occurs because initially when there is a loss of nephrons there is a compensatory hypertrophy of residual nephrons so single nepron GFR may more than double

Answer 65

Inulin Clearance

Answer 66

Iohexol Clearance (Ominpaque)

Answer 67

1. Reduction in kidney function 2. Proteinuria 3. Hypertension

Answer 68

1. Provide adequate nutritional support 2. Correct deficits and excesses in fluids, acid-base, and electrolytes 3. Amerliorate CS of CDK 4. Provide renoprotective therapy to slow the progression of CKD

Answer 69

1. Feeding a renal diet (best evidence) 2. Ensure adrequet nutrition (feeding tube maybe needed) 3. Provide omega-3 polyunsaturated fatty acids (most in renal diets)

Answer 70

1. Maintain Phosphorus 2. Maintain potassium 3. Correct metabolic acidosis (bicarbonate) 4. Maintain hydration

Answer 71

○ Want below 4.5 mg/dl in Stage II, below 5 mg/dl in Stage III, and below 6 mg/dl in Stage IV Controlled with renal diet and intestinal phosphate binders

Answer 72

○ Metabolic acidosis in CKD primarily from impaired renal ammmoniagenesis, impaired excretion of acid and impaired resorption of bicarbonate may also occur § Metabolic acidosis in RTA from impaired bicarbonate resorption (proximal RTA) or impaired urine acidification (distal RTA)

Answer 73

1. Anemia (Epo supplementation) | 2. GI upset (acid blockers, antiemetics, and sucralfate)

Answer 74

1. Reduce proteinuria (ACEi and renal diet) 2. Control hypertension (cats - amlodipine, dogs - ACEi + amlodipine) 3. Provide calcitriol (to prevent secondary renal hyperparathyroidism and improve appetite/energy)

Answer 75

``` Description of AKI • Risk • Injury • Failure • Loss • End Stage Renal Failure ```

Answer 76

○ Initiation Phase: This is when injury is occurring § Extension phase – during this ischemia, hypoxia, inflammation, and cellular injury continue leading to cellular apoptosis and necrosis § This phase is usually < 48 hours § May not see any abnormalities ○ Maintenance Phase: characterized by azotemia and may last days to weeks, oliguria (< 1 ml urine/kg/hr) or anuria may occur here ○ Recovery Phase: azotemia improves and renal tubules repair, marked polyuria may occur here (from osmotic diuresis from accumulated solutes

Answer 77

1. Furosemide 2. Osmotic diuretic - Mannitol or 20% dextrose 3. Dopamine CRI

Answer 78

Furosemide

Answer 79

1. Proteinuria (proteinuria, nonproteinuria, borderline) | 2. Hypertension

Answer 80

o Evidence of dietary therapy (n-3 polyunstaurated fatty acids (PUFA)) (Brown et al 1998), and ACE-I in dogs and cats to lower UPC, glomerular filtration pressures, and limiting structural changes in kidneys, and/or slow the decline in GFR § Benefit of diet (n-3 PUFA supplementation, and Protein, Na, Phos restrictions): Jacob et al 2002 for dogs and Elliott et al 2000 and Plantinga et al 2005 for cats = Unable to determine precise factors that improved outcome (ie used commercial diets) § Benefit of ACE-I (Grauer et al 2000 and King et al 2006)

Answer 81

Organs most prone to damage from systemic hypertension: 1. Heart, 2. Kidney, 3. Brain, and 4. Eyes

Answer 82

Goal: Reduce systolic BP < 160 mmHg to minimize risk of extrarenal end organ damage

Answer 83

Stage 1: < 1.4 mg/dl Stage 2: 1.4-2 mg/dl Stage 3: 2.1-5 mg/dl Stage 4: >5 mg/dl

Answer 84

Stage 1: < 1.6 mg/dl Stage 2: 1.6-2.8 mg/dl Stage 3: 2.9-5 mg/dl Stage 4: >5 mg/dl

Answer 85

``` Based on UPC Nonproteinuria (NP) = < 0.2 (dogs and cats) Borderline proteinuria (BP): 0.2-0.4 (cats), 0.2-0.5 (dogs) Proteinuria (P): > 0.4 (cats), > 0.5 (dogs) ```

