Urinary and endocrine Flashcards

Question

Treatment of oliguria/anuria

Answer 1

Oliguria - <1ml/kg/hr in the hydrated and perfused patient Anuria – little to no urine in the hydrated and perfused patient Loop diuretics e.g. furosemide – no good evidence for improved outcomes in AKI, however may be justified to prevent fluid overload and allow increased volumes of e.g. nutrition (tube feeding). Furosemide is nephrotoxic in the poorly hydrated patient. Osmotic diuresis – mannitol – no good evidence for improved outcomes despite many theoretical benefits, may also cause AKI itself. Dopamine – increases afferent renal blood flow, but not GFR, no evidence for improving outcomes. Fenoldopam – increases urine output, no evidence for improved outcomes yet. Ca2+ channel antagonists – diltiazem – afferent renal vasodilation; some none significant findings supporting improved resolution of azotaemia and urine output, other study showing no significant increase in GFR or UO. Renal Replacement Therapy – Dialysis Indicated for the non-responsive patient to fluid therapy or acute poisoning e.g. lilly/ethylene glycol toxicity in cats. Peritoneal dialysis – the first opinion option. - Peritoneal catheter is placed - Dialysate solution (glucose containing) is infused, left anywhere from 20 minutes to a few hours, to allow for diffusion, then drained. - Repeated as needed - Complications are moderate, including causing a septic abdomen. - Moderately improved outcomes. Haemodialysis – the referral option. - Requires dialysis machine and specific training - Improved outcomes

Answer 2

Suspected urinary tract infection – Amoxy-Clav is a good first line choice for e.coli, Doxycycline for Lepto. Metabolic acidosis – Hartmann’s (Careful if considering sodium bicarbonate, could worsen hypernatraemia if present, and if lung function is impaired can paradoxically cause CNS acidosis) Tachyarrythmias – ECG for VTACH and consider lidocaine Hyperkalaemia – Glucose, insulin, bicarbonate or beta agonist. Hypertension – not uncommon and further damages the kidneys – amlodipine. Avoid ACE inhibitors which reduce afferent renal blood flow. Nutrition – catabolic disease; feeding tube

Answer 3

PUPD Anorexia Weight loss Dehydration Pallor Vomiting and diarrhoea Mucosal ulcers Uraemic breath

Answer 4

Dogs - Westie - Boxer - Shar pei - Bull terrier - Cocker spaniel - CKCS Cats - Persian - Abyssinian - Siamese - Ragdoll - Burmese - Russian blue - Maine coon Age - Can be juvenile if underlying familial disease - Polycystic kidney disease Older animals if not - age assocaited disease processes Comorbidities - Hyperthyroid, hypercalcaemia, heart disease, periodontal disease, cystitis, urolithiasis, diabetes Previous AKI Nephrotoxic drugs - NSAIDs, aminoglycosides, sulphonamides, polymyxins, chemotherapeutics

Answer 5

Nephron damage - progressive and irreversible Other nephron GFR increased to compensate - capillary wall damage, more plasma protein filtration, further glomerular and tubulointerstitial damage Nephron loss - reduced total GFR, build up of products normally excreted (urea), uraemic crisis Reduced renal function, reduced EPO production - non regenerative anaemia Reduced metabolism and excretion of parathyroid hormone - renal hyperparathyroidism - osteodystrophy

Answer 6

Early stage - I or II - rarely picked up this soon - Abnormal renal imaging/known insult or - Persistant elevation/increasing creatinine/SDMA or - Persistant renal proteinuria Later stages II or IV - Consistent clinical signs - Azotaemia/persistently elevated creatinine/SDMA AND USG <1.035 cats <1.030 dogs - Dehydration and azotaemia with isosthenuria or <1.030 is inappropriate - should be more

Answer 7

Serum creatinine - product of muscle metabolism - Produced at constant rate and excreted via kidney - Muscle atrophy/cachexia can decrease - Can increase after feeding - starved sample - Only increases with >75% nephrons already lost SDMA - produced by all nucleated cells at constant rate and cleared by kidneys - Not affected by muscle mass - Increases at 40% nephron loss - earlier More expensive test, less available, and less sensitive

Answer 8

Treat underlying cause if possible/known Slow progression by managing risk factors Recommendations vary by stage - monitor and control - Proteinuria, hypertension and hyperphosphataemia Diet - very important from stage II onwards later stage - treat secondary anaemia, acidosis, nausea, maintain hydration, ensure adequate nutrition

Answer 9

Build up of urea and other toxins normally excreted in kidneys to intolerable levels - Due to end stage CKD, AKI, acute on chronic AKI (ischaemic, toxic - exacerbating existing CKD) Clinical signs - Vomiting, nausea - Anorexia - Lethargy - Depression - Oral ulcers - Melena - GI ulcers - Anaemia - Weakness - Hypothermia - Muscle tremours - Seizures

