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CVSOH 4 > Nephrology and Urology > Flashcards

Nephrology and Urology Flashcards

1
Q

Apart from vascular, traumatic and toxic, what other classification of disease is often responsible for acute injury?

A

Inflammatory

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2
Q

What is the characteristic of azotaemia?

A

Increase urea with/without increased creatinine in the blood

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3
Q

Define uraemia.

A

The clinical syndrome arising from azotaemia

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4
Q

What is pre-renal azotaemia?

A

Reduction in renal blood flow or increase protein catabolism/GI haemorrhage (bleeds means delivering a huge amount of protein to the kidney that normally functioning kidneys wouldn’t be able to deal with it).

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5
Q

What is the USG of pre-renal azotaemia?

A

The kidney will be doing everything they can do to conserve water = azotaemia with concentrated urine

> 1.030 in dogs
1.035 in cats

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6
Q

What is renal azotaemia?

A

Fewer functional nephrons. The kidneys are unable to conserve water so azotaemia with dilute urine

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7
Q

What is the USG of renal azotaemia?

A

< 1.030 in dogs
< 1.035 in cats

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8
Q

What are 2 examples of post-renal azotaemia?

A

Urinary tract obstruction > back-pressure

Urinary tract rupture > urine leakage > reabsorption of waste products

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9
Q

How is post-renal azotaemia diagnosed?

A
  • Identify with history, imaging with/without effusion analysis. Uroabdomen: [creatinine]fluid > [creatinine]serum
  • Free abdominal fluid
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10
Q

You are presented with a 9 year old cat for a dental treatment. Pre-operative bloods identified increased urea and creatinine. You collect a urine sample – specific gravity is 1.018. What classification of azotaemia does this cat have?

A

Renal

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11
Q

Define acute kidney injury.

A

Sudden organ damage and association dysfunction, usually severe clinical signs. Causes fatal injury, complete recovery, partial recovery to chronic disease. Acute nephron damage/dysfunction

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12
Q

What is chronic kidney disease?

A

Chronic nephron loss > gradual decline in renal function

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13
Q

Why are the kidneys so susceptible to toxic and ischaemic injury?

A

As they weight 0.5% of body weight but get 20% of cardiovascular output so are very sensitive to CVS changes/lesions or toxic lesions

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14
Q

What is the effect of severe acute kidney injury on urine output? How does this effect prognosis?

A

Most commonly = anuria/oliguria
Less commonly = polyuria

Polyuric has better prognosis as at least they are able to excrete the waste products with lots of water, anuric/oliguric cannot and so this is what is fatal progressively

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15
Q

What are the physiological consequences of acute kidney injury?

A
  • Failure of excretion of nitrogenous waste products
  • Acid base disturbances
  • Electrolyte disturbances
  • Fluid balance disturbances
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16
Q

What is the effect of failing to excrete nitrogenous waste due to acute kidney injury?

A
  • Azotaemia = increased serum urea, creatinine
  • Increased phosphate
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17
Q

What is the effect of electrolyte disturbances due to acute kidney injury?

A
  • Hyperkalaemia with an/oliguria
  • Various with polyuria
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18
Q

What is the presentation of acute kidney injury?

A
  • Often uraemic – lethargic, inappetant, nauseous/vomiting, diarrhoea
  • With/without dehydrated/hypovolaemic
  • Increased or decreased temperature
  • With/without renomegaly – symmetry? Cats may get asymmetry from AKI
  • With/without renal/abdominal pain
  • With/without concurrent signs due to other affected organ systems
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19
Q

What are the possible concurrent signs from other organ systems with presentation of acute kidney injury?

A
  • Hypocalcaemia – tremors, seizures (ethylene glycol)
  • Icterus, petechiae – leptospirosis causes acute kidney and liver injury
  • Cutaneous lesions
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20
Q

What are the possible aetiologies of acute kidney injury?

A
  • Toxic – toxins, drugs
  • Ischaemic – hypoperfusion
  • Infectious – leptospirosis, pyelonephritis, CRGV
  • Metabolic – elevated Ca:P product or condition causing high calcium and phosphate that may cause kidneys to mineralise
  • Uncorrected pre/post renal progressing to renal azotaemia
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21
Q

What is CRGV?