Answer 86

``` Based on systolic BP Minimal Risk: < 150 mmHg Low Risk: 150-159 mmHg Moderate Risk: 160-170 mmHg High Risk: > 180 mmHg ```

Answer 87

Microcytosis

Answer 88

Hypocalcemia = ↑ PTH by posttranscriptional mechanism (parathyroid gland membrane Ca-sensing receptor to stabilize PTH ribonucleic acid)

Answer 89

↑ PTH → 1. ↑ Renal Ca reabsorption from ascending Loop of Henle, distal tubule, and collecting tubule 2. ↑ Ca reabsorption from bone 3. Enhancing formation of calcitriol (1,25-dihydroxycholecalciferol) from 25-hydroxycholecalciferol by kidneys

Answer 90

Calcitriol promotes ↑ Ca by: 1. Enhancing absorption of Ca from intestine 2. Facilitating PTH effects on bone (resulting ↑ Ca → ↓ PTH) ® Independent of Ca: Calcitriol inhibits synthesis and storage of PTH by activating Vitamin D receptors (VDR) → ↓ PTH gene transcription

Answer 91

Independent of Ca: Calcitriol inhibits synthesis and storage of PTH by activating Vitamin D receptors (VDR) → ↓ PTH gene transcription

Answer 92

® Levels of phos influence intestinal Ca and Phos absorption via renal calcitriol production ® ↑ Phosphorus (hyperphosphatemia) inhibits renal 1-a hydroxylase activity (renal conversion of 25-hydroxycholecalciferol to calcitriol (active form of Vit D)) ® ↓ Calcitriol → Phos retention and hyperphosphatemia which ↓ phos intestinal absorption ® If ↓ Phos = ↑ Calcitriol → ↑ Intestinal absorption of phosphate

Answer 93

PTH blocks proximal tubule from resorbing phos = phosphaturia

Answer 94

Inciting Event = Retention of Phosphorus dt ↓ renal excretion

Answer 95

o Hyperphosphatemia → ↑ PTH (direct effects of phos on parathyroid gland and ↓ renal production of calcitriol by inhibiting renal 1-a hydroxylase activity o Hyperphosphatemia may also complex with iCa (thus ↓ iCa) = leading to further ↑ PTH § ↑ PTH → phosphaturia (phosphate in serum to normal range) · Secondary hyperparathyroidism long term is the “trade off” for short term serum control of Phos levels o As renal dz progresses, capacity to prevent hyperphosphatemia is insufficient and loss of nephrons means less calcitriol produced

Answer 96

Secondary hyperparathyroidism long term is the “trade off” for short term serum control of Phos levels o As renal dz progresses, capacity to prevent hyperphosphatemia is insufficient and loss of nephrons means less calcitriol produced § Persistent calcitriol deficiency may cause parathyroid gland hyperplasia and hypertrophy with sustained automonous PTH secretion (tertiary hyperparathyroidism) = Resistant to conventional medical interventions (may need surgical reduction in renal mass to normalize PTH levels) § Thus need to maintain calcitriol in CKD to prevent tertiary hyperparathyroidism, since calcitriol is antiproliferative effects, ↓ PTH gene transcription, and represses parathyroid cell proliferation

Answer 97

1. ↓ Hyperphosphatemia and mechanisms underlying phosphate rentention 2. Restore adequate levels of active Vitamin D (calcitriol) 3. Normalize serum Ca

Answer 98

1. ↓ Dietary Phosphorus (serum phos < 6 mg/dl; ideal 4.5-5.5 mg/dl) § CKD diet have 75% less phos = helps to ↓ or normalize PTH levels in most patients with CKD Stage II and many patients with CKD Stage III (diet alone is not sufficient for Stage IV) 2. Intestinal phosphate binders (Aluminum, Ca, lanthanum): Bind irreversibly to phosphate in intestinal lumen, bound phosphate nonabsorbale, cations are released and may be absorbed § Sevelamer hydrochloride (Renagel): Polymer that does not release cations, very expensive and not more effective 3. Calcitriol (once serum phos < 6 mg/dl) § Since Calcitriol ↑ intestinal absorption of BOTH Ca and phos, failure to correct hyperphosphatemia prior can result in an ↑ Ca x Phos product = soft tissue mineralization

Answer 99

Since Calcitriol ↑ intestinal absorption of BOTH Ca and phos, failure to correct hyperphosphatemia prior can result in an ↑ Ca x Phos product = soft tissue mineralization

Answer 100

· Enhanced survival, appetite, activity, alertness, and interactivity with owners o Improved survival in dogs with Stage III and IV (Polzin et al 2005); unknown in cats o Failed to confirm benefit of reducing CS of CKD (hard since studies performed in animals with stable disease that were not showing overt CS and phos aggressively managed thus less hyperparathyroidism) · ↓ PTH secretion · Systemic Role in direct activation of VDR (humans, Vit D promotes longer survival independent of Ca, Phos, or PTH) o Dog studies showed little effect of calcitriol on survival and differences in Serum Phos, Ca, PTH levels o Humans: Paricalcitol (selective activator of VDR), more efficacy to side-effect profile, less morbidity, and better survival

Answer 101

· Randomized controlled clinical trial – Calcitriol prolonged survival and forestall development of uremic crises with Stage III and early Stage IV o Rate of progression of CKD was slower in animals getting calcitriol = renoprotective effect (same effects seen in humans) · Calcitriol INDICATED in dogs with Stage III and early Stage IV o Should be started even if PTH is not high (hard to manage hyperparathyroidism thus early intervention or prophylaxis) o Unknown values in dogs with Stage I and II Cats with CKD · Insufficient data (1 yr randomized, controlled study for Stage II, III, IV failed to show clinical benefit of calcitriol in cats with CKD

Answer 102

o Long term hyperparathyroidism with parathyroid hyperplasia = deficiency of VDR on hyperplasic parathyroid cells = hyperparathyroidism that is refractory to calcitriol · Calcitriol can induce formation of VDR on parathyroid cells, thus if long standing deficiency consider a prolonged calcitriol course or “pulse” therapy

Answer 103

May induce formation of greater numbers of VDR on parathyroid cells, making gland more responsive to action of calcitriol, may also minimize likelihood of inducing hypercalcemia (promoting intestinal Ca absorption) o Actions on newly formed intestinal cells leaving Crypts of Lieberkuhn (ability of cells to absorb Ca dependent on exposure to calcitriol during development) o Calcitriol has short T1/2 (4-6 hrs), thus less frequency administration means that less cells are exposed to calcitriol and thus less are primed to enhance Ca absorption

Answer 104

Hypercalcemia

Answer 105

hyperphosphatemia, hypercalcemia, ↑ Ca x Phos product

Answer 106

Selective VDR activators: paricalcitol (Zemplar) and doxercalciferol = less changes in Ca and phos levels with adequate control of hyperparathyroidism (No reports in dogs or cats)

Answer 107

· Serum Ca, iCa, phos, and PTH levels MUST be monitored (check q2-4 weeks until dose is stable), then recheck q3-6 months · Goal of Therapy: Maintain serum phos, Ca, and PTH levels within normal limits

Answer 108

Reduced in GFR initiates development of hyperparathryoidism by promoting phosphorus retenion and hyperphosphatemia Phosphorus retention suppressess the renal enzyme (1-alpha hydroxylase) - conversion of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol (calcitriol) = Most active form of Vitamin D Calcitriol deficiency, hypocalcemia, and hyperphosphatemia = contribute to development of hyperparathyroidism and parathyroid gland hyperplasia

Answer 109

Intermittent hemodialysis (IHD) and Continuous Renal Replacement Therapy (CRRT)

Answer 110

· Removes uremic toxins from blood by diffusion · Blood from patient carried in disposable tubing (extracorporeal circuit) → Dialyzer (artificial kidney) with porous membrane (Size and charge are major determinants of which particles are filtered) → Blood returned to patient o Small to middle sized molecules (urea and Crt) diffuse through pores into dialysate solution on other side o Large molecules (albumin and cells) remain in blood

Answer 111

· Citrate via CRI into extracorporeal circuit to bind calcium to prevent coagulation in circuit (thus need to give CaCl centrally in patient to avoid hypocalcemia, also need to check blood Ca to adjust both doses) o Citrate CONTRAINDICATED with hepatic dysfunction

Answer 112

· Most common = ARF (Goal of ACUTE dialysis: Resolve life threatening disorders (hyperkalemia, pulmonary edema), control uremia (↓ uremic complications), allowing time for renal repair o Leptosporsis, bacterial pyelonephritis, toxic nephropathy (ethylene glycol, lily ingestion, grapes/raisins, aminoglycosides), renal ischemia, ureteral obstruction (to tx acute uremia syndrome prior to sx; 1-3tx before sx or 2-4 tx prior to renal transplantation) · CHRONIC Dialysis: Control CS associated with CKD for the rest of patient’s life

Answer 113

· Certain drugs and toxins can be removed (low MW with little protein binding are readily removed) o IDH with charcoal perfusion cartridge in series with dialyzer (filters blood across microencapsulated charcoal beads to absorb toxic compound) o Consider that doses of medications may need to be adjusted since they will also be lowered

Answer 114

Therapeutic plasmapheresis (plasmapheresis cartridge = large pores to allow removal of albumin and globulins to separate plasma from cellular components)

Answer 115

· Anuria or oliguria that does NOT respond to volume expansion and diuretics o Volume overload (pulmonary edema or pleural effusion dt inappropriate urine output relative to IVF rate) · Hyperkalemia (start medical management with insulin, dextrose, bicarb, Ca) – Rapid removal of K with IHD · Severe uremia (BUN> 100 mg/dl, Crt <> 10 mg/dl) or uremia that does not respond to medical management in the first 24 hours o Humans: Earlier dialysis started in renal failure improves outcome and likelihood of return of renal function · For CKD: Failure of medical management to control CS of uremia (anorexia, lethargic, vomiting) – Need to place feeding tube · For toxins: Start ASAP (ex: Antifreeze, get dose of 4-methylpyrazole (dogs) and ethanol (Cats) to slow the metabolism of ethylene glycol

Answer 116

· IHD: Efficient method of solute removal = Good for ARF, CKD, acute toxicities, and fluid removal o Severe uremia (rapid ↓ urea can lead to untoward effects, first few IHD tx are short, 3-7 short daily tx to gain gradual control, followed by 4-5 hr duration tx 3 times/week, performed until patient regains renal function) o If severe uremia in unstable patient (first tx long 6-> 24hrs with slow blood flow to gradually control uremia to reduce complications = slow low-efficiency dialysis) · CRRT: Good for ARF and fluid removal (applied for short duration) o Blood flow 2-3 ml/kg/min compared to IHD 5-20 mk/kg/min and slow dialysate flow rate (8-34 ml/min compared to 500 ml/min in IHD): Net fluid removal rate based on patient’s hydration (solute cleranace, 0-35ml/kg/min) o Clinical improvement (increased urine putput, etc) may prompt decreased blood or dialystae flow rate to wean patient off of CRRT