Answer 10

CKD - Older - >3 weeks - Weight loss, reduced appetite, PUPD, renal insult - ongoing - BCS and coat quality reduced, small hard kidneys, enlarged possible - K+ normal/reduced, non regenerative anaemia USG <1.035 - inappropriately dilute Sediment usually not active though possible if UTI Possible proteinuria ARF - Any age - <48hours - Sudden onset, nephrotoxin, urinary obstruction - Good BCS, kidneys possibly enlarged and painful, possibly small bladder - Increased K+, metabolic acidosis, very unwell for severity of azotaemia - Haem often normal - USG usually 1.008-1.015 but can be any if bladder not empty since onset - Urine casts/proteinuria/cell debris, possible glucosuria

Answer 11

IVFT- Hartmann’s * Replace dehydration + ongoing losses * Care if AKI not to over perfuse- measure urine * If can measure blood gases- assess for acidosis * Bicarb if pH <7.2 or serum bicarb < 12 * Treat nausea/GI ulceration * Omeprazole +/- H2 Blockers +/- sucralfate * Antiemetics e.g. maropitant * Pain relief – opioid – care with dosage and excretion Nutritional support- Important! * Appetite stimulants- Mirtazapine * Feeding tubes (Nasogastric) * Beware food aversion-DO NOT introduce renal diet in hospital

Answer 12

Renal diseases - Glomerular disease - fanconi - Polycystic kidney disease - Pyelonephritis - Nephrotoxin exposure - Neoplasia Extrarenal issues - Hypertension - Cardiac disease - Hyperthyroidism - Diabetes - Urolitiasis/obstruction - Cystitis - Neoplasia - Hypercalcaemia

Answer 13

Primary Stress/environment Idiopathic (prevalence >12% in healthy cats >10 yrs) Secondary Iatrogenic (e.g. glucocorticoids) Systemic disease including CRF, Cushing's, hyperT4, hypoT4, DM, obesity, pheochromocytoma or primary hyperaldosteronism Concern- end organ damage if sustained Diagnosis Based on repeated measurements of systolic blood pressure (SBP) – consistent technique and equipment. Beware white coat effect! * Approx 20% of CKD patients have BP at diagnosis * A further 10-20% will develop BP over time- monitor! Treat if SBP reliably and consistently >160 mm Hg and evidence of EOD (CKD = evidence) Hypertension - Renal injury - Renal sensory nerves stimulated - Sympathetic pathways upregulated to improve renal perfusion - Renin release - Angiotensin > angiotensin I - Angiotensin I > Angiotensin II - Receptor binding > vasoconstriction and aldosterone release > More Na+ absorption - hypertension Treat with ACE inhibitors - inhibit Angiotensin > angiotensin I -Enalapril Or CCB - calcium channel blockers - amlodipine CCB in cats first ACE in dogs first Low salt diet

Answer 14

Bacterial invasion of renal pelvis and parenchyma Diagnosis on - Clinical signs - fever, abdo pain, PUPD - Haematology - neutrophilia with left shift - US - renal pelvis dilatation with hyperechoic mucosa, altered cortex, medulla echogenicity NOT pyelocentesis as high risk - culture urine Treat with renally excreted drugs - amoxicillin, amoxyclav Avoid aminoglycosides - acute tubular necrosis

Answer 15

Metastatic spread site CKD signs if bilateral or underlying issue Primary is rare

Answer 16

Hereditary condition - Persians Cysts present from birth - increase in size and no with age Age of clinical signs 7 years Large irregular kidneys US - hypo/anechoic spherical cavities

Answer 17

disease of proximal tubule - reduced resorption of solutes - dogs loss of glucose, Na+, K+, phosphorus, bicarbonate, albumin, amino acids Idiopathic Hereditary - gradual onset - Basenji Gentamycin nephrotoxicosis Signs PUPD and weight loss +/- signs of uraemia Diagnosis - Increased urinary fractional excretion of glucosa, Na+, K+, phosphorus, and bicarbonate in urine, despite normal plasma concentrations Treatment - supplement oral NaCl, K+, and bicarb if serum concentration is low

Answer 18

Can be secondary to advanced CKD or primary and worsen/cause CKD Glomerular damage - low molecular weight proteins - albumin and antithrombin pass into urine - protein losing nephropathy Signs consistent with CKD, uraemia or can be non specific - weight loss, lethargy Diagnosis - Haem/biochem - likely as for CRF by may not be azotaemia - Likely hypoprotenaemia Urinalysis - Proteinuria - May still be able to concentrate urine - Hyaline casts common as proteins line tubules Common primary forms * Immune complex glomerulonephritis * immune complexes in the glomerular capillary wall, > inflammatory change * Idiopathic (most) or associated with neoplasia, rickettsial diseases, SLE, heartworm, pyometra, chronic septicaemia or adenovirus. * Familial glomerulopathies in several breeds including Bernese Mountain Dogs, English Cocker Spaniels, English Springer Spaniels, Doberman, Greyhounds and more. * Amyloidosis (non familial form) * Chronic inflammation results in protein deposition in glomerulus * Glomerulosclerosis * Currently poorly characterised but IDed at histology CATS- less common than in dogs Most common causes- neoplasia, systemic inflammatory diseases, chronic FeLV/ FIV/ FIP

Answer 19

Uncommon result of protein losing nephropathies PLNs, pathogonomic for glomerular disease Pitting oedema/ascites/pleural effusion Hypoalbuminaemia Hyperlipidaemia - TGs and cholesterol Treatment Antiproteinurics - slow nephron damage and increase plasma oncotic pressure ACE inbibitors - Enalapril Anticoagulants - risk of thromboembolism as lost alongside albumin - aspirin or clopridogrel - minimise platelet aggregation Fluid removal - only if severe impairment of respiratory, heart, QoL as result Will reform as RAS upregulates and worsens hypovolaemia - Abdominal/pleural tap - Frusemide, Spironolactone (K+ sparing)

Answer 20

Vitamin D from diet - absorbed through gut - to liver - metabolised to active calcitriol PTH - parathyroidhormone secreted in response to low calcium levels - pulls from bone and from urinary filtrate and increased CA absorption from gut - negative feedback loop on PTH once levels increased In clinic tests tend to be false high - EDTA bind to calcium for fake result

Answer 21

3 forms - ionised calcium - bound calcium - Complexed calcium Makes up total calcium PTH monitors ionised calcium - body needs tight regulation of this to control metabolic processes Bound fractoin - albumin, eggs Complex - travelling partnered with phosphate, lactate So a low albumin can give low bound calcium so low result - need to analyse just ionised calcium really And phosphorus - when elevated will increased complexed calcium - total can be high when physiologically the animal is low

Answer 22

Decreased calcitriol and reduced calcium absorption - so increased PTH Hyperphosphataemia - increased complex fraction of calcium - Serum total calcium normal or high - Ionised calcium low or low-normal - high serum PTH

Answer 23

Calcium and phosphorus will complex/precipitate when concentration of both is high - mineralisation in tissues Prediction by calcium phosphate product Restricted water - reduced volume - reduced renal perfusion - so increased phosphate levels - so not urgent if hydration is maintained

Answer 24

Increased PTH activity - primary hyperparathyroidism - parathyroid adenoma Activity of PTH like substances - humoral hypercalcaemia of malignancy - PTH related peptide PTHrP - secreted by some tumours Increased vitamin D activity - drives calcium out of gut and bone in high levels - dietary/toxin, granulomas (macrophages - can do final activation step for vitaminD) Osteolysis - local destruction of bone, tumour, or marrow Hypoadrenocorticism, feline idiopathic hypercalcaemia, raisin toxicity

Answer 25

Decreasingly common Malignancy Hypoadrenocorticism - addisons Primary hypoparathyroidism Chronic renal failure Vitamin D toxicosis Granulomatous diseases

Answer 26

Decreasingly common Malignancy Hypoadrenocorticism - addisons Primary hypoparathyroidism Chronic renal failure Vitamin D toxicosis Granulomatous diseases

Answer 27

Decreasingly common Idiopathic hypercalcaemia Renal failure - total mainly, occasionally iCa Malignancy - lymphoma and squamous cell carcinoma Primary hyperparathyroidism

Answer 28

PUPD Vomiting Anorexia Muscle weakness Dehydration Lymphadenopathy Rubber jaw - osteopenia Consequences of urinary calculi Collapse, seizure, weakness - hypocalcaemia

Answer 29

Review history - Diet - supplements, brand, grapes, raisins - Access to vitamin D - supplements, rodenticide, psoriasis medication, certain plants Signalment - primary hyperparathyroidism - middle aged to geriatric - Keeshond breed Less so, Dachshund, golden retriever, poodle, labrador retriever

Answer 30

If Calcium high and PTH high - PT problem If Ca high PTH low - external to PT problem

Answer 31

Determine urgency by Ca x P Fluids/diuresis - Fluids + frusemide - care check on potassium Glucocorticoids - prednisolone Bisphosphanates Treat underlying cause If primary hyperparathyroid - will remove parathyroid - others will have shrunk so may become hypocalacemic - need to aim for subclinical hypocalcaemia so parathyroid glands can regain function

Answer 32

Parathyroid dependent Primary hypoparathyroidism spontaneous immune mediated functional hypomagnesaemic post-surgical e.g. feline hyperthyroidism Demand exceeds supply or mobilization periparturient tetany (eclampsia) nutritional deficiency of calcium or vitamin D e.g. all meat diets, severe GI disease pancreatitis with fat necrosis [PTH and Calcitriol resistance syndromes]

Answer 33

Parathyroid dependent Primary hypoparathyroidism spontaneous immune mediated functional hypomagnesaemic post-surgical e.g. feline hyperthyroidism Demand exceeds supply or mobilization periparturient tetany (eclampsia) nutritional deficiency of calcium or vitamin D e.g. all meat diets, severe GI disease pancreatitis with fat necrosis [PTH and Calcitriol resistance syndromes]

Answer 34

Muscle fasciculations or tremours Face rubbing Biting and licking at paws or body Hypersensitivity to external stimuli Stiff, stilted gait Ataxia Tetanic seizures Respiratory arrest Weakness Agitation Anxiety Vocalisation Aggression Panting Hyperthermia Cataracts Lengthening of ST segment and QT interval on ECG Third eyelid prolapse in cats

Answer 35

History, lab results - rarely PTH, iCa and Mg measurements IV calcium Monitor for bradycardia Aim for subclinical hypocalcaemia - stimulate PT tissue Oral supplementation only if diet is insufficient Vitamin D to promote calcium uptake

Answer 36

Reduced insulin → Reduced glucose uptake into cells → metabolic deficit Glucagon → Lipolysis → Fatty Acids → Acetyl CoA → Ketones Ketones → Acetoacetate, β-hydroxybutyrate, acetone Acetoacetate and β-hydroxybutyrate are acidic → Metabolic Acidosis Metabolic acidosis and inadequate cellular energy → inappetence, nausea, reduced mentation, vomiting → dehydration, renal hypoperfusion and electrolyte derangements → Death Insulin levels are not always low in these patients – so consider other concurrent disease leading to insulin resistance through increased cortisol, catecholamines or glucagon.

Answer 37

Often new diabetics Middle aged to older animals Since diagnosis - PUPD non resolved, weight loss continued. Progressive lethargy, anorexia, vomiting Clinically - dehydrated and hypovolaemic through fluid loss Other signs: Abdominal pain – pancreatitis common Hepatomegaly – Diabetic hepatopathy (dogs), hepatic lipidosis (cats) Body condition loss (they may still be obese though!) Mental dullness – headache!

Answer 38

Usually straight-forward – history and clinical signs are a strong clue. - Diabetes M → Hyperglycaemia and glucosuria - Ketones → β-hydroxybutyrate is the most abundant - Blood ketones is ideal; usually tests for β-hydroxybutyrate - Urine ketones less ideal; usually tests for acetoacetate so false negatives - Metabolic Acidosis → Blood gas machine e.g. EPOC/iSTAT Other findings: - Anaemia and left shift neutrophilia common (cats also have increased Heinz body formation – oxidative damage to RBC)) - Elevated ALP, ALT due to hepatic effects (cats may be jaundiced) - Electrolyte derangements - Pseudohyperkalaemia or hypokalaemia, hypophosphataemia, hyponatraemia, hypochloraemia and hypocalcaemia. - Bacteriuria – culture and sensitivity is sensible (concurrent UTI 20% dogs)

Answer 39

Hypovolaemia/dehydration and metabolic acidosis mask the true extent of electrolyte disturbances – in particular potassium and phosphate. - Pseudo-hyperkalaemia - Acidosis, haemoconcentration, hypo-insulinaemia or reduced sensitivity - Correction and insulin therapy rapidly reveal true total body hypokalaemia - Do not dive in with insulin straight away! Fluid therapy plan. - Hartmanns - Restore volume status and hydration rapidly – see fluid therapy workshop - Arguably restore deficit quickly over 6-12 hours. - Reduces glucose significantly alone (mechanism not fully understood) - Reveals true extent of electrolyte disturbances allowing treatment - Monitor electrolytes closely (q2-4h) As hydration restores hypokalaemia and hypophosphataemia may unmask. * Severe hypokalaemia – profound muscle weakness and respiratory arrest when extreme * Severe hypophosphataemia – weakness, myocardial depression, arrythmias and haemolysis or seizures in extreme cases. Hypokalaemia - Potassium supplementation – dose rate dependant on severity (table in formulary) – CRI or spiked fluids. - High rates can cause bradyarrythmias – at highest doses (>0.5mEq/kg/hr) consider ECG monitoring (reduce if arrythmias noted) - Monitor and adjust q4-6h Hypophosphataemia - CRI of potassium phosphate 0.03-0.12 mM/kg/hr - Take care as contains potassium too Hyponatraemia (hypochloraemia) - Sodium is pushed intracellularly in response to hyperglycaemia - Maintains normal osmolality - As glucose corrects – sodium should also correct Hypocalcaemia - Only correct if clinical signs noted e.g. muscle twitching/tremors - Usually corrects with fluid therapy and restoration of renal perfusion - Dose rates in the formulary Hypomagnasemia - Rarely done in routine practice as measurement of magnesium is difficult - Questionable accuracy - If doing poorly – could be an option Once hydration is restored, focus switches to achieving normoglycaemia (mild hyperglycaemia) until the patient begins eating, drinking and is BAR. This is via regular neutral insulin administration or insulin CRI - CRI is considered more effective and titratable - BG > 15 mmol/L → 0.05IU/kg/hr - BG 10-15 mmol/L → 0.025IU/kg/hr - BG <10 mmol/L → 0.025IU/kg/hr and start 5% dextrose supplementation at maintenance - If BG <7.5 mmol/L → stop insulin and restart once >10 mmol/L again. Once the patient is eating (any food at this point) and stable then slowly switch back to routine insulin regime as per long term DM control. If the patient is persistently anorexic – consider tube feeding

Answer 40

Survival to discharge – 70% (Good but not perfect) <10% dogs relapse Up to 40% cats relapse

Answer 41

Rare (<5%) but important. Pathogenesis is similar to DKA, but a small amount of insulin and hepatic glucagon resistance reduce lipolysis so ketones are not elevated. Hyperglycaemia → osmotic diuresis → haemoconcentration → hyperglycaemia Diagnosis: - BG > 33.3 mmol/L - Absence of urinary ketones - Serum osmolality > 350 mOsm/kg (see PUPD Lecture) - Alternative version for the calculation: - 2 x (Na + K mEq/L) + (glucose in mmol/L) + (BUN in mmol/L) Treatment – fluid therapy is key again; however rapid correction of hyperglycaemia (and hypernatraemia) lead to an osmotic gradient across the blood brain barrier – rapid cerebral oedema is possible → seizure, coma, death Therefore – aim to restore deficit over 24-48h, but monitor glucose and sodium very closely – maximum rate of reduction is: - Glucose <3mmol/L/h - Sodium 0.5-1mmol/L/h Insulin therapy should only be started once normo-volaemic and hydrated as per DKA – alter insulin doses if glucose is reducing too quickly. Prognosis in the short term is guarded (~60%) but long term survival is probably poor (one feline study reported 12% > 2 months)

Answer 42

Calculi/uroliths located anywhere along urinary tract

Answer 43

DOG Almost always UTI Magnesium ammonium phosphate - MAP Supersaturation of urine by MAP - struvite urolith Risk factor - retention of urine, any condition predisposing to UTI - diabetes mellitus, hyperadrenocorticism Susceptible breeds - miniature schnauzer, Shih tzu, Bichon CAT Almost all sterile Risk factors - abnormal retention of urine Formation of concentrated urine - moisture content of food, water intake Urine alkanising metabolites in diets

Answer 44

Poorly understood Hypercalcaemia, hyperoxaluria, hypocitraturia - Increased intestinal absorption of calcium or reduced renal tubular absorption, renal tubular resorption mechanisms overwhelmed Recurrence common Risk factors - Acidifying diets - Oral calcium supplements given outside of meal times - Excessive dietary protein - Formation of concentrated urine

Answer 45

Uric acid, sodium urate or ammonium urate Impaired conversion of uric acid to allantoin - increased concentration of uric acid in serum and urine 5-8% of uroliths Dalmations and black russian terriers Often associated with PSS (portosystemic shunt) - due to impaired hepatic metabolism of uric acid and ammonia - so urate uroliths also associated with breeds predisposed to PSS - yorkshire terrier Risk factors - High purine intake - glandular meat Persistent aciduria in predisposed animal

Answer 46

Cystinuria – inborn error of metabolism caused by defective tubular resorption of cysteine and other amino acids Breeds with genetic mutations include Newfoundlands, Labradors, Australian cattle dogs, mastiffs and bulldogs Not all cystinuric dogs develop cysteine uroliths – cystinuria is a predisposing factor Predominantly intact male dogs affected Risk factors: Genetic predisposition to cystinuria Acidic, concentrated urine Urine retention

Answer 47

Pure Calcium Phosphate uroliths - less than 1% of all uroliths in dogs and cats Often a minor component of Struvite and Calcium Oxalate uroliths Risk factors: Excessive dietary calcium, primary hyperparathyroidism UTI – with urease producing bacteria

Answer 48

Impaired Xanthine oxidase activity leads to hyperxanthinaemia and xanthinuria Familial or congenital defect e.g. CKCS Allopurinol therapy can lead to acquired xanthinuria Risk factors: Genetic predisposition Acid urine, highly concentrated urine Urine retention Allopurinol treatment