A

Cutaneous and renal glomerular vasculopathy – Alabama rot

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22
Q

What is the presentation of CRGV?

A

Skin lesions are rare with other causes of AKI – clots in blood vessels causing ischaemic skin lesions

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23
Q

How is CRGV diagnosed?

A
  • Acute azotaemia with exclusion of pre-renal and post-renal causes – non-azotaemic AKI is possible
  • Often hyperphosphataemic
  • Potassium variable – increased if anuric/oliguric, decreased if polyuric
  • Metabolic acidosis
  • With/without changes related to underlying cause
  • Rule out addison’s – can look like AKI
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24
Q

What are the specific urinalysis findings with CRGV?

A
  • Submaximally concentrated urine with/without proteinuria/glucosuria due to tubular damage
  • Casts, crystals
  • Inflammatory cells/bacteriuria
  • Bacterial culture and sensitivity (ideally cystocentesis sample) - polynephritis
  • Calcium oxalate dihydrate may be found in normal cats and dogs
  • Calcium oxalate monohydrate = ethylene glycol toxicity
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25
Q

How can imaging exclude post-renal causes in acute kidney injury diagnosis?

A

Ureteric obstruction > pelvic dilation

Urinary tract rupture > free fluid

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26
Q

What can be seen of acute kidney injury on ultrasound?

A
  • Renal size normal to renomegaly
  • Pyelonephritis may lead to pyelectasia
  • With/without cortices, peri-nephric fluid
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27
Q

What can be seen of acute kidney injury on radiography?

A

With/without renomegaly and radio-opaque uroliths

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28
Q

When may renal cytology FNA be indicated?

A

Rarely. Use if suspect renal lymphoma – black band around the kidney. Thrombocytopathia?

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29
Q

Which infectious disease may cause acute kidney injury? How is this tested?

A

Leptospirosis

Serology, PCR (blood first 5-7 days of illness, urine thereafter)

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30
Q

What other specific test can you do in acute kidney injury?

A

Specific tests for toxins such as ethylene glycol. Potentially toxicology for owner peace of mind if there is concern someone has poisoned the cat in the neighbourhood

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31
Q

How is acute kidney injury managed?

A
  • Remove underlying cause - stop known nephrotoxic drugs, f recent ingestion of substance – gastric decontamination/adsorption
  • Supportive management, pending renal recovery. Manage fluid balance, electrolytes, uraemic toxins, nausea, pain
  • Specific treatment where available
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32
Q

How is initial fluid therapy done in acute kidney injury?

A
  • Correct any hypovolaemia (pre-renal component) within 1-2 hours
  • Once euvolaemic, correct any dehydration
  • Replace over 6 hours
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33
Q

What are the potential contraindications for initial fluid therapy in acute kidney disease?

A
  • Overhydration - kidneys made oedematous are work more poorly
  • Clinically significant cardiac disease
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34
Q

What are the risks of anuria/oliguria?

A
  • Progressive azotaemia
  • Metabolic derangements
  • Life threatening potassium increase
  • Volume overload > worse outcome
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35
Q

What are the risks of polyuria?

A

Dehydration, hypovolaemia, potassium wasting, hypokalaemia

Easier to manage, better prognosis because can excrete uraemic toxins

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36
Q

How is ongoing fluid therapy for acute kidney injury done?

A
  • Hartmann’s
  • 2ml/kg/h maintenance obsolete in patients with increased or decreased urine output
  • Match ins with out
  • Re-evaluate every 1-4 hours
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37
Q

What are the consequences of hyperkalaemia caused by acute kidney injury?

A
  • Reduced pacemaker activity – may be bradycardic
  • Can lead to ventricular fibrillation and cardiac arrest - wide QRS, spiked T, flattened P
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38
Q

How is hyperkalaemia by acute kidney injury managed?

A
  • Restore renal perfusion
  • Calcium gluconate IV – does not address hyperkalaemia but stabilised cardiomyocyte membranes
  • Redistribute potassium intracellularly
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39
Q

How is potassium redistributed intracellularly to manage hyperkalaemia caused by acute kidney injury?