Answer 117

Rapid decline in blood osmolality caused by removal of solutes (esp urea) by dialysis · Results in the osmoles are removed from the blood faster than diffuse from the intracellular compartment = intracellular hyperosmolaity = cellular swelling (leading to CNS signs like seizures and mentation changes) · Higher Risk with: Severe Azotemia, Smaller Blood Volume, preexisiting neurologic signs · Thus use: Slow, low-efficiency dialysis or CRRT to lower the likelihood of this complication

Answer 118

· 40-60% patients with ARF treated with dialysis survive (depending on the etiology) o Infectious causes of ARF: 60-70% survival rate o Hemodynamic and metabolic causes: 40-56% survival rate o Toxic Causes (ethylene glycol): 20-30% survival rate · Extends time to allow for renal repair and recovery o Can take 4 weeks to 3-6 months after renal injury

Answer 119

1. FeLV 2. FIV 3. Toxoplasmosis Concern since patient will need to undergo immunosupression

Answer 120

If moderate azotemia (Crt < 6 mg/dl) consider medial management (G-tube, fluids, dietary, EPO) – survival times parallel renal transplant survival times in these patients

Answer 121

No! | Screening (FeLV, FIV, IgG/IgM Toxo titers, imaging of kidneys, blood type)

Answer 122

Dog Lymphocyte Antigen (DLA)

Answer 123

Enteroplication in DOGS: High incidence in dogs of intussuspection follow allograft implantation, also helps to administer opioids pre-op and intra-op (NOT needed in cats)

Answer 124

Cyclosporine: Calcineurin inhibitor with specific anti-T cell activity Ketoconazole can be added to dose reduce the cyclosporine

Answer 125

· 80% cats survive perioperative period and discharged; 60% survive to 6 months after sx (Adin et al 2001) · 42% cats remaining alive at 3 yrs · Overall median survival 22 months (Matthews and Gregory, 1997) o Median Crt 8 mg/dl and medical options exhausted o Improves QOL and duration but not to normal cats lifespan · Harder to predict in dogs, small number of transplants performed and variation in drugs used o Survival in experimental dogs exceeds those with naturally occurring renal dz § Only about 50% dogs survive first 2 months after kidney transplantation, high rate of opportunistic infections may occur in patients with long term survival (Gregory et al 2006)

Answer 126

stoma site complications in 46% dogs (may be dt impaired immune function, increased susceptibility to infection, delayed wound healing dt malnutrition and/or uremia)

Answer 127

20% dogs will remove their own G-tubes (Elliott et al 2000) = ER situation, peritonitis, new tube needs to be placed ASAP If tube in for < 7 days, check with radiographic contrast leakage, may need laparotomy

Answer 128

Hypertension in 19.4% felines and 61% canine with renal dz (exact cause unknown – interactions btwn heart, kidney, endothelial signaling, and autonomic NS)

Answer 129

o Hypertensive retinopathy/choroidopathy: Retinal edema, tortuous vessels, hemorrhage, retinal detachment (cats come in for acute blindness) o Some cats, hypertension will precede azotemia with early CKD o Murmur, arrhythmia, gallop rhythm secondary to hypertension = cardiac muscle hypertrophy o Hypertensive encephalopathy: Head tilt, ataxia, depression, seizures (hypertension overwhelms cerebral vasculature autoregulatory mechanisms)

Answer 130

ACEi | As long as there is no end-organ damage

Answer 131

o Blocks conversion of Ang I to Ang II (powerful vasoconstrictor), systemic vasodilation when blocked o Ang II directly promotes Na absorption in proximal tubules → IV Expansion o Ang II stimulates aldosterone release = Na and water reabsoprtion o Can worsen azotemia therefore check renal values (start at lowest possible dose)

Answer 132

Since 50% of cats failure to respond to ACEi = Calcium channel blockers (amlodipine)

Answer 133

o Blocking influx of Ca needed to cause smooth muscle contraction and thus ↓ systemic vascular resistance (amlodipine: long acting, q24 hr dosing, and gradual effect)

Answer 134

§ Humans and dogs: Ca channel blockers may worsen renal dz (paradoxic effect that Ca Channel blockers preferentially dilate the afferent arteriole of glomerulus = glomerular hypertension) · Therefore DO NOT use in dogs as monotherapy! (Same effect is NOT seen in cats) § Cats treated with amlodipine live longer and with fewer hypertensive complications (safe as monotherapy in cats)

Answer 135

Horrible facial excoriations

Answer 136

May protect the heart, brain, and kidneys from effects of hypertension, may also help to reduce hypertensive-induced fibrosis of target organ Spironolactone: ↓ Na resorption and K excretion

Answer 137

By activating RAAS - Na resorption (water follows)

Answer 138

1. Blood Loss, 2. RBC destruction, 3. Failure of bone marrow to produce RBCs o Can have > 1 etiology in CKD (Normally = blood loss and lack of RBC production)

Answer 139

· Dogs = gastric edema, vasculopathy, glandular atrophy, mineralization, submucosal artertitis, less common (ulceration or necrosis) (Peters et al 2005) · Can have significant GI bleeding in certain patients: GASTRIN (polypeptide from G cells in stomach, renally excreted) o Cats with CKD = ↑ Gastrin levels (but relationship btwn gastrin and Crt is not linear) (Goldstein et al 1998) o Persistent ↑ Gastrin = gastric hyperacidity and mucosal erosions (esp if administering NSAID or steroids) o Upper GI Bleedings (hematemesis, melena, hematochezia) · May not see melena if amount of bleeding is very small · Uremic enterocolitis = Marked large bowel diarrhea with frank blood

Answer 140

Chief Uremic Hemostatic Changes = IMPAIRED platelet FUNCTION

Answer 141

1. Defective platelet cyclooxygenase = ↓ thromboxane A2 production 2. Abnormal concentrations of large multimers of von Willebrand factor (total von Willebrand factor is normal) 3. Abnormal intracellular cyclic adenosine monophosphate 4. Abnormal intracellular Ca mobilization · All cause impaired subendothelial adhesion of platelets and abnormal platelet aggregation

Answer 142

· EPO: Hematopoietic growth factor, stimulates erythrogenesis in anemia, deficiency most common with CKD · EPO Production: Peritubular interstitial cells of the outer medulla and inner cortex (MAIN), about 10-15% in liver o Renal hypoxemia (anemia or hypoxia) result in EPO release = Stimulate RBC growth and differentiation of colony-forming unit-erythroid cells of bone marrow (takes about 5 days to see new RBCs in circulation) o EPO also induced hemoglobulin and RBC membrane protein synthesis and facilities RBC release from bone marrow o With CDK and reduced renal mass: Less EPO produced (Relative EPO Deficiency)

Answer 143

· Humans with CKD and poor nutrition = o Vitamin B deficiencies: B12 (cobalamine), folic acid, niacin, B2 (riboflavin), and B6 (pyridoxine)→ All important in erythropoiesis o Variety of uremic toxins result in poor bone marrow response § Not evaluated in dogs or cats · Protein-calorie malnutrition can contribute to nonregenerative anemias · Iron deficiency (needs iron therapy, but if anemia of chronic inflammatory disease iron overdose is possible)

Answer 144

1. Serum iron (mobile form of iron) 2. total iron binding capacity (indirect measurement of transferrin, serum carrier molecule of iron) 3. ferritin (storage form of iron)

Answer 145

o Iron def anemia: All results low and decreased iron stores in bone marrow (more invasive test!) o Chronic Inflammatory Anemia: Serum iron low, transferrin low to normal (iron sequestration), ferritin normal to increased

Answer 146

1. Recombinant human EPO (r-HuEPO) | 2. Darbepoetin

Answer 147

Iron (either oral - ferrous sulfate or IM - iron dextran)

Answer 148

Produce anti-EPO antibodies!!! □ 60-100% dogs getting r-HuEPO developed anti-EPO antibodies, clinically significant anemia reported in 20-70% of dogs and cats getting EPO (presumptively related to anti-r-HuEPO antibodies) ® Antibodies develop within first few months, but can have late onset as well ® Antibodies suppress native EPO action on bone marrow precursor cells = profound anemia ◊ Precipitous ↓ PCV following response to treatment (retics will ↓ to zero prior to drop in PCV) } Stop EPO therapy and consider transfusion } Antibodies can decline over 2-12 months, anemia secondary to EPO antibodies can be reversed, but patient may be transfusion dependent for weeks to months (anemia that required EPO will persist, thus many animals are euthanized)

Answer 149

Hypertension (humans and CATS): Noted in 60% of cats, thus check BP

Answer 150

Derivative of r-HuEPO with more attached carbohydrates to slow clearance and ↓ freq of administration

Answer 151

Addition of carbohydrate moieties of darbo may shield protein backbone from immunologic exposure and thus less likely to cause antibody formation (anti-r-HuEPO antibodies are directed against protein component)

Answer 152

Life span of transfused RBC SHORTED if patient uremic

Answer 153

Color of serum changes (red): Crt underestimated and BUN/electrolytes not affected

Answer 154

· Caused by ascending migration of pathogenic organisms from distal urogenital tract (normally present in distal urogenital tract and host defense is altered to allow colonization) o Normal micturition o Normal Anatomy: High pressure zone within urethra, surface characteristics of urothelium, urethral peristalsis, length of urethra, male dogs (prostatic secretions: Ig and antibacterial components), good blood supply and flow, ureterovesical flap valves, ureteral peristalsis o Mucosal Defense: Antibody production, surface layer of gylcoasminoglycans, intrinsic mucosal antibacterial properties, rapid turnover of urothelial cells o Urine Properties: Antimicrobial = pH (caution from Vaden), hyperosmolaity, Tamm-Horsfall mucoproteins, high concentration of urea and organic acids

Answer 155

E. coli Proteus spp Klebsiella spp Pseudomonas aeruginosa

Answer 156

Staph spp Strep spp Enterococcus spp

Answer 157

Cystocentesis: >1000 (dogs/cats) Catheterization: >10,000 (dog) and > 1000 (cat) Voiding: >100,000 (dog) and > 10,000 (Cat)

Answer 158

Minimum Inhibitory Concentration = Lowest drug concentration that inhibits microbial growth (NOT all bacteria are killed) o In vitro MIC depends on ability to reach given concentration in the plasma

Answer 159

· Breakpoint = Arbitrary criterion, set at point at which majority of all isolates for that microbe are inhibited (determined by National Committee for Clinical Laboratory Standards) · The further the MIC for individual organism is from the breakpoint, the more likely a drug is effective

Answer 160

· General Rule: Avoid choosing a drug when MIC is approaching the breakpoint (“intermediate susceptibility), if selected use dose that his at high end of normal dosing, also consider that if drug excreted through kidney, it may reach higher levels in the urine that may be effective

Answer 161

If empirical tx: Board –Spectrum = Cephalosporins (good against E. coli and Staph), TMS o Avoid fluoroquinolones: Inherent resistance of many gram positive bacteria and development of resistance patterns in gram negative organisms (esp E. coli)

Answer 162

o Relapse = UTI caused by same organism that recurs after stopping tx (most occur quickly but can be months, Freitag et al 2006) = · Relapsing Infection = Infection recurs rapidly after stopping tx, with same organism with same sensitivity pattern o Reinfection = UTI caused by a different organism that recurs at variable intervals after tx stopped

Answer 163

· Relapsing Infection = Infection recurs rapidly after stopping tx, with same organism with same sensitivity pattern o Problem: Organism is in deep seated niche within urinary tract and is “protected” (bacteria killed in urine but abx cannot reach bacteria in deep tissue) § Sources: Chronic pyelonephritis, prostate, struvite uroliths, any submucosa or location associated with partially obstruction (uretherolith)

Answer 164

Experimentally uropathagenic E. coli can enter host bladder epithelial cells and remain quiescent for period time before leaving the cell and replicating again

Answer 165

· Reinfection with a different organism at variable intervals o Problem: Multiple! Poor systemic immune function (Cushings, immunosuppressive drugs), loss of antimicrobial properties of urine (Glucosuria, poor concentrating ability), anatomic abnormalities (stricture, urolith, previous sx, neoplasa), physiologic predisposition (urine retention from neurologic dx, decreased urethral sphincter tone)

Answer 166

o About 30% of dogs, no identifiable underlying reason is noted (esp in females, Sequin et al 2003) – Assumed to be defect in local immunity

Answer 167

· Original causative bacteria continues to be present during therapy that should be effective (based on UC +Sen) o Diagnosed: ONLY by performing a UC while that patient is receiving the ABX (misconception: that all UC will be negative when a patient is on ABX, only true if drug is effective, not true if organism is resistant)

Answer 168

· Infection with a different organisms in the face of tx for the original organism · Diagnosed ONLY by performing UC during therapy (normally associated with indwelling urinary tubes)

Answer 169

§ ABX that penetrate the renal tissue: trimethoprim, chloramphenicol, nitrofurantoin, some quinolones, aminoglycosides (not recommended for long term use dt nephrotoxicity) · Optimum duration unknown – 4-6 weeks recommended

Answer 170

· Suppressive therapy is used in animals with no underlying abnormalities that can be corrected = low dose long term administration of ABX to assist in UTI control (Sequin et al 2003) o Single dose of effective ABX once daily (normal dose given, but give at night to help concentrate in the urine) o Should be started when the infection is under control (negative UC) o Drugs for Suppressive Therapy: Trimethoprim, nitrofurantoin (neurologic and heaptic toxicity), cephalexin, and enrofloxacin § Risks: ABX resistance and/or drug toxicity

Answer 171

Not treating unless CS present o Risk: Infection could become systemic

Answer 172

ABX with prostatic penetration: Trimthoprim, chloramphenicol, quinolone

Answer 173

Local antiseptic (tris-ethylenediaminetetraacetic acid) and urinary antiseptics (methenamine mandelate)

Answer 174

Rads: 2.5-3.5X length of L2 (dogs); 2.4-3X length of L2 (cats)

Answer 175

Primary renal neoplasia

Answer 176

Renal neoplasia (lymphoma), granulomatous infiltration (due to FIP), perinephric pseudocysts, hydronephrosis, and polycystic kidney disease

Answer 177

Renal Cell Carcinomas

Answer 178

Renal Cell Carcinomas

Answer 179

o Site of metastasis: Regional lymph node, liver, and contralateral kidney; CNS (spine, spinal cord, and brain); and lungs (Klein et al., 1988) o Local Extension: Ipsilateral adrenal gland and abdominal serosal surfaces

Answer 180

Histologic types of RCC → tubular (most common), papillary, tubulopapillary, solid/undifferentiated forms (Henry et al., 1999)

Answer 181

o Nephrectomy → tx of choice for solitary renal tumors without azotemia or metastasis (partial nephrectomy in humans if not locally extensive) o No standardized adjuvant chemotherapy protocols → respond poorly to most agents (doxorubicin, cisplatin, and Interferon-α)

Answer 182

o Primary renal hemangiosarcoma may be less aggressive than visceral hemangiosarcoma § Slower rate of progression; ¯ frequency of macroscopic metastasis at diagnosis (Locke and Barber, 2006) § Mean survival: 278 days (14 dogs); worst outcome hemoperitoneum § Chemotherapy: Doxorubicin-based protocol likely is appropriate, others not evaluated

Answer 183

o NCSU: 24% primary renal tumors (dogs) → hemangiosarcomas

Answer 184

Nephroblastoma Called Wilm's tumor (humans) o Nephrectomy may be curative, + adjunctive chemotherapy when histology suggests a less differentiated, more aggressive tumor o Sites of mets: Spinal cord (most common)

Answer 185

Spinal cord

Answer 186

syndrome of bilateral multifocal renal cystadenocarcinomas, nodular dermatofibrosis, and uterine leiomyomas o Affected dogs have mutation in 1 allele of folliculin (protein of unknown function) · Long term prognosis is POOR, due to metastatic disease and renal failure (common), mean age at death 9 yrs · Treament o Nephrectomy = contraindicated → both kidneys affected o Chemotherapy possible, but no successful reports (paclitaxel and pirfenidone)

Answer 187

Evaluation of diffuse skin nodules (mean age 8 yrs)

Answer 188

Renal Lymphoma

Answer 189

Acute renal failure (up to 80%)

Answer 190

Acute renal failure (up to 80%) What virus is strongly associated with development of renal lymphoma in cats? FeLV strongly associated with development of renal lymphoma (50% affected cats are FeLV +)

Answer 191

CHOP § About 60% achieve complete remission → mean duration of remission 372 days (median 127 days), mean survival 408 days (median 169 days) (Mooney et al., 1987) § Nephrectomy is not recommended → both kidneys invariably are affected § Azotemia improves dramatically with tx of lymphoma, so renal failure is not cause of death in most, but residual renal damage may persist

Answer 192

1. involvement of other organ systems (particularly CNS) 2. FeLV infection 2. Severity of renal failure (Mooney et al., 1987)

Answer 193

primary renal lymphoma, RARELY have involvement of other organs o Nephrectomy is possible in dogs if unilateral (only if azotemia and urine concentrating is ok), followed with chemotherapy

Answer 194

Transitional Cell Carcinomas | o Not renal origin, but they invade renal parenchyma

Answer 195

Carcnimoas | Renal Blood Flow = 15% of total CO

Answer 196

1. Polycythemia → secondary to excess production of erythropoietin → most common paraneoplastic syndrome 2. Extreme leukocytosis → Excess production of granulocyte-macrophage colony-stimulating factor 3. Hypertrophic osteropathy Palpable firm swelling of distal long bones (most prominent in metaphyseal regions) can be VERY painful § May occur with extreme leukocytosis 4. Hepatopathy: ↑ ALP, GGT (no ↑ bilirubin), common in humans, reports in dog with sarcomatoid RCC

Answer 197

· Polycythemia → secondary to excess production of erythropoietin → most common paraneoplastic syndrome o Not true paraneoplastic syndrome, as it may results from renal tumors ¯ O2 levels → excessive EPO production by nonneoplastic renal epithelial cells o Could be incidental finding or patient presents with epistaxis or CNS signs (disorientation, seizures) o Measure serum erythropoietin (question value!), since erythrocytosis and renal mass are enough for dx o Reports with renal carcinomas, fibrosarcoma, and lymphoma; cats: renal carcinoma o Nephrectomy can resolve polycythemia but mets of functional cells may prevent resolution

Answer 198

· Azotemia → Paraneoplastic hypercalcemia, secrete PTHrp or other humoral factors that ↑ calcium release from bones and promote calcium absorption from GIT o Hypercalcemia of malignancy: Higher serum calcium and phosphorus → more likely to develop kidney dz than those with hyperparathyroidism o Kidney damage from mineralized tubular basement membranes, dysregulated renal tubular cell mitochondrial function, dehydration 2nd to hypercalcemia-induced polyuria, changes in GFR

Answer 199

1. Diuresis (0.9% NaCl) 2. Loop diuretics (Lasix): ↑ renal Ca excretion (once hydrated) 3. Bisphosphonate drugs: Inhibit osteoclast function and↓ mobilization of Ca stores from bone □ Pamidronate is highly effective 4. Prednisone: Promote calciuresis (may worsen long-term prognosis)

Answer 200

· Kidney disease high in humans with monocolonal gammopathies 2nd to multiple myeloma or B-cell lymphoma o Obstruction of renal tubules by light chains, toxicity to renal tubules dt resorption of proteins, deposition of Ig light chains within renal parenchyma; ¯ renal perfusion by hyperviscosity, tumor infiltration into kidney o Cast nephropathy (obstruction of renal tubules and tubular cell toxicity): Not definitively described in dogs/cats § Humans: Light chains lead to amyloidosis and fibrillary nephropathy □ Rare reports of light chain associated amyloidosis in dogs/cats § Humans with multiple myeloma: Fanconi syndrome (not reports in dogs/cats)

Answer 201

§ Leiomyosarcoma § Adrenal adenocarcinoma § Parathyroid adenoma (membranoproliferative glomerulonephritis) § Hemangiosarcoma § Osteosarcoma (microalbuminuria) § Mast cell tumor (membranous glomerulopathy) § Mammary tumors and Sertoli cell tumor (reactive amyloidosis) § TCC § Bronchogenic adenocarcinoma § Lymphoma (microalbuminuria)

Answer 202

· Tumor Lysis Syndrome: Secondary to massive release of intracellular content (phosphorus, uric acid, potassium): After chemo for lymphoma is a rare cause of renal failure o Humans: Precipitation of uric acid, calcium phosphate, or hypoxanthine in renal tubules, cytokine-induced perturbations in renal blood flow → rapid renal failure, often death § TX: Rehydration (to improve renal perfusion), alkalinization of urine (inhibit uric acid precipitation) and tx hyperkalemia and hypocalcemia

Answer 203

``` Platinum compounds (primarily cisplatin) Streptozotocin Methotrexate (dogs - uncommon) ```

Answer 204

Doxorubicin (unknown mechanism)

Answer 205

Lomustine (CCNU) - VERY rare

Answer 206

Hiamalyan and Persian

Answer 207

1. CaOx | 2. Dried Solidified Blood Calculi

Answer 208

o Sensitivity of abdominal rads for dx of ureterolithiasis: 81% (Kyles et al., 2005a) § AUS: Sensitivity for dx ureterolithiasis: 77% (Kyles et al., 2005a) § Combo of Abdominal Rads + AUS: Sensitivity of 90%

Answer 209

o Fluid diuresis (+/- diuretics; furosemide, mannitol) § Humans: IV Glucagon: Relaxation of ureteral smooth muscle = Promotes passage of calculi □ NO effect in cats (0.1mg per cat IV) § Humans: α-adrenergic antagonists (prazosin, tamsulosin), amitriptyline (a tricyclic antidepressant), and calcium channel blockers □ No reports in dogs and cats (??? But there is a report of 8 cats with amitriptyline)

Answer 210

12 month survival 66% (dying related to chronic renal insufficiency or recurrent ureterolithiasis (Kyles et al., 2005b)

Answer 211

§ Recovery of renal function about removal: Duration and extent of obstruction o Research dogs: Almost completely recovered after 4 days of relief, 46% GFR returned after 14 days of obstruction, almost NO GRF returned after 40 days of obstruction o Optimal time has not been determined in cats; reported median interval btwn dx and sx = 3 days (Kyles et al., 2005b)

Answer 212

§ 12 month survival was 91% (many dying from chronic renal insuffuicency, recurrent ureterolithiasis, or nonregenerative anemia)

Answer 213

Hypocitraturia (risk factor for CaOx stones since citrate is chelated to calcium – more soluble salt) o Citrate supplementation helpful in humans; No studies in cats Potassium citrate

Answer 214

Hill's feline x/d Purina NF RC: Feline SO

Answer 215

Crushing/fragmenting uroliths by shock waves or laser energy

Answer 216

Extracorporeal shock wave llithotripsy (SWL), electrohydraulic lithotripsy, laser lithotripsy ○ SWL: Neprholiths, ureteroliths (Adams and Senior, 1999) ○ Electrohydraulic lithotripsy: Urocystoliths in larger females = REPLACED with safer methods ○ Laser lithotripsy: Using rigid or flexible endoscope § Humans: Holmium: YAG (Ho:YAG) laser for intracorporeal lithotripsy § Percutaneous nephrolithotomy → Procedure of choice for large staghorn nephroliths § Ho:YAG can efficiently fragment uroliths from dogs regardless of chemical composition (Wynn et al., 2003) § Implanted urethroliths in male dogs safely fragmented by Ho:YAG laser (Davidson et al., 2004) § Successful removal of bladder and uretheral calculi in dogs with laser lithotripsy fragmentation (Adams and Lulich, 2006)

Answer 217

Transurethral cystoscopy and laser lithotripsy → stone-free status in 80% male dogs and 100% female dogs (Adams and Lulich, 2006)

Answer 218

· Minimally invasive stone removal = Reduced postprocedureal dysuria and hematuria · Shorter than sx · Owner preference · If recurrent uroliths: Can be performed repeatedly to avoid cystostomy

Answer 219

· Presence of ACTIVE urinary tract infection o ↑ intravesicular pressure during voiding urohydropropulsion may induce vesicoureteral reflux = ascending pyelonephritis o Small perforations of bladder wall = spread of microbes into abdominal cavity o Perioperative ABX given to animals that have current UTI or prior UTI → fragmentation of infected uroliths may liberate viable bacteria from inner layers of uroliths · Coagulopathy: Intraluminal or periurethral hemorrhage · Obstruction of urinary outflow distal to urolith (urethral stricture): Hard to pass cystoscope and remove fragments

Answer 220

· Laser fragmentation: Photothermal mechanism that can induce chemical alterations in stone composition (Chan et al., 1999) o Not clinically relevant in most stone types o Converts uric acid uroliths into small quantities of cyanide (can be absorbed into systemic circulation) but risk of clinical toxicity is VERY low (Teichman et al., 1998) § Unable to detect cyanide in fluids during procedure, but still need constant irrigation of saline and frequent evacuation of bladder to prevent cyanide from accumulating

Answer 221

Laser Fragmentation o Converts uric acid uroliths into small quantities of cyanide (can be absorbed into systemic circulation) but risk of clinical toxicity is VERY low (Teichman et al., 1998) § Unable to detect cyanide in fluids during procedure, but still need constant irrigation of saline and frequent evacuation of bladder to prevent cyanide from accumulating

Answer 222

Classified as idiopathic feline lower urinary tract disease, idiopathic cystitis, or interstitial cystitis

Answer 223

· CS subside within 5-7 days (without tx) in up to 92% of cats with acute nonobstructive idiopathic cystitis (Barsanti et al., 1982, Kruger et al., 2003; Osborne et al., 1996) · CS may recur and again subside without tx: 40-50% of cats with acute idiopathic cystitis experience recurrence of CS within 1-2 yrs (Barsanti et al., 1982; Kruger et al., 2003)

Answer 224

· Subset of cats that CS persist for weeks to months or recur frequently → chronic idiopathic cystitis o Spectrum of clinical manifestations associated with similar etiologic factors or entirely different mechanism of disease · Fewer than 15% of cats with acute idiopathic cystitis will develop chronic forms

Answer 225

· Empirical tx for hematuria, dysuria, and pollakiuria – BUT only 1-3% have bacteria noted at onset of CS of lower urinary tract disorders in young-middle aged cats · USELESSNESS for ABX in abacteriuric cats with lower urinary tract disease have been documents (Barsanti et al., 1982) · Tx with ABX has been perpetuated by misinterpretiation of “pseudobacteria” in unstained urine sediment and failure to perform UC ○ 89% of unstained feline urine sediments reported as + bacteruria by light microscopy were sterile on UC → Reduce false-positive bacteruria using a modified Wright-stain (Diff Quik)

Answer 226

· Amitriptyline hydrochloride (Elavil): tricyclic antidepressant drug with anticholinergic, antihistaminic, sympatholytic, analgesic, and antiinflammatory properties o Humans: Months for antidepressant actions to be evident, BUT rapid onset of other properties § Used in humans with interstitial cystitis (randomized placebo controlled, double masked study found that 63% on amitriptyline for 4 months rated good or excellent compared to 4% of placebo group) o Uncontrolled study in cats (severe recurrent idiopathic cystitis): CS ↓ in 60% (9/15) cats treated with amitriptyline for 6 months (Chew et al., 1998) o Randomized double-masked, placebo-controlled clinical trial in short term (7day) amitriptyline in 31 cats with acute nonobstructive idiopathic cystitis, amitriptyline did NOT reduce duration of pollakiuria and hematuria (Kruger et al., 2003) § CS recurred sooner and with higher frequency in amitriptyline treated cats than placebo § Adverse events: Urinary tract infection, sedation, hyperbilirubinemia, ↑ ALT o Placebo-controlled study in cats: No difference in severity of CS after short-term (7 days) with amitriptyline and amoxicillin compared to placebo and amoxicillin (Kraijer, Fink-Gremmels, and Nickel, 2003) o Thus short term tx may not work; but it is unknown if the long-term use may be helpful (studies needed) o Use amitriptyline in cats with severe chronic idiopathic cystitis that are not responding to other tx § If no change in CS in 2-4 months, taper over few weeks and then stop this medication □ Humans: Abrupt discontinuation = Withdrawal syndrome (GI somatic, neurologic, and psychiatric disturbances)

Answer 227

Glucocorticoids · Small, double-blind, placebo-controlled study: Antiinflammatory prednisolone (1 mg/kg PO q12hrs for 10 days) = NO benefit in ¯ CS or duration of CS in affected cats (Osborne et al., 1996) Nonsteroidal Antiinflammatory Drugs · NSAIDs more effective when inflammation has causes sensitization of pain receptors to normally painless mechanical and chemical stimuli Studies in cats needed

Answer 228

For 24-72 hrs may be beneficial in alleviate acute “flare-ups” Studies in cats needed

Answer 229

· Pollakiuria may be associated with pain, bladder fullness, urgency → Related to inflammation induced stimulation of bladder sacral sensory afferent nerves → sensation of pain or fullness/urgency → premature micturition reflex = inappropriate or involuntary voiding of small quantities of urine o Detrusor contraction: Cholinergic parasympathetic efferents → anticholinergics agents may help with pollakiuria and urge incontinence · Propantheline (Pro-Banthine): potent nonselective muscarinic antagonist = ¯ force and frequency of uncontrolled detrusor contractions = No benefit in cats · Oxybutynin chloride (Ditropan) / Tolterodine (Detrol): synthetic tertiary amine muscarinic receptor antagonists o Humans: Used for overactive bladder and urge incontinence No studies in cats

Answer 230

· Transitional epithelium of bladder covered by glycocalyx composed of hydrated glycoconjugates (glycoproteins and glycosaminoglycans (GAGs) o Urothelial GAGs minimize adherence of microorganisms and crystals to bladder urothelium and limit movement of urine proteins and other solutes from bladder lumen to other surrounding tissue · Defects in surface GAGs leading to ↑ urothelial permeability hypothesized as causative factors in pathogenesis of feline idiopathic cystitis (Human interstitial cystitis) · Pentosan Polysulfate (Elmiron) o Oral and intravesicular of GAG (humans): Reduced transitional cell injury = May benefit SOME cats ( no studies in cats) · Glucosamine and Chondroitin Sulfate o Glucosamine: Amino sugar made in body (important intermediate in formation of GAGs) o Chondroitin Sulfate: Most abundant GAG in bladder surface GAG layer § 6 month randomized placebo controlled study with oral glucosamine: NO difference in CS (Gunn-Moore and Shenoy, 2004) o Combination of glucosamine and chondroitin has NOT been evaluated (potential synergism)

Answer 231

1. Dietary management - more canned food (increased water intake) 2. Stress management 3. Environmental Enrichment

Answer 232

· Feline facial pheromone fraction F3 (Feliway): Synthetic pheromone o Application to living environment as adjunctive therapy o Randomized double-blind, placebo-controlled, crossover study (9 cats): NO significant difference in CS, behavior, or overall health (Gunn-Moore and Cameron, 2004)

Answer 233

Mucous or mucocrystalline plug secondary to feline lower urinary tract disease OR CaOx stones

Answer 234

Cardiovascular compromise (check MM, CRT, pulse quality, rate) o Slow HR → Hyperkalemia → Check ECG and serum potassium § NOTE: In cats hyperkalemia can have normal to rapid HR o Metabolic Acidosis o Ionized Hypocalcemia

Answer 235

Hyperkalemic induced cardiac conduction changes (tall positive or large negative T-waves, diminished or absent p-waves, prolonged, P-R intervals, widened QRS complex, since waves (end-stage when QRS and T waves merge) – Association of increasing K levels with abnormalities is inconsistent o NOTE: Can see ventricular tachycardia with hyperkalemia (or sinoventricular rhythm with intraventircular conduction delay)

Answer 236

Driving potassium intracellularly or by removal of K from body = Effect is transient o Calcium gluconate: Direct antagonism of cardiac effects of hyperkalemia (50-100 mg/kg IV over 2-3 mins with ECG monitoring, since Ca can induce arrhythmias) § Effects are immediate (lasting 20-30 mins) § SHOULD be the FIRST drug in hyperkalemic cats o Regular Insulin: Promotes intracellular movement of K (0.1-0.25U/kg IV bolus, followed by slow bolus of 1-2 g of 25% glucose per unit insulin to prevent hypoglycemia) § Effects within mins to 1 hour (monitor BG for several hours after administration of insulin) o Sodium Bicarbonate: Lower K by raising pH and driving K into cells § Effects within 30-60 mins, persists for hours

Answer 237

Hypocalcemia

Answer 238

· Post-obstructive diuresis is profound (esp 24-48 hrs later) – May exceed 120 ml/hr in some cats

Answer 239

· If multiple obstructive events → perineal urethrostomy | o Complications: Stricture formation, recurrent UTIs, does NOT eliminate underlying cause

Answer 240

urethral folds, moist epithelial seal, primary smooth muscle | · Urethral outlet resistance maintained by smooth and striated muscle components of urethra

Answer 241

Activation of terminal α-adrenergic receptors Non-selective agent = Phenoxybenzamine (dog); Prazosin: Potent (dogs/cats) Uroselective α1-antagonists (terazosin, doxazosin, tamsulosin) – Humans

Answer 242

Benzodiazepine (diazepam, alprazolam)

Answer 243

``` Enhance by activating terminal receptors for parasympathetic input or antagonizing the (sympathetic) adrenergic input on β-receptors in detrusor muscle o Bethanechol (parasympathomimetic agent): Primary tx for detrusor atopy or dysfunction ```

Answer 244

primary sphincter mechanism incompetence

Answer 245

Combined reproductive hormone and α-agonists to see synergistic effects (allows estrogen to “prime” the urethral receptors for α-agonist treatment – both drugs can be reduced over time

Answer 246

§ Estrogen diethylstilbestrol (DES), stilbestrol, estriol, and conjugated estrogens (Premarin) improve urethral resistance by increasing α-adrenergic receptor responsiveness and improving urethral vascularity and other mucosal epithelial characteristics □ Can be used with phenylpropanolamine (PPA) = May be synergistic when combined □ Improves 60-80% of treated dogs ® BM suppression unlikely but owners should be warned § Gonadotropin-releasing hormone (GnRH) analogs – Suppress sex hormone release □ Theory: Chronically unsuppressed FSH and LH release (because of lack of negative feedback) in spayed dogs may contribute to urinary incontinence ® GnRH analogs = Reduced FSH and LH over time □ Leuprolide, buserelin, and deslorelin (Reichler et al 2003)

Answer 247

· α-agonists (sympathomimetic drugs) o Phenylpropanolamine, phenylephrine, and pseudoephedrine o SE: restlessness, tachycardia, systemic hypertension, anorexia, GI side effects, and aggression and other behavioral changes

Answer 248

o Urethral tone, smooth muscle (MAJOR component) o Mucosal integrity, vasculature, and connective tissue surrounding the urethra o Healthy urothelium o Surface tension from glandular secretions o Pliability of the mucosa o Bladder position o Exposure to vesicourethral junction and proximal urethra to intraabdominal pressure § Studies have linked urethral position/length and vesicourethral angle to incontinence (Gregory, 1994; Gregory et al., 1996) § Incontinence: Short urethra and intrapelvic bladders o Hormone Status § 20% of neutered females will develop a degree of urinary incontinence (75% within 3 yrs of neutering) □ Decreased estrogen (woman) associated with loss of uretheral muscle tone, urethral vascular atrophy, decreased glandular secretions ® Increasing FSH and LH may play a role, but mechanism is unknown (Reichler et al., 2005) o Other factors: breed, body weight, tail docking

Answer 249

§ Old English sheepdogs, Doberman pinschers, GSD, boxers, weimeraners, rotties, Irish setters □ Labs have a decreased risk (Holt and Thrusfield, 1993) □ Large and giant breed dogs (Over 20kg), small breed are at decreased risk

Answer 250

§ 20% of neutered females will develop a degree of urinary incontinence (75% within 3 yrs of neutering) □ Decreased estrogen (woman) associated with loss of uretheral muscle tone, urethral vascular atrophy, decreased glandular secretions

Answer 251

Lympathomimetic drugs, estrogens, periurethral injections, and colposuspension

Answer 252

· 32 FS dogs refractory to PPA, tx with periurethral collagen injection (Arnold et al., 1996) o 52% were continent after 1 or 2 injection w/o PPA o 75% if PPA added o No complications observed o 19% (6) continent for longer than 30 months after 1st injection · 40 dogs over 7 yrs(Barth et al., 2005) o 68% dogs were continent for mean of 17 months (1-64 months) after injection o Additional 25% with 60% continent after addition of α-agonist therapy o Side effects in 15% (stranguria, hematuria, vaginitis) · 29 FS dogs (34 collagen injecitons) (Byron et al., 2005) o 6 had ectopic ureters (6 had corrective sx) o 66% complete continence immediately after the injection, additional 32% were improved o 55% achieved full continence after additional of medical tx o Mean duration of continence = 12.1 months w/o other tx o Client satisfaction 88%, 76% were 100% satisfied · Repeated injection of collagen: Enhancing the previously placed blebs or additional of new blebs = Improved response and reinduction of continence

Answer 253

Greyhound AkaGreenetrack Disease or Alabama Rot Syndrome of skin ulcerations, edema, and renal dysfunction

Answer 254

Hemolytic-uremic syndrome (HUS)

Answer 255

Carbamoylared Hb High levels of CaHb in humans and dogs with CKD urea exists in equilibrium with cyanate which can react with valine groups on Hb

Answer 256

TOENAIL creatinine!!

Answer 257

compensatory hypertrophy, acute inflammatory renal diseases (interstitial nephritis or glomerulonephritis), metabolic nephropathies, portosystemic shunt, toxic insult, and diffuse infiltrative neoplasia (LSA)

Answer 258

reduction in kidney function within 48 hours defined by the occurrence of at least one of the following: (1) an absolute increase in serum creatinine concentration of at least 0.3 mg/dl (26.4 mmol/L), (2) an increase in serum creatinine concentration of more than 50% of baseline, (3) oliguria of less than 0.5 ml/kg/hr for more than 6 hours

Answer 259

Acute Kidney Injury Network

Answer 260

Significant association btwn increasing severity of AKI and mortality, even with minimal increases in creatinine concentration that previously were not considered important.

Answer 261

Based on 2 retrospectives: 10-17% For cats - 20-21.3%

Answer 262

``` preexisting renal disease** dehydration and volume depletion decreased CO **Heart dz** advanced age** (>7) fever hypotension hypertension, hypoalbuminemia sepsis electrolyte imbalances acidosis hyperviscosity syndromes liver disease administration of nephrotoxic drugs** administration of radiocontrast media pancreatitis diabetes mellitus anesthesia** surgery (Humans: decreased renal perfusion) ```

Answer 263

Retinol-binding protein (URBP) - Freely infiltered by reabsorbed in proximal tubular (if increased = Proximal tubular damage) In SIRS dogs: increased URBP to UC compared with healthy =>presence of increased quantities of URBP could occur from direct tubular damage as an indication of AKI or from competition with other HMWPs for tubular binding sites

Answer 264

N-acetyl-β-d-glucosaminidase (NAG) | γ-glutamyl transpeptidase

Answer 265

Decrease in survival was significant with both mild and severe changes in creatinine concentration ion (dogs: 38-46% compared to 84%; cats 48% compared to 85% - but more significant for cats with more severe AKI) About 50% that survive will develop CKD!

Answer 266

NO reports of HA-AKI | But there are reported in humans with sepsis (blackbox warning)

Answer 267

1. Dipstick colorimetric | 2. Sulfosalicylic acid (SSA) precipitation test = Turbidity

Answer 268

Dipstick: Mainly albumin; 30 mg/dl D: 81%/48% C: 90%/11% SSA: Albumin Globulins Bence Jones Proteins 5 mg/dl D: 73%, 64% C: 58%, 25%

Answer 269

Radiographic contrast agents Penicillin, cephalosporins, sulfisoxazole Thymol (a urine preservative) Unknown Reasons

Answer 270

Performed Poorly = High # false positive results NEITHER USEFUL for albuminuria in cats = NEED to use species specific ELISA NOTE: Cats with CKD the accuracy of dipstick and SSA improved (likely dt high amount of proteinuria)

Answer 271

Microalbuminuria is defined as concentrations of albumin in the urine that are higher than normal (>1.0 mg/dl) but below the limit of detection using conventional urine dipstick tests (<30 mg/dl).

Answer 272

Suggests dz progression

Answer 273

1. increased glomerular filtration of plasma proteins associated with intraglomerular hypertension, structural abnormalities of the glomerular capillary wall, or the presence of immune complexes or vascular inflammation in the glomerular capillaries. 2. Decreased reabsorption of filtered plasma proteins due to tubulointerstitial disease

Answer 274

Dogs: 0.2-0.5 Cats: 0.2-0.4

Answer 275

the cutoff value of 0.2 for UP/C ratio resulted in an unacceptable number of false-negative results.

Answer 276

Neoplasia, infection, polyarthritis, hepatitis, hyperadrenocorticism, immune-mediated hemolytic anemia, and systemic hypertension are common concurrent medical problems

Answer 277

iral diseases, neoplasia, immune-mediated disease, polyarthritis, and systemic hypertension

Answer 278

Nonazotemic: TX if UPC 1-2 Azotemic: Tx if UPC >0.5 dogs or >0.4 cats

Answer 279

Reduction in dietary protein (renal diet) Omega-3 FA (found in most renal diets) ACEi If higher magnitude - Aspirin Supportive care: Control hypertension, edema, and thrombolic potential

Answer 280

(1) monitoring for and treatment of underlying NIN disorders, (2) reduction of proteinuria, and (3) management of uremia and other complications of renal failure

Answer 281

Intraglomerular hydrostatic pressure

Answer 282

ACEi (ENALAPRIL) - Considered standard of care for glomerular dz in dogs

Answer 283

no evidence that one ACE inhibitor is pharmacokinetically superior to others in either dogs or cats

Answer 284

Serum aldosterone concentrations increase over time in people treated with maximal dosages of ACEi or Angiotensin II receptor blockers

Answer 285

Reducing the dosage of ACE inhibitor, ARB, or spironolactone; feeding a reduced-potassium diet; or administering a gastrointestinal potassium binder (e.g., Kayexalate)

Answer 286

WEAK, only 10-15 mmHg

Answer 287

induce preferential dilation of the afferent glomerular arteriole, thereby increasing intraglomerular hydrostatic pressure, as well as RAAS activation in dogs and potentially also cats (based on Atkins work) THUS, some recommend that in dogs/cats with CKD that you need a ACEi as well

Answer 288

increases net fluid extravasation from vascular beds (edema) and simultaneously widens glomerular endothelial pore size (proteinuria)

Answer 289

Remove some of it (QOL) | Lasix initially and then spironolactone

Answer 290

Day-to-day UP/C variations of up to 50% in dogs and 90% in cats have been described, and therefore averaging results of two to four UP/C ratios measured over a 3- to 5-day period is ideal for estimating the severity of proteinuria in an individual patient.

Answer 291

``` Variable prognosis (dead to years!) Concurrent azotemia - negative prognostic indicator ``` 605 days in nonazotemic nonnephrotic dogs with glomerular dz 45 days in azotemic nonnephrotic dogs with glomerular dz

Answer 292

HX that suggests animal is at increased risk of CKD = Expsoure to nephrotoxin, breed, high prevalence of infectious dz, or old age)

Answer 293

IRIS CKD Stage 2-NP-AP3(c), where NP indicates absence of proteinuria and AP3(c) denotes arterial blood pressure associated with a high risk of target-organ damage and evidence of complications secondary to high blood pressure present at initial staging

Answer 294

IRIS CKD Stage 4-BP-RND, where BP denotes borderline proteinuria and RND indicates that the risk of target-organ damage associated with arterial blood pressure was not determined

Answer 295

IRIS CKD Stage 3-P-AP0(nc), where P denotes proteinuria and AP0(nc) designates an arterial pressure status associated with minimal or no risk of target-organ damage accompanied by no evidence of hypertensive complications

Answer 296

Late IRSI CKD Stage 2 Dog: 1.4- 2.0 Cat: 1.6-2.8

Answer 297

Albumin <2

Answer 298

1. Restrict dietary sodium 2. Calcium channel blocker (amlodipine) 3. Icrease dose of amlodipine Add ACEi to CCB tx

Answer 299

1. Restrict dietary sodium, 2. Start ACE inhibitor therapy at the standard dosage. 3. Double the dose of ACE inhibitor (this will improve antihypertensive efficacy in some patients). 4. Combine the ACE inhibitor with a CCB (e.g., amlodipine). Caution: see step 4 earlier for cats. 5. Add hydralazine to combined ACE inhibitor and CCB treatment.

Answer 300

early in the course of CKD, and many cats with IRIS CKD Stage 2 disease already have increased blood parathyroid hormone (PTH) concentrations even when blood phosphate concentrations remain within reference limits

Answer 301

Reducing phosphorus intake may be benficial

Answer 302

For dogs with IRIS CKD Stage 3 or 4 there is evidence that judicious use of calcitriol prolongs survival when phosphate is controlled and ionized calcium and PTH are monitored

Answer 303

``` Na Bicarbonate K citrate (esp if hypokalemic) ```

Answer 304

CATS! | Consider potassium gluconate

Answer 305

1. COX-1: Housekeeper 2. COX-2, inducible form in inflammation and other dz states 2. COX-3 or splice variant of COX-1 - Poorly understood

Answer 306

Both isoenzymes (COX-1 and COX-2) are constitutive and inducible in the kidney and both contribute to the control of renal blood flow, GFR, renin release, and cytoprotection NOT a big deal in normal animals BIG deal in at risk patients!

Answer 307

1. Acute cortical nephrotoxicity (acute hemodyanmic insult) | 2. Chronic meduallary cytotoxicity (chronic cytotoxic insult)

Answer 308

Hemodynamically mediated acute cortical nephrotoxicity = Classical AKI

Answer 309

``` ECF depletion (dehydration) Systemic hypotension General anesthesia Dietary salt restriction Diuretic use Administeration of antihypertensive drugs Higher NSAID dose Hypoalbuminemia Genetic factors? ```

Answer 310

Loss of renoprotective effects of vasodilatory prostaglandins Primary effects: Decreased renal blood flow and GFR

Answer 311

Inhibition of COX-1 more important than inhibitor of COX-2

Answer 312

Early: Renal cells and casts in sediment, renal enzymuria, proteinuria, microalbuminuria Intermediate: Serum electrolyte changes, reduced urine concentration Late: Rising creatinine!!

Answer 313

Dogs are more susceptible than people Cat unknown

Answer 314

``` Chronic dehydration Chronic hypotension or multiple acute bouts of hypotension Administration of antihypertensive drugs Higher NSAID dose Hypoalbuminemia Genetic factors? ```

Answer 315

Loss of cytoprotective effects of prostanoids Effect - Necrosis of medullary interstitial and tubular cells (papillary necrosis)

Answer 316

Inhibition of COX-2 more important than inhibition of COX-1

Answer 317

Early: NONE!!! Intermediate: Renal enzymuria, decreased concentrating ability Late: Electrolyte abnormalities, acid-base changes, rising creatinine

Answer 318

Dogs are more susceptible than people Cat unknown

Answer 319

Dt potential for GI toxicity

Answer 320

1. Initiation 2. Extension (ishcemia, hypoxemia, inflammation, cellular injury) 3. Maintenance (urine production variable) 4. Recovery (marked polyruia possible, tubular repair, can take ks to months)

Answer 321

Partial restoration of renal tubular function and osmotic diuresis of accumulated solutes

Answer 322

Dopamine infusion

Answer 323

Fenoldapam (selective dopamine D1 receptor agonist) Renoprotective in humans Few studies in normal dogs and cats - Beneficial effects on GFR and urine volume

Answer 324

hyponatremia and hypokalemia

Answer 325

Amlodipine

Answer 326

1. Severe azotemia (creat >10) 2. Lack of improvement or worsening with IVF and supportive care 3. Concurrent dz (pancreatitis or sepsis)

Answer 327

Ability to remove larger molecules from blood than can diffusion HARD since ultrafiltrate must be calculated and replaced

Answer 328

Purely convection | positive transmembrane pressure forces fluid (ultrafiltrate) out of the blood, hemoconcentrated blood returned

Answer 329

Purely convection positive transmembrane pressure forces fluid (ultrafiltrate) out of the blood, ultrafiltrate is replaced with a sterile balanced electrolyte solution

Answer 330

Diffusion therapy Blood enters the dialyzer, where it is divided into thousands of strawlike semipermeable membranes that are bathed in dialysate Movement of molecules is based on their relative concentrations in dialysate

Answer 331

diffusive aspects of CVVHD with the convective aspects of CVVH Blood flowing through the dialyzer's semipermeable membranes are bathed in dialysis solution and exposed to a positive transmembrane pressure so that both diffusion and ultrafiltration guides the movement of solutes

Answer 332

Systemic heparinization | Regional citrate infusion

Answer 333

39% dogs UTI (no CS) with chronic skin dz that got steroids compared to 18% w/o steroids IVDD sx dogs that got dexSP = 11.4X more likely to have +UC than w/o dex sp HAC: 46% found to have UTI, CS rare

Answer 334

Dogs: UTI in 24-37% (few had CS) Cats: 12-13% UTIs (CS in 14-445)

Answer 335

Emphysematous cytitis - E.coli

Answer 336

12% (none had CS)

Answer 337

Morbidly obese dogs (>45% body fat)

Answer 338

45% dogs with U cath develop UTI | Increased with age (by 20% with each year), duration of catheterization (27% each day), and antimicrobial use (by 454%)

Answer 339

CKD (twice yearly) | DM and HAC

Answer 340

Culture of uroliths and bladder mucosa may be more sensitive!

Answer 341

Bacterial virulence factors | Host muscoal response (cytokine production)

Answer 342

Uropathogenic E. coli (35-50% UTIs) | Posses genes and virulence factors that allow colonization and persisitence in urinary tract

Answer 343

Cell entry: Pili (fimbriae) = Type 1 pilia (tip of adhesin, FimH = binds to monomannose molecules) Disrupt and increased host cell mobilization = = Penetrate deeper layers, permits bacterial persistence despite host defenses and ABX

Answer 344

High dose Clavamox (25 mg/kg PO q8hrs) BEFORE carbapenems

Answer 345

Used to prevent reinfection in an animal documented to develop UTIs three or four times per year or more Bedtime dosing (max bladder contact time) at 30-50% daily therapeutic dose

Answer 346

Proanthocyanidins - UPEC antiadhesion effects Abstract in dog urine (similar effects) No in vivo studies!

Answer 347

methenamine hippurate = Dissociated to formaldehydrate = Bactericidial

Answer 348

Polysulfated glycosaminoglycans (Elmiron) - Though that bladder urothelium is protected by a glycosaminoglycan layer that accounts in part for its capacity to tolerate constant contact with urine and also helps prevent bacterial adhesion

Answer 349

Fosfomycin (Monurol) - Similar B-lactams, BUT is NOT inactivated by ANY class of B-lactamases

Answer 350

Deliberate induction of asymptomatic bacteriuria with a specific E. coli strain (that cannot express primary adhesins but has superior biofilm-forming capacity) has been shown in murine models and in humans to successfully prevent establishment of a range of UPEC strains in the bladder NOT shown in dogs

Answer 351

Bacteriophages, noted to work in dog and cat urine, but no in vivo studies

Answer 352

Cats: 1/3 Dogs: 2/3 (65-70%( will have concurrent UTI

Answer 353

dried solidified blood calculi, mucus plugs, and radiolucent uroliths

Answer 354

Up to 2-3 months

Answer 355

Amitripytline

Answer 356

Glucagon | No shown in vet med

Answer 357

one in vitro canine ureteral study morphine was found to have spasmogenic effects (even after naloxone given)

Answer 358

H2receptor blockers

Answer 359

ACEi | Angiotensin receptor blocker = Losartan

Answer 360

``` Mg Citrate Pyrophosphate Nephrocalcin Tamm-Horsfall glycoproteins ```

Answer 361

``` Uric acid (seen in min Schnauzers) Foreign material ```

Answer 362

Potassium citrate (alkalinzing agent, and provide citrate to inhibit formation of CaOX) Thiazide diuretics (inhibit Na/Cl cotransporter, Ca reabsorption promoted)

Answer 363

Lowest at night | Highest during the day

Answer 364

insufficient dietary purine (protein) reduction, insufficient urine alkalization, insufficient urine dilution, insufficient allopurinol administration

Answer 365

excessive allopurinol administration in relation to insufficient dietary purine (protein) reduction, insufficient urine alkalization, or insufficient urine dilution

Answer 366

Minilaparotomy-assisted cystotomy

Answer 367

Specific, Measurable, Action oriented, Realistic, Time-driven/Timely, and Rewarded For cat environmental enrichment

Answer 368

For idiopathic renal hematuria | silver nitrate and povidone-iodine = flush into renal pelvis

Answer 369

Subcutaneous Ureteral Bypass device

Answer 370

<5mm in female dogs and 3mm in male dogs or cats

Answer 371

NOT proven, but some people think so, you can try it in refractory cases

Answer 372

When bladder overactivity is a cause or consequence of incontinence in dogs

Answer 373

Phenoxybenzamine - Nonslective a-antagonist Prazosin - Selective a1-antagonist Tamsulosin - Uroselective a1 antagonist in male prostate Dantrolene - Relaxant of striated muscle (important in cat urethra)

Answer 374

Bethanechol - Parasympathomimetic

Answer 375

cholinesterase inhibitors (pyridostigmine)***, β-blocking agents, dopaminergic antagonists, prostaglandins, and prokinetic agents (cisapride and metoclopramide***)