Nephrology/Urology Flashcards
1
Q
List the clinical signs associated with renal amyloidosis in cattle.
A
Mature animals with:- Chronic diarrhoea.- Weight loss.- Poor productivity.- +/- Generalised or ventral oedema.- +/- Enlargement of the left kidney on rectal (non-painful).- +/- stable foam on urine.
2
Q
What clinical pathology abnormalities will be seen in cattle with renal amyloidosis?
A
- Marked proteinuria.- Marked hypoalbuminaemia.- Advanced dz: azotemia.- Chronic, active dz: hyperfibrinogenaemia, hyperglobulinaemia.
3
Q
What two diseases cause prolonged proteinuria in cattle? How would you differentiate between the two in the live animal?
A
- Renal amyloidosis and glomerulonephritis.- Renal biopsy.
4
Q
Describe the pathophysiology of renal amyloidosis in cattle.
A
- Chronic inflammatory disease e.g. TRP, mastitis –> circulating serum amyloid A; abnormal catabolism of SAA or inherent abnormality in SAA –> misfolding of SAA and deposition of amyloid fibrils which are resistant to proteolysis in glomerulus –> sustained albuminuria.- Dxa: GIT wall oedema or amyloid deposition in GIT.- Renal or pulmonary thrombosis: loss of low-molecular weight anticoagulant proteins through the compromised kidney.
5
Q
Described the gross and histopathology of kidneys of cattle with amyloidosis.
A
- Gross: large, yellow-tan to white kidney, waxy quality of renal parenchyma; generalised oedema.- Histo: amyloid deposition in glomerulus, interstitium and tubule lumen (congo red –> light pink or bright green under polarised light).
6
Q
What is the prognosis associated with renal amyloidosis?
A
Hopeless.
7
Q
What is the common common route of infection in cattle with pyelonephritis and what are the two most common aetiologic agents?
A
- Ascending infection from the lower urinary tract e.g. urogenital trauma during calving, abnormal vulvar conformation, urine retention, catheterisation.- Corynbacterium renale - contagious; adhere to urinary tract epithelium via pH-mediated pili i.e. adherence enhanced in alkaline urine and dec in acidic urine.- Escherichia coli - faecal contamination.
8
Q
List bacteria that have been implicated in causing pyelonephritis of haematogenous origin in cattle.
A
Salmonella, Staphylococcus, Streptococcus, P. aeruginosa and T. pyogenes.{Corynbacterium pseudotuberculosis (small ruminants)}.
9
Q
List the clinical signs of acute pyelonephritis in cattle.
A
- Sudden reduction in feed intake.- Sudden reduction in milk production.- Fever.- Tachycardia.- Tachypnoea.- Dehydration.- Rumen stasis, mild colic.- Scleral injection.- +/- signs of cystitis: dribbling urine, swishing tail, arched stance after urinating, discharge on distal vulva.- +/- L kidney large, painful, smooth on rectal palpation.
10
Q
List the clinical signs of chronic pyelonephritis in cattle.
A
- Vague clinical signs: weight loss, muscle wasting, poor growth, anorexia, diarrhoea, reduced milk production.- Pale mucous membranes due to anaemia.- There may be no abnormal behaviour or posturing during urination.- +/- loss of lobulation in L kidney on rectal (may not be pain or enlargement).
11
Q
Describe ultrasound findings in acute pyelonephritis.
A
- R kidney in 12th ICS and R paralumbar fossa.- L kidney: L paralumbar fossa or per rectum.- Renal enlargement, abnormal kidney shape, dilated renal calyces, flocculent echogenic material in the renal pelvis and ureter.
12
Q
Describe clinicopathologic abnormalities in cattle with pyelonephritis.
A
- Neutrophilic leukocytosis w hyperfibrinogenaemia.- If more chronic expect hyperglobulinaemia and hypoalbuminaemia (renal loss).- Chronic: anaemia (dec EPO and renal loss).- Bilateral pyelonephritis –> azotemia and isosthenuria = poor Px.- Haematuria, proteinuria, bacteria; USG 1/005-1.020.
13
Q
Describe the epidemiology of pyelonephritis in cattle.
A
- Israeli study: prevalence 0.3-2.7%.- Female predisposed due to short urethra and potential contamination and trauma from breeding/parturition.- Majority of cases w/in 90d of calving.- C. renale is difficult to eliminated on a herd level once established.
14
Q
List necropsy findings in cattle that have died from pyelonephritis.
A
- Bladder has evidence of haemorrhage, ulceration and fibrin deposition of epithelial surfaces; may extend through urethra.- Polypoid growths may develop with chronicity.- Ureters may be enlarged and filled w purulent debris.- Kidney(s) enlarged, may have grey, odourless exudate in renal pelvis, medulla and cortex (acute) or abscess (chronic).
15
Q
Describe the treatment of pyelonephritis in cattle
A
- Agressive and long-term ABs: penicillin; if coliform infection and no response after 96h gent, ceftiofur, TMPS.- Diuresis with oral or IV fluids to remove necrotic debris and bacteria from the UT.- Nephrectomy if unilateral pyelonephritis that is unresponsive to medical therapy.- Perform urinalysis and urine culture 1wk after stopping therapy to confirm efficacy.
16
Q
What is the prognosis for cattle with pyelonephritis?
A
- Treatment more efficacious if instituted early.- Case fatality/cull rates of 18-47% reported.- Recrudescence rate of 9.4% reported.
17
Q
Describe the pathophysiology of glomerulonephritis in cattle.
A
- Immune-mediated damage to the glomerulus.- Reported w acute septic dz, cattle w BVD and fascioliasis, mesangiocapillary GN in landrace lambs, preg tox in ewes.- Ab may be directed against host or foreign Ag in the vascular endothelium, mesangial cells or BM of the glomerulus or Ag-Ab complexes may deposit –> complement activation, chemotaxis of leukocytes –> glomerular injury –> inc glomerular permeability.
18
Q
List clinical signs displayed by ruminants with glomerulonephritis.
A
- Weight loss or poor productivity.- Chronic diarrhoea.- Lethargy.- Generalised oedema.- Kidneys maybe mildly enlarged, non-painful on rectal.- Signs of concurrent dz: BVD, fascioliasis, preg tox.- Mesangiocapillary GN of Landrace lambs: 1d-3mo old, dull, ataxic, appear blinds, seizures, fine muscle tremors, colic.
19
Q
Describe clinicopathologic abnormalities in ruminants with glomerulonephritis.
A
- Heavy proteinuria.- Mild anaemia.- Hypoalbuminaemia.
20
Q
Describe prognosis for ruminants with glomerulonephritis.
A
- Treatment not described.- Prognosis poor.- Mesangiocapillary GN of Landrace lambs not invariably lethal; some lambs may survive to adulthood.
21
Q
Describe congenital defects of the kidneys reported in ruminants.
A
- Renal cysts: common in cattle; no clinical significance unless multiple (polycystic kidney dz).- Renal agenesis: most common renal defect in lambs.- Renal oxalosis: inherited in Beefmaster calves –> weakness, lethargy, anorexia, dehydration, dxa, alopecia w/in wks of birth due to accum of Ca oxalate crystals.- Extopic ureter: rare in ruminants.
22
Q
Describe urinary tract neoplasias (not related to bracken fern ingestion) in ruminants.
A
- Primary bladder tumours reported in 0.05% cattle in Nth Am abattoirs = adenomas, papillomas, TCCs.- Fibropapillomas and SCC of genitalia may impinge upon urethra.- Renal carcinoma has been reported in cattle.- Nephroblastoma has been reported in a ewe and a lamb.- Urinary tract involvement occ seen w lymphosarcoma.
23
Q
Haemolytic uraemic syndrome occurs in people following ingestion of E. coli O157:H7. It has been reported in 4 horses and 2 cattle. Describe the pathophysiology and clinical findings in cattle with HUS.
A
- Thrombotic microangiopathy disorder charac by microangiopathic haemolytic anaemia, thrombocytopaenia and renal failure; normal clotting times.- Cattle CSx: severe progressive anuric renal failure, acute haemolytic anaemia and consumptive thrombocytopaenia; haemolysis and tendency to bleed.- Necropsy: renomegaly, renal infarcts, scattered petechial and ecchymotic haemorrhage w/in renal parenchyma, ATN, fibrin thrombi in glomerular capillaries.
24
Q
List aetiologic agents of acute renal failure in ruminants.
A
- Aminoglycosides.- Tetracycline.- Ionophores.- Ethylene glycol.- Oxalate-containing plants.- Vitamin C or D overdose.- Oak, acorns, pigweed, Easter lily, phildendron, ponderosa pine, cocklebur, jessamine.- Myoglobin.- Haemoglobin, methaemoglobin.- Arsenic, mercury, cadmium, chromium, lead, zinc.
25
Q
List clinical signs of acute renal failure in ruminants.
A
- Non-specific; freq presented for poor appetite, diarrhoea or epistaxis.- May be anuric, oliguric or polyuric.- Depression, nasal discharge, ileus, melena and mild free-gas bloat may be present.- If concurrent septic dz: fever, scleral inj, tachycardia.- Acid-base, elec, fluid imbalances –> weakness.- Uraemia –> saliva w ammonia smell, enceph signs.
26
Q
List clinicopathologic abnormalities in cattle with acute renal failure.
A
- CBC: if inflammatory condition affecting renal tubules: neutropaenia or left shift.- Azotemia: elevated BUN (maybe as influenced by rumen physiology); elevated creatinine.- HypoNa, hypoCl, variable K +/- hyperMg, hyperPO4, hypoCa.- Metabolic alkalosis (acidosis in calves w concurrent dxa).- Urinalysis: proteinuria, haematuria, granular casts, FE sodium >4%.
27
Q
Describe the pathophysiology of acute renal failure in ruminants.
A
- Reduced blood flow/ischaemia in kidneys: secondary to blood loss, septicaemia, endotoxaemia, severe dehydration from mastitis, metritis, enteritis, rumen acidosis or intestinal accidents, heat stress (lambs) –> infarction of renal cortex, renal v thrombosis, damage to tubular BM.2. Bacterial infection: bilateral pyelonephritis –> destruction of nephrons by bacterial toxins and host inflam resp.3. Pigment nephrosis: haemoglobin/myoglobin –> renal vasoconstriction and tubular obstruction from protein coagulation.4. Toxic nephropathies: various mech e.g. sulphonamides –> deposition of insoluble precipitates in renal tubules, NSAIDs –> dec Pg synth and medullary crest necrosis, aminoglyc –> cell death of tubules thru mitochond inj.
28
Q
Outline the treatment of acute renal failure in ruminants.
A
- Remove offending toxin or source: rumenotomy, activated charcoal, heavy metal chelators.- Promote diuresis through IVFT (IV, oral or rumen) and diuretic meds (furosemide or mannitol until urinating).- Correct acid-base and electrolyte derangements.- Additional therapy if indicated in specific cases: broad-spectrum ABs, plasma, PPN or transfaunation.
29
Q
Describe leptosira bacterial structure and transmission.
A
- Motile, gram-negative, obligate aerobic, tightly coiled spirochetes 0.1-0.3um diam and 6-20um length.- Persist in chronic infections of renal tubules of maint host –> little or no dz.- Transmitted to incidental host through urine from maint host (directly or contam feed/enviro).- Causes multi-organ dz in incidental hosts e.g. abortions, repro failure, kidney, liver or CNS dz.- Survives in warm, moist enviro for 6mo; survives short period if dry and cold; doesn’t survive freezing.- Seasonal incidence higher in Summer/Autumn in temperature regions or rainy season in warm climates.
30
Q
Describe epidemiology of leptospirosis in cattle.
A
- Cattle are primary maintenance host reservoir of L. interrogans serovar hardjo type hardjopragitno (UK) and L. borgpetersenii servo hardjo type hardjobovis (worldwide).- Also maint or incidental host for L. interrogans serovar pomona and L. interrogans serovar grippotyphosa.- Serovars hardjo, pomona and grypotyphosa most often implicated in renal infection in cattle; renal dz caused by lepto in small ruminants rare but may serve as carriers.- Urine/renal/seroprev varies in US from 2-47%.- Infection w host-adapted serovar hardjo –> mild dz; overt losses attrib to effects on reproduction.- Incidental infection w non-host adapted strains –> acute severe renal dz (particularly in calves).
31
Q
Describe clinical presentation of host-adapted Leptospira serovar hardjo infection in cattle.
A
- Asymptomatic.- Chronic interstitial nephritis; renal dys rarely observed.- Infertility, stillbirth, abortion and birth of weak calves.- Milk-drop syndrome/flabby udder: fever, agalactia, mastitis, milk yellow/red-tinged and thick; udder soft.
32
Q
Describe clinical presentation of non-host-adapted Leptospira serovars infection in cattle.
A
- Severe systemic disease in calves > adult cattle.- Haemolytic anaemia (some L. serovars prod haemolysins), hepatitis, interstitial nephritis, tubular nephrosis, fever, anorexia, lethargy, dec milk prod, petechiation.- Agalactica and mastitis in lactating cows; +/- abortion.- Renal lesions result from damage to vascular endothelium, pigement nephropathy, interstitial nephritis –> azotemia, proteinuria, pyuria, granular casts, +/- haemoglobinuria.
33
Q
Describe the pathophysiology of leptospirosis in cattle.
A
- Leptospires ingested or penetrate external mucosa surfaces and scarified skin, mutliply, enter bloodstream thru lymphatics or direct penetration of blood vessels.- Bacteraemia 4-7d –> infection multiple organisms.- Leptospires become localised in mammary gland, kidney or genital tract; appear to be protected from IR.- Leptospires cleared from body OR chronic infection of renal prox tubules/repro tract occurs –> shedding for wks to months (non-adpated) or years (host-adapted).- Virulence factors: toxin effect of lipopolysaccharide, adhesion to cells and extracellular matrix, bacterial motility, haemolysins and iron sequestration.
34
Q
How is leptospirosis diagnosed in cattle?
A
- Microscopic agglutination test (MAT) is most widely-used serologic test: detects ABs to specific serovars, but cross-reactivity occurs b/w related serovars.- Acute infection: four fold inc b/w acute and convalescent sample or conversion from -ve titre to titre >100.- Chronic infection: titres may be -ve, inc, dec, static.- L. shedding in urine or semen can be assessed via culture (often unrewarding), PCR, phase-contrast or dark-field microscopy, FA, nucleic acid hybridisation or immunblot.- Urine testing: admin furosemide, discard first sample, clean vulva of gross debris, collect and test 2nd sample.- Histo renal tissue: Warthrin-Starry or Levaditi stains.
35
Q
Outline treatment of leptospirosis in cattle.
A
- Oxytetracycline for 5-7d (reported clinically effect but not proven); PPG/ampicillin (efficacy in cattle unproven).- IV or oral fluids, blood transfusions, diuresis if ARF.- Oxytet, ceftiofur, tilmicosin and tulathromycin have been shown effective in clearing renal shedding in herds.
36
Q
What is the prognosis associated with leptospirosis in cattle?
A
- Varies w virulence of serovar involved, host immunity, extent of renal lesions.- Guarded prognosis in azotemic cattle as >75% nephrons affected in such cases, therefore even if acute dz tx, may –> chronic interstitial nephritis and fibrosis.
37
Q
Outline strategies to prevent leptospirosis in cattle herds.
A
- Draining or fencing off standing water.- Maintaining a dry, clean environment.- Limiting rodent and wildlife contact with cattle and their feed and water.- For host-adapted strains, eliminate renal carrier state.- Vaccination (pentavalent vacc) is considered effective at preventing losses but may not consistently prevent renal colonisation w host adapted hardjobovis.- Recommended at a young age followed by annual boosters to prevent initial renal colonisation.
38
Q
Describe the aetiology of enzootic haematuria of ruminants.
A
- Chronic (1-3 mo) ingestion of bracken fern (Pteridium aquilinum).- Toxins in plant –> haemorrhagic cystitis –> chronic or intermittent haematuria.- Chronic ingestion + bladder infection w BPV-2 –> bladder neoplasm of epithelial, mesenchymal or mixed origin.- NB distinct from acute Bracken Fern toxicity –> acute coagulopathy or fulminant septicaemic crisis assoc w severe bone marrow suppression.
39
Q
Outline clinical signs of enzootic haematuria in ruminants.
A
- Group of animals grazing same pasture or cutting of hay.- First CSx is protracted, poss intermittent haematuria +/- blood clots in urine.- Chronic blood loss –> tachycardia, tachypnoea, exercise intol, pale MM, dec productivity and body condition.- May palpate bladder wall thickening per rectum.- +/- dysuria, pollakiuria, obstr of bladder trigone (tumour) or urethra (clot).
40
Q
Describe diagnostic test findings in cattle with enzootic haematuria.
A
- Ultrasound: bladder thickening, irregularly shaped bladder wall.- CBC: severe anaemia; may see low platelet, seg neut and lymphocyte counts.- Urinalysis: haematuria, proteinuria, +/- pyuria.
41
Q
Describe the pathophysiology of enzootic haematuria in ruminants.
A
- All parts of the plants are toxic to sheep and cattle.- Several compounds in bracken fern possess irritant, mutagenic, immunosuppressive or carcinogenic activities incl ptaquiloside, quercetin and alpha-ecdysone.- May cause recrudescence of latent BPV-2 through immunosuppression.- Mutagenic compounds interact w BPV-2 in bladder to induce local neoplasia.- Bladder carcinomas from cows w enzootic haematuria express COX-1 and COX-2 at a high level compared to normal controls.
42
Q
Describe the epidemiology of enzootic haematuria in ruminants.
A
- Described in America, UK, Aus, Europe.- Occurs most in US in Pacific Northwest and upper Midwest.- Plant grows best in well-drained, fertile coils and is often localised in open areas of forests; poisoning occurs in ruminants grazing pasture itself or hay w bracken fern.- Primarily adult sheep and cattle; haematuria seen in cattle 2-3yo, neoplasia 3-7y after grazing commences.- Up to 90% adult cattle affected in endemic areas.
43
Q
Describe the necropsy findings in ruminants with enzootic haematuria.
A
- Tissue pallor from anaemia.- Bladder wall thick and mucosa haemorrhagic and ulcerated.- Histo bladder wall: capillary engorgement, intramural haemorrhage, metaplasia of bladder epi, several type of bladder tumours.- Metastasis of epi neoplasms to regional LNs or other organs can occur.
44
Q
Describe the treatment and prevention of enzootic haematuria in ruminants.
A
- Tx limited to reduction or elim of bracken fern in diet.- Haematuria will cease if bracken feeding is discontinued before onset of tumour formation.- Early culling may help prevent low productivity from anaemia and neoplasia.
45
Q
Describe the clinical signs of ulcerative posthitis and vulvitis of small ruminants (‘Pizzle Rot’).
A
- Begins as a moist ulcer at/near mucocutaneous junction of the prepuce, covered by a scab, focal swelling, painful.- Spreads along mucosal surface inside the prepuce –> entire prepuce swollen, dysuria, vocalise during urination.- May progress to fibrous adhesions between penis and prepuce, restriction of urine egress due to swelling of glans penis or impairment of breeding soundness (blood/exudate in ejaculate, penis adhesions, scarring prepucial orifice, suppuratives urethritis.- Weight loss in chronic cases.- Ewes/does: ulcerative lesions on vulva and perineum, gross vulvar enlargement, dysuria.- Ddx: orf, ulcerative dermatosis (poxvirus), urolithiasis, caprine hervesvirus-1.
46
Q
Describe the pathophysiology of ulcerative posthitis and vulvitis in small ruminants.
A
- Corynebacterium renale: aerobic, gram-positive, pleomorphic, club-shaped bacteria; normal flora of skin and external genitalia.- Bacteria contains enzyme urease.- High-protein diet –> inc ammonia in rumen –> urea elim thru kidneys –> C. renale proliferate in alkaline urine and urease hydrolyses urea to ammonia –> chemical irritation and ulceration of prepuce and surrounding skin.
47
Q
Describe the epidemiology of ulcerative posthitis and vulvitis in small ruminants.
A
- Males > females.- Risk factors: inc/excessive dietary protein (>16%, as low as 12%) e.g. alfalfa hay or lush legume pastures.- Inc plane of nutrition in intact males prior to breeding.- Breeds w dense wool or hair e.g. Merino, Angora.- Organism persists in wool, hair and scabs for up to 6mo and can survive freezing in scabs/exudative material.- Can occur in single or multiple animals; venereal transmission reported.- Causes losses from debilitation caused by pain, incapacitation of breeding animals, loss of breeding soundness, deformation of external genitalia.
48
Q
Outline the treatment of ulcerative posthitis and vulvitis in small ruminants.
A
- Reduction of protein and non-protein nitrogen intake.- Isolate affected animals.- Clip hair around affected region and apply topical ABs.- Systemic ABs in severe cases e.g. penicillin, oxytet.- NSAIDs if required for pain/inflammation.- Sx of severe strictures to allow normal urine flow.
49
Q
Describe the prognosis associated with ulcerative posthitis and vulvitis in small ruminants.
A
- Response to tx optimal early in infection before deformation of prepuce or vulva as a result of fibrosis.- Changes for full recovery poor if dietary protein not restricted.- Complete recovery of breeding soundness unlikely if internal ulcerative posthitis.
50
Q
Describe the common signalment of ruminants with urolithiasis.
A
- Common metabolic dz in all livestock spp.- Castrated small ruminants at greatest risk.- Dx in single animal suggests whole herd is at risk due to important of diet/enviro factors in pathogenesis.- Can occur as epidemics or indv disorder.
51
Q
Describe the clinical presentation of acute urethral obstruction secondary to urolithiasis in ruminants.
A
- Impacted calculi –> urethral trauma and bladder distension –> stranguria and abdo pain.- CSx: restless, swish tail, grind teeth, stranguria, vocalise, tachycardia, tachypnoea, mild bloat sec to rumen stasis.- Stranguria may result in rectal prolapse.- Visible dilation or palpable pulse in urethra at midline of perineum proximal to obs may occur.- Anuria or urine dribbling.- May see blood or crystals on prepuce.- Distended bladder on abdo/rectal palpation.- Most common site of obstruction = sigmoid flexure in cattle and urethral process in sheep and goats.- NB always ultrasound kidneys as hydronephrosis –> poor Px.
52
Q
Describe the clinical presentation of chronic urethral obstruction secondary to urolithiasis in ruminants.
A
- Uncommon, but may occur if calculi cause partial obstruction of urethra and still allow for urine flow.- CSx: slow/intermittent urine flow during voiding, lethargy, dec appetite, thin BCS if renal failure has developed.- Rectal may reveal small bladder with thick wall.- DDx for urine dribbling: neuro dz, previous urethral trauma –> stricture formation, congenital anomalies of urogenital tract, infection, neoplasia, internal ulcerative posthitis.
53
Q
Describe the clinical presentation of urethral rupture secondary to urolithiasis in ruminants.
A
- Common complication of urethral obstruction.- Wall of urethra undergoes pressure necrosis –> leakage of urine into s/c tissue of perineum and ventral abdo.- Sequelae: cellulitis, penile adhesions, urethral fistula formation, urethral stricture, erection failure.- CSx: depression, inappetence, bilaterally symmetric pitting oedema in ventral perineum, inguinal region, prepuce and ventral abdo, may –> gangrenous necrosis.
54
Q
Describe the clinical presentation of urinary bladder rupture secondary to urolithiasis in ruminants.
A
- Prolonged bladder distension secondary to urethral obs –> pinpoint perforations, tears or necrosis of large areas of bladder wall.- Most common location for rupture is dorsum of the bladder fundus.- Rupture –> relief of stranguria.- CSx 1-2d post-rupture: abdo distension, depression, anorexia, weakness, dehydration, shock; breath may smell of ammonia; may ballot fluid wave in abdo; death.- U/s –> free fluid w collapsed or partially filled bladder.- Abdominocentesis: larve vol blood-tinged fluid.
55
Q
Describe the clinical presentation of ureterolithiasis and nephrolithiasis in ruminants.
A
- Acute ureteral obs may present w severe colic if obs is complete, or absent/milder colic.- Enlarged ureter/L kidney may be palpated rectally.- Rectal/transabdo u/s may aid dx.- May see evidence on u/s of pyelonephritis (necrotic debris/calculi may be released into ureter from infected renal pelvis) or ureteral or renal rupture.- If no signs of colic may be see non-specific signs of illness –> serum chem/urinalysis/ultrasound for definitive dx.
56
Q
Describe the procedure of examination of the urethral process for stones/sand-like grit in small ruminants.
A
- Sedation: diazepam or acepromazine +/- butorphanol; recomm to avoid xylazine as inc urine production.- Can admin epidural instead of/as adjunct to sedation; 1ml/15kg 2% lignocaine, no more than 15ml.- Prop sheep/goat on rump w spine perpendicular to floor.- Apply lidocaine jelly to prepuce, exteriorise penis by pushing sigmoid flexure cranially from base of scrotum and pull sheath caudally.- Inspect/palpate urethral process and amputate w scalpel blade if stones/grit palpated.
57
Q
Describe clinicopathologic findings in ruminants with acute and chronic urethral obstruction.
A
- CBC/chem may be WNL if acute.- May see hyperglycaemia and stress leukogram.- Dec water intake –> haemoconc and azotemia.- Chronic obst: hypoNa, hypoCl, hypoCa, hyperP, severe azotemia w isosthenuria.- Haematuria and proteinuria are consistent abnormalities; crystalluria is variable finding; +/- pyuria.
58
Q
Describe clinicopathologic findings in ruminants with bladder rupture.
A
- HypoNa, hypoCl, hyperP, uraemia, haemoconc.- K+ conc is variable, depending on appetite and time prior to dx; bladder rupture usually –> hyperK in animals but in ruminants K is usually low or normal due to anorexia, salivary potassium excretion and aldosterone release.- Peritoneal fluid:serum creat 2:1 or greater.- May see leukocytosis and hyperfibrinogenaemia secondary to peritoneal inflammation.
59
Q
Describe clinicopathologic findings in ruminants with ureterolithiasis and nephrolithiasis.
A
- Azotemia and secondary hydronephrosis most severe if condition is bilateral.- Chronic: hypoNa, hypoCl, hypoCa, hyperP, severe azotemia w isosthenuria.- Pyuria present w traumatic urethritis, cystitis or secondary bacterial infection.
60
Q
Describe the pathophysiology of urolithiasis in ruminants.
A
- Mucopolysaccharides, ions, organic acids in urine act as intrinsic inhibitors of crystallisation of calculogenic ions.- Calculus formation initiated if supersaturation of urine w crystalloids exceeds capabilites of these inhibitors –> crystalloids rendered insoluble and precipitate out of urine.- Dietary, enviro, management factors interact to determine degree of supersat of urine w calculogenic minerals.- pH: struvite (Mg amm phos), Ca phos, Ca carb less soluble in alkaline urine; Ca ox not affected by pH, silica debatable.- Rare cause and rare consequence of UTIs in ruminants.- Vit A defic may create nidus for calculi formation through desquamation of epi cells/altered cell surface charac.- Ad lib feeding may dec calculi formation, as 1-2 feedings/day –> ADH release after feed –> urine conc.- Water hardness may be sig, partic Mg content.
61
Q
Describe factors influencing development of phosphatic urinary calculi in ruminants.
A
- High phosphorus (grain-based) diet –> struvite (Mg amm phos) or apatite (Ca phos) calculi.- Ca:Phos outbreaks of urolithiasis.- Struvite dev primarily affected by Mg content in diet; Mg > 0.6% DM.- High dietary K+ alters DCAD –> inc risk uroliths.- Pelleted rations –> inc risk phosphatic uroliths; dec saliva prod w pellets –> dec GI phos loss –> inc renal excr.- Struvite uroliths: white or grey, smooth, radiopaque, easily broken; single stone or sand-like debris.
62
Q
Describe factors influencing development of silica urinary calculi in ruminants.
A
- Ruminants grazing native rangeland grasses of western North America; silica content higher in mature grass.- Periods of water deprivation –> water and Na resorption by kidneys –> highly conc urine –> silic acid conc and polymerises to polysilicic acid –> binds to urinary mucoproteins and becomes insoluble.- Incidence may be inc by dietary defic of Cu and Zn and high dietary Ca:PO4 content > 2.8:1 (opp to struvite!).- Silica uroliths are hard, smooth, white to brown, radiopaque, often layered; 20% mucoprotein, 75% silicon dioxide and variable amounts Ca ox and Ca carb.
63
Q
Describe factors influencing development of calcium-based urinary calculi in ruminants.
A
- Two main types: Ca oxalate and Ca carbonate.- Ca carb common in small ruminants grazing lush, rapidly growing clover pastures or fed alfalfa hay, high in Ca, low in PO4 and Mg, high oxalate content.- Oxalate binds GI Ca –> inc urinary Ca excretion; ruminal bacteria metabolises oxalate to bicarb –> alkaline urine; both factors –> inc Ca carbonate calculogenesis.- High oxalates, low Ca in diet and dec water intake –> inc risk of Ca oxalate uroliths.- Ca carb uroliths: round, smooth shape, golden colour.- Ca oxalate uroliths: dense, hard, white to yellow, smooth or jagged.
64
Q
Describe the epidemiology of urolithiasis in ruminants.
A
- Gender: obs urolithiasis almost exclusively dz of males; testosterone –> inc urethral diameter, therefore castration (esp prior to puberty) = risk factor. - Season: inc incidence in late Autumn and Winter: limited water avail, inc silica content, higher number of young, growing male animals; higher risk in arid months of year in warmer climates.- Age: tendency in younger ruminants, maybe due to management factors e.g. high grain rations.- Other: inherent indv diff in animals’ mineral metabolism or urinary tract health.- Breed: higher risk in African Pygmy goats; truley higher risk or management facts due to pet status?
65
Q
List surgical treatment options for management of urolithiasis in ruminants.
A
- Amputation of obstructed urethral process.- Perineal urethrostomy.- Prepubic urethrostomy.- Urethrotomy.- Cystotomy.- Tube cystotomy.- Bladder marsupialisation.
66
Q
Describe medical management options for treatment of urolithiasis in ruminants.
A
- Tranquillisers: antispodic effect on urethra and relaxation of retractor penis muscle –> relaxation of sigmoid flexure (NB low success of NSAIDs, IVF, tranquillisers alone).- Percutaneous drainage of bladder prior to Sx or as adjunct to medical therapy.- Percutaneous inj of Walpoles soln into the bladder –> dec urine pH to 4-5 to dissolve uroliths in bladder/urethra.- Pre-operative stabilisation of hypovol and correction of electrolyte abnorm e.g. hypertonic followed by 0.9% NaCl.- If hyperK can give IV dextrose, sodium bicarb or insulin to move K into cells.- Slow drainage of urine from abdo cavity to reduce pressure on diaphragm and slow progression of metabolic derangements. - Peri-operative ABs to prevent UTIs.
67
Q
Describe factors of management which can prevent or decrease the risk of urolithiasis in ruminants.
A
- Perform ration and urolith analysis to ID dietary factors.- Goal: dilution of urine to reduce urinary concentration of calculogenic mineral ions.- Dietary management of phosphotic calculi:– Ca:P 2:1 or greater; dec grain (high phos), inc Ca w alfalfa or other legumes.– 0 mEq DCAD diet w ammonium Cl –> urine pH 6-6.5.– Inc long-stemmed forage –> inc saliva –> inc P excr.- Dietary management of silica calculi:– Cannot change silica content or range grasses.– Can only add salt to inc water intake; up to 15% DM NaCl or 1% NH4Cl.– Dec Ca:P from 2:1 to 1:1 –> trend towards less calculi.- Dietary management of Ca carb uroliths:– Supplement hay w grass hay instead of alfalfa alone.– Salt grass hay to inc water intake.– NH4Cl to inc water intake and acidify urine.- Water management: clean feeders, in shade in Summer, warmed in Winter, multiple sites, check regularly.
68
Q
Can serum creatinine concentration at presentation be used to predict survival in horses with renal failure?
A
- Yes.- Non-survivors (mean = 9.4mg/dL) had higher creatinine concentrations than survivors (mean = 6.1mg/dL).Ref: J. Vet. Intern. Med. 2011; 25(6):1426–1430.
69
Q
Are serum calcium concentrations different in horses with acute renal failure and chronic renal failure?
A
- Mean serum calcium concentration was significantly higher in horses with CRF than ARF.- Cases of ARF were more likely to be normocalcaemic or hypocalcaemic, whereas CRF cases were more likely to be normocalcaemic or hypercalcaemic.Ref: J. Vet. Intern. Med. 2011; 25(6):1426–1430.
70
Q
What is the complication rate associated with renal biopsies in horses? What complications are seen?
A
- Study of 151 biopsies in horses 48h-30y old.- 11.3% had complications (9% minor, 2.3% major).- 0.7% mortality rate (fatal haemorrhage).- Haemorrhage (7/17).- Colic (6/17).- Macrohaematuria (4/17)- Microhaematuria (2/17).- Pyrexia (2/17).- Abortion (1/17 - no evidence linking directly to biopsy).- Death (1/17).Ref: J. Vet. Intern. Med. 2011; 25(3):532-539.
71
Q
List risk factors for complications when performing renal biopsies in horses.
A
- Biopsy of left kidney.- Diagnosis of neoplasia.- Low urine specific gravity.- NB No association with complications was found for age, sex, breed, institution, presenting complaint, other initial clinicopathologic data, biopsy instrument, needle size, or use of ultrasonographic guidance.Ref: J. Vet. Intern. Med. 2011; 25(3):532-539.
72
Q
What is the likelihood of obtaining a diagnostic sample following renal biopsy in horses? What is the agreement of diagnosis from biopsy with that at necropsy?
A
- Biopsy specimens yielded sufficient tissue for a histopathologic diagnosis in most cases (94%).- Dx had only fair (72%) agreement with PM findings.Ref: J. Vet. Intern. Med. 2011; 25(3):532-539.
73
Q
Is renal replacement therapy safe and efficacious in adult horses?
A
- Study performed with horses in stocks for 6h, connected via a commercial renal replacement machine with blood flow rate 250 mL/min; dialysate rate 3,000 mL/h; prefilter replacement pump 3,000 mL/h; and postfilter replacement pump rate 2,000 mL/h. Balanced electrolyte solution was used as dialysate and replacement fluid.- Renal replacement therapy was successfully performed in horses, resulting in a mean creatinine clearance of 0.127 mL/kg/min (68.9 mL/min) and urea reduction ratio of 24%. - No adverse effects were detected although a significant decrease in rectal temperature was observed (P .007). A significant increase in serum phosphorus (P .001) and decrease in BUN (P .04).Ref: J. Vet. Intern. Med. 2013; 27(2):308-316.
74
Q
Describe the risk factors for development of calcium carbonate urolithiasis in goats.
A
- The breed with the highest odds of developing calcium carbonate uroliths was Nigerian Dwarf.- Breeds with the lowest risk of developing calcium carbonate uroliths included mixed, Anglo-Nubian or Nubian, and Toggenburg. - Goats of African descent (Pygmy, Nigerian Dwarf, Boer) had significantly higher odds of developing calcium carbonate uroliths than did those of non-African descent.- Goats that were > 4 yo.- Males were approx 196 times as likely to develop calcium carbonate uroliths as were females.- Calcium carbonate uroliths were sig more likely to be collected in Autumn, Summer and Winter than in Spring.Ref: J Am Vet Med Assoc 2015;247(3):293–299.
75
Q
What are the conventional treatment principals of acute renal failure (ARF) therapy?
A
- Reversal of inciting or underlying cause.- Judicious administration of IV fluids.- Correction of electrolyte and acid-base abnormalities.Ref: JVIM 2013; 27: 308-316.
76
Q
When should renal replacement therapy (RRT) be instituted in cases of ARF?
A
- If ARF remains refractory to conventional treatment.- Renal indications: reduced GFR –> solute imbalance; oliguria –> ECF overload.- Non-renal indications: facilitating clearance of drugs, toxins, toxic metabolites or inflammatory cytokines.Ref: JVIM 2013; 27: 308-316.
77
Q
Describe the way in which continuous renal replacement therapy (CRRT) purifies the blood.
A
Blood is passed through thousands of semipermeable membranes and blood is purified via diffusion, convection (solvent drag) and adsorption (adhesion).Ref: JVIM 2013; 27: 308-316.
78
Q
List the advantages of CRRT over haemodialysis.
A
- Slow, continual process allows for better control of blood pressure, electrolyte and acid-base balance.- Convective process allows for more effective removal of larger molecules with limited diffusibility.- Ability to use pre-packaged sterile fluids vs pure dialysate.Ref: JVIM 2013; 27: 308-316.
79
Q
Describe the reported procedure for CRRT in the horse.
A
- Sedation: initial bolus followed by CRI of detomidine.2. Anti-coagulation: initial bolus followed by CRI of heparin.3. Fluids: double lumen dialysis catheter in jugular vein; CRRT extracorporeal circuit with 1.5m2 filter was connected to the horse for 6h removing 250ml/min blood and dialysate rate set at 3000ml/h; dialysate and replacement fluid = Plasmalyte.4. Free choice access to feed and water throughout.Ref: JVIM 2013; 27: 308-316.
80
Q
Outline the reported side effects of CRRT in horses.
A
- Hypothermia: progressive decrease in rectal temperature over 6h; due to cool IV fluids and/or detomidine CRI.- Mild dec in HR/RR.- Occasional transient arrhythmias: proposed due to detomidine CRI not CRRT.- Thrombocytopaenia: due to heparin admin.- Haematoma formation at catheter sites: due to heparin admin.- Hyperphosphataemia: mechanism unknown.Ref: JVIM 2013; 27: 308-316.
81
Q
Compare the creatinine clearance rate achieved in CRRT with that achieved by peritoneal dialysis and that of the healthy horse.
A
- CRRT: 0.127mg/kg/min.- Peritoneal dialysis: 0.0322 mL/kg/min (intermittent) to 0.1054 mL/kg/min (continuous).- Normal horse: 1.7-2.7ml/kg/min.Ref: JVIM 2013; 27: 308-316.