A
  • Glucose in hartmann’s – stimulate endogenous insulin release which will cause cells to uptake with potassium
  • With/without exogenous insulin (neutral) – requires regular BG monitoring
  • Sodium bicarbonate is rarely indicated even in referral, requires acid base monitoring
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40
Q

How are acute kidney injuries managed?

A
  • Fluid balance – post AKI polyuria may be profound
  • Renal perfusion – systemic blood pressure, avoid hypertension
  • Electrolytes – supplement as necessary
  • Azotaemia
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41
Q

What is the antidote for NSAID induced acute kidney injury?

A

Misoprostol

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42
Q

What is the specific antidote for pyelonephritis causing acute kidney injury?

A

Antibiotics. Clavulanate potentiated amoxicillin = reasonable choice pending culture

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43
Q

What is the specific antidote for leptospirosis induced acute kidney injury?

A

Clavulanate potentiated amoxicillin IV (pending results/if too sick for oral doxy.) Doxycycline (2 weeks, orally) to eliminate carrier state

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44
Q

What is the specific antidote for ethylene glycol toxicity induced acute kidney injury?

A

Ethanol (or 4-methylpyrazole) within 8 hours ingestion

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45
Q

What is the adjunctive management for acute kidney injury?

A
  • Consider dose reductions for renally metabolised drugs
  • Manage nausea – maropitant, metoclopramide
  • Manage GI haemorrhage (may > nausea) – omeprazole (reduce 50%), sucralfate
  • Analgesia (opioids) if required
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46
Q

What are the other considerations for acute kidney injury management?

A
  • If feeding liquid food incorporate into fluids ins calculation
  • Manage hypertension with amlodipine
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47
Q

What is done if there is persistent anuria?

A
  • Double check – euvolaemic, euhydrated
  • No post-renal disease – obstruction, rupture
  • Frusemide single dose, expect response 20-60 minutes, may repeat
  • Still a anuric, indication for renal replacement, prognosis guarded if cannot respond to single dose
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48
Q

What is the prognosis of acute kidney injury?

A
  • Approximately half of survivors have CKD
  • All survivors should be considered as CKD IRIS stage 1 at minimum
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49
Q

What is chronic kidney disease?

A
  • Functional and/or structural disease of over 3 months duration
  • Gradual, progressive, irreversible, nephron loss
  • Management aimed at protecting remaining nephrons and managing clinical consequences
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50
Q

Why is evidence of chronic kidney disease not seen until late in the disease?

A
  • Loss 50% nephrons = 1 kidney loss or 50% function in each, still subclinical
  • Loss 67% = lose concentrating ability
  • Loss 75% = become azotaemic
  • Loss 100% nephrons = decreasing quality of life
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51
Q

What are the possible aetiologies of chronic kidney disease?

A
  • Chronic interstitial nephritis (CIN) – end stage of many pathological processes. Original inciting cause of the injury is not possible to tell
  • Glomerulonephropathy
  • Undiagnosed/untreated infections
  • Chronic obstructive disease
  • Congenital – PKD, renal dysplasia
  • Lymphoma
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52
Q

What is the genetic test for polycystic kidney disease?

A
  • Cheek swab or EDTA blood sample
  • Negative cats > ICC PKD register
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53
Q

What is the pathogenesis of chronic kidney disease?

A
  1. Asymptomatic/undiagnosed initial insult > decreased GFR
  2. Compensatory hypertrophy of remaining nephrons
  3. Leads to progressive nephron loss, progressive decreased GFR
  4. Loss of electrolyte/water regulation
  5. Loss acid/base regulation
  6. Failed excretion of organic solutes
  7. Impaired renal hormone synthesis – calcitriol (vitamin D), erythropoeitin (EPO)
  8. Hypertension; cause vs. consequence
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54
Q

What are the findings from the history of a clinical presentation of chronic kidney disease?

A
  • PUPD – in cats, major differentials are diabetes mellitus ad hyperthyroidism
  • Weight loss
  • Lethargy, weakness
  • Inappetance
  • Vomiting with/without diarrhoea with/without haematemesis/melaena. May see constipation secondary to dehydration
  • With/without signs associated with hypertension - blindness, neurological
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55
Q

What are the findings from the examination of a clinical presentation of chronic kidney disease?