Answer 49

Lower urinary tract signs - dysuria, haematuria, pollakiuria +/- signs of urinary obstruction Urate - signs of PSS

Answer 50

Urinalysis – Not as helpful as you might think! pH is useful – partly clue to urolith type, but also for monitoring treatment/dietary management Need to rule out UTI – and if present, must treat especially if struvite uroliths Crystals can be misleading- once a urolith has formed, minerals are more likely to be deposited on the surface of the urolith than to form new crystals, so crystals are often absent when uroliths present If crystals present, may not represent urolith composition – eg struvite crystalluria often seen in dogs with calcium oxalate uroliths as urine is therapeutically alkalinised. Imaging Is key! Radiography vs ultrasound: ?GA/sedation needed Radiography: Radiopaque uroliths – Calcium Oxalate, Struvite, Calcium phosphate Radiolucent uroliths – Xanthine Variable – Urate, Cysteine# Struvite - usually round/faceted, appear smooth Calcium oxalate - more irregular US - accoustic shadowing - remember gravity when deciding if mass or urolith Can be done conscious Will pick up radiolucent uroliths A diagnosis of urolithiasis without knowing the composition makes it impossible to select effective management

Answer 51

Treatment - medical Analgesia – usually NSAID Antibiotic if concurrent UTI (e.g. with Struvite) – culture and sensitivity as will usually need prolonged course if uroliths present Specific urolith treatment – Urate – Allopurinol – Xanthine Oxidase inhibitor – for dissolution – takes at least 4-6 weeks, sometimes required long term Not effective if PSS – need to manage the shunt Calcium Oxalate Not amenable to dissolution (dietary management is for prevention of recurrence) Struvite Prescription struvite dissolution diet (acidifying) Urate Low-purine, alkalinising diet (contraindicated if pregnant/lactating) Cysteine Alkanising, lower methionine protein content Calcium phosphate - Not amenable to dissolution Xanthine Low purine, alkalinising

Answer 52

Treatment - surgery Which uroliths? Calcium Oxalate, Calcium phosphate, and larger Struvite uroliths Cystotomy, urethrotomy (see surgery lecture, also practical to come  ) If blocked – try and push urolith(s) back into bladder by retrograde urohydropulsion Cystotomy – rarely an emergency – remember lower ASA risk if planned not emergency, can ensure adequate personnel available, do in morning so time to recover and usually home same day Post-op – warn owner of likely haematuria, need to monitor urine output, watch for dysuria Peri and post op analgesia – Opiod, NSAID If Struvite suspected, take urine sample for C & S (unless done recently)

Answer 53

Calcium Oxalate High moisture alkalinising diet – but monitor for Struvite crystalluria Monitor – monthly urinalysis, aim for SG < 1.020 (dogs) & < 1.030 (cats) and pH >6.5 Correct any hypercalcaemia Struvite High moisture acidifying diet – but care re CaOx crystalluria Monitor urine pH & SG (as for CaOx but want pH < 7 Ensure UTI fully resolved – repeat C & S at end of antibiotic course Urate High moisture alkalinising diet Some dogs require long term Allopurinol Cysteine High moisture alkalinising diet Dogs – consider castration, will reduce recurrence if have sex-linked genetic predisposition Calcium Phosphate High moisture diet; senior diets may be useful due to lower protein Xanthine High moisture alkalinising diet

Answer 54

Nephrectomy * renal and ureteral neoplasia * trauma * persistent renal haematuria * polynephritis associated with polycystic disease * end-stage hydronephrosis * single renal cysts associated with renal disease * renal or perirenal abscessation * chronic end-stage pyelonephritis * renal disease associated with ectopic ureter Renal biopsy - cortex not medulla * Investigation of proteinuric renal disease * Renomegaly (or renal mass) * Familial renal disease * renal amyloidosis * renal dysplasia * polycystic kidneys * basement membrane disorders * tubular dysfunction (Fanconi's syndrome) * Acute renal failure Nephrotomy * Removal of renal calculi Normal functioning of the contralateral kidney is a prerequisite for performing nephrectomy Presence of azotaemia or persistent isosthenuria is a contraindication for nephrectomy Do not ligate artery and vein together - could create artery-venous fistula * Renal pain * Haemorrhage * Haemoabdomen * Haematuria * Retroperitoneal and peritoneal urine leakage (uroabdomen) * Urinary tract infection * Compromise of renal function (renal failure)

Answer 55

* Calculi (urolithiasis) * Biopsy * Tumour * Ureteral ectopia Minimal handling – urothelium – oedema with handling – obstruction of ureters and harder closure Use stay sutures Absorbable monofilament (e.g., polydioxanone, polyglyconate, poliglecaprone, glycomer 631) * Size * 4/0 or 3/0 cats * 4/0, 3/0 or 2/0 dogs * Pattern * One-layer – full thickness (simple interrupted, simple continuous, continuous inverting (e.g., Connell, Cushing, Lembert) * Two-layer * Submucosal / mucosa * Seromuscular Knots on inside give substrate for crystals to form * Haemorrhage * Haematuria * Haemoabdomen * Peritoneal urine leakage (uroabdomen) * Urinary tract infection (cystitis) * Urothelial oedema * Dysuria * Small bladder volume * Reflex dyssynergia

Answer 56

Urinary diversion in animals with either: * functional or mechanical obstruction of the bladder or urethra * excessive urine retention (atonic bladder) * Post bladder / urethral surgery (urinary bypass)

Answer 57

Uncommon, represent 0.5-1.7% of all neoplasms in dogs * Benign tumours uncommon * Most common in middle-aged to older animals * No breed predilection has been found * Commonest malignant tumour is renal carcinoma * usually, it is unilateral, located at one pole of the kidney, and well demarcated * size varies from microscopic to several times that of the normal kidney * metastasise early to various organs; the opposite kidney, lungs, liver, and adrenals are involved most commonly Nephroblastomas (embryonal nephroma, Wilms’ tumour) arise from vestigial embryonic tissue * They are seen in young animals and, in dogs, are most commonly diagnosed at < 1 yr of age * There is no breed predilection * Males are affected twice as commonly as females * Nephroblastomas are usually unilateral but are occasionally bilateral * They can grow to immense size; it is not uncommon to have virtually the entire abdomen occupied by tumor * Metastasis may occur to regional lymph nodes, liver, and lungs Kidneys are a common site of metastatic or multicentric neoplasms * Metastatic lesions may be unilateral or bilateral * Lymphosarcoma is the most common multicentric tumor involving the kidneys * As many as 50% of dogs and cats with lymphosarcoma have renal lesions Haematuria, dysuria, stranguria, and pollakiuria are the most common signs * Animals with ureteral obstruction and unilateral hydronephrosis may show signs of abdominal pain and have a palpable, enlarged kidney * Signs of uraemia may be apparent in animals with bilateral reteral obstruction and hydronephrosis or with urethral obstruction * The bladder wall may be thickened, and a cord-like urethra or urethral mass(es) may be palpable rectally Diagnosis * History * Clinical signs * Ultrasonography * Urinalysis * Radiography (contrast) * Computed tomography Treatment * Treatment of majority of renal neoplasms except lymphosarcoma involves surgical removal * Unilateral nephrectomy is usually required * Lymphosarcoma is best managed by combination chemotherapy * Chemotherapy is generally ineffective against renal tumours other than lymphosarcoma

Answer 58

Rare in dogs and cats Mean age 9 years Primary neoplasms more likely to be malignant than benign - transitional cell carcinoma May be solitary or multiple papillary like projections form mucosa, or diffuse infiltration Highly invasive and metastasise frequently - regional lymph nodes and lungs Can cause chronic obstruction and secondary hydronephrosis, and secondary UTIs Diagnosis History Haematuria Neoplastic cells in sediment Biopsy Treatment Excision Poor prognosis Radiation or chemo with vinblastine, chlorambucil to prolong life Stent urethra

Answer 59

* Intraluminal – Plugs – Uroliths – Sloughed tissue * Mural or extraluminal – Neoplasms – Strictures – Anomalies – Reflex dyssynergia * Intraluminal – Sloughed tissues – Inflammatory cells and clots – Increased production of mucoprotein * Mural or extraluminal – Inflammatory swelling – Muscular spasm – Strictures Iatrogenic * Tissue damage – Retrograde flushing solutions – Catheter trauma – Catheter-induced foreign body reaction – Catheter-induced infection * Post surgical dysfunction

Answer 60

Post renal urinary tract obstruction will result in * Severe azotaemia * Hyperkalaemia * Metabolic acidosis Relief from - Urethral catheterisation - Therapeutic cystocentesis Remove urethral plugs by - restraint, muscle relaxants and reverse flushing

Answer 61

Retrograde positive contrast urethrocystograpy - Survey radiograph abdominal films - Contrast study - Abdominal US

Answer 62

* Tube cystotomy and urethral stenting * Perineal urethrostomy (based on Wilson-Harrison technique) * Prepubic urethrostomy * Subpubic urethrostomy (transpelvic urethrostomy) * Stabilise and referral * Stabilise and perform PU * Euthanase

Answer 63

* Haemorrhage * Wound dehiscence * Subcutaneous urine leakage * Urinary incontinence * Urinary tract infection * Urethral (stoma) stricture

Answer 64

Filling The sympathetic nervous system predominates: * Positive stimulus (via alpha-adrenergic fibres) causes urethral smooth muscle contraction (prevents leakage) * Inhibition of detrusor muscle (via beta- adrenergic fibres) allows passive filling of the bladder The somatic nervous system (voluntary): Stimulates urethral striated muscle contraction (for sudden or prolonged increases in bladder pressure) Urination The parasympathetic nervous system dominates: * When threshold is reached, stretch receptors in the bladder wall stimulate detrusor muscle contraction = detrusor reflex * Urethral sphincter muscles relax * Micturition reflex = detrusor reflex and inhibition of sympathetic and somatic stimulation to bladder and ureters

Answer 65

Behavioural - stress, pain, instinct, cognitive dysfunction Polyuria Increased urinary frequency - pollakiuria Impaired control - neurogenic, non neurogenic (anatomical or functional disorder) History Ask for pattern in urination habits Does animal seem conscious of urination? Rule out behavioural problems Ask if any other concurrent symptoms Is the patient also polydipsic (has this been measured?) Any change in diet? Clinical examination Can you palpate the bladder? (rectal palpation in horses) Do the genitalia look normal? – is it painful to palpate – are uroliths present? Is the neurological exam normal including anal tone? Check for urine scalding Neurological examination Urination Can you observe urination or ask owner to film? Is stream of urine continuous or intermittent? What is the appearance of the urine? Urinalysis Including SG, microscopy, culture and sensitivity (cystocentesis) CBC, biochemistry, bile acids, electrolytes (and species specific: FeLV, T4) Rule out our causes of polyuria Access renal function Imaging Plain abdominal radiographs Ultrasonography to access bladder and urinary tract Contrast radiography/urethrogram Cystoscopy

Answer 66

True urinary incontinence: the patient is unaware that they are leaking urine. Usually due to poor sphincter functionality. (Uncommon in cats)

Answer 67

Urge incontinence: the patient is aware that they need to urinate but may have lack of control. Can be caused by bladder irritation or seen as inappropriate urination

Answer 68

Overflow incontinence: the patient is (usually) unaware that they are urinating, occurs when urine pressure within the bladder is greater than the urethra. Considered a ‘voiding’ rather than storage disorder.

Answer 69

Cerebral lesions - rare - loss of voluntary control - Bladder can empty normally but at inappropriate times Brainstem L7 lesions - upper motor neurone bladder - autonomic bladder Damage to brain or higher spinal cord Absent voluntary micturation Bladder is hard to express Increased urethral sphincter tone High volume urinary retention Development of automatic bladder - bladder emptying when threshold reached not under voluntary control S1-S3 or nerve root lesion - lower motor neurone bladder Paralytic bladder Damage to sacral spine/pelvic plexus/tail pull in cats * Absent voluntary micturition * Bladder is atonic, flaccid and easy to express * Concurrent reduced perineal reflex and anal tone, may have tail paralysis * Atonic urethral sphincters * Absent detrusor reflex * Can result in overflow incontinence when full

Answer 70

Most common non-neurogenic cause of canine incontinence * Normally presents as intermittent involuntary leaking of urine when dog is relaxed (sleeping) or excited * Can occur concurrently with ectopic ureters * Patient may have good/bad leaking days * May be congenital (less common, and some may resolve post 1-2 seasons) * Uncommon presentation: male entire or castrated dogs Most common - female, spayed, older, large breed, overweight Sympathomimetic agents = aim to mimic the ‘storage’ of urine phase Phenylpropanolamine; propalin (vetoquinol) and urolin (dechra) - alpha-adrenergic mechanism - Good rapid response (>75% of female dogs will improve) - Can use in male dogs/cats - Possible adverse effects: restlessness, aggression, tachycardia, weight loss Oestrogens = acts on oestrogen receptors on sphincters Estriol; Incurin (intervet) and enurace (janssen) - Takes longer to get a response - Cannot use in males/entire bitches or cats - Adverse effects: oestrogenic effects (appears ‘in season’)

Answer 71

Congenital: * Intersex patients (rare)– may have combination of genital and reproductive organs resulting in different anatomy or functional problem Ectopic ureters * Incontinence observed shortly after birth * Bladder is bypassed and urine may empty into vagina or urethra * Grossly ureter could look normal, but ‘burrows’ along bladder submucosa into “intra-luminal” position. * Can occur concurrently with other abnormalities * Secondary infection is common (including pyelonephritis) * Treatment: surgical Other * Detrusor instability: an overactive bladder presenting as pollakiruria. Most animals have underlying cystitis, irritating the bladder lining and over stimulating the detrusor reflex. = URGE INCONTINENCE

Urinary and endocrine Flashcards

(95 cards)