A
  • Catabolic state
  • Typically dehydrated
  • With/without weakness – hypokalaemic myopathy > neck ventroflexion
  • With/without uraemic ulcers, with/without uraemic halitosis
  • With/without hypertensive retinopathy
  • Kidneys typically small and irregular on palpation – may be large if lymphoma
  • ‘Rubber jaw’
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56
Q

What is the pathogenesis of renal secondary hyperparathyroidism/rubber jaw?

A
  1. Decreased GFR > decreased phosphate excretion
  2. Increased serum phosphate
  3. Parathyroid secretion
  4. Decreased phosphate and increased calcium – ineffective as inadequate renal function to excrete increased phosphate
  5. Progressive increased phosphate
  6. Persistent parathyroid hormone release
  7. Bone resorption resulting from increased parathyroid hormone activity
  8. Rubber jaw – R2PTH. Clinically most recognised in renal dysplasia
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57
Q

What diagnostic test is needed to confirm a renal azotaemia in a cat?

A

Urine specific gravity less than 1.035

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58
Q

How is chronic kidney disease diagnosed?

A
  • Azotaemia is increased urea and creatinine, not until 75% GFR loss
  • With inadequately concentrated urine not until 67% GFR loss
  • GFR = gold standard measure of renal filtration
  • SDMA = benefits and limitations, equally prone to limitations of creatinine (increases with pre, renal and post renal azotaemias)
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59
Q

How might chronic kidney disease appear on urinalysis?

A
  • Submaxillary concentrated urine
  • Evaluate for proteinuria
  • Sediment examination for casts and crystalluria
  • Cytological examination – EDTA sample for inflammatory sediment or atypical cells
  • Culture and sensitivity – cystocentesis, plain sample
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60
Q

How may chronic kidney disease be diagnosed from bloods?

A

Haematology – anaemia (normocytic, normochromic)

Serum biochemistry
- Azotaemia
- With/without increased phosphorous
- With/without increased/decreased calcium
- With/without decreased potassium – very end stage causes increase

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61
Q

What other diagnostic tests might be done for chronic kidney disease?

A
  • FIV (/FeLV)
  • Systolic blood pressure
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62
Q

What might be assessed from radiography about chronic kidney disease?

A
  • Renal size and architecture
  • Ureteroliths
  • Ureteric obstruction
  • Pyelonephritis
  • Lymphoma
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63
Q

How is IRIS staged?

A
  1. Creatinine
  2. Substage by proteinuria
  3. Substage by blood pressure
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64
Q

How is fluid balance managed for chronic kidney disease?

A
  • Encourage oral intake
  • Subcutaneous fluids
  • Oesophageal tube – nutrition, fluid, medication
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65
Q

How is the progression of chronic kidney disease delayed?

A
  • Renal diet
  • Control hypertension, proteinuria, hyperphosphatemia, hypokalaemia
  • Avoid further insults
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66
Q

Which nutrients are restricted in renal diets?

A

Protein
Phosphorus
Sodium

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67
Q

Which nutrients are supplemented in renal diets?

A

Omega-3 PUFAs
Vitamin E
Synergistic with PUFAs
B vitamins
Potassium in cats
Soluble fibre

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68
Q

How is calorific intake managed in chronic kidney disease?

A
  • Important to avoid protein calorie malnutrition
  • Avoid introducing prescription diets in the hospital or syringe feeding
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69
Q

What are the possible causes of inappetence in chronic kidney disease?

A
  • Dehydration
  • Hypokalaemia
  • Nausea, mirtazepine, maropitant
  • Uraemic gastropathy, omeprazole, sucralfate
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70
Q

How is hyperphosphataemia from chronic kidney disease managed?

A

Phosphate restriction slows progression and so prolongs survival

  • Renal diet
  • If inadequate decreased phosphorous > phosphate binder
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71
Q

What are the contributors to hypokalaemia caused by chronic kidney disease?

A

Inadequate dietary intake
Renal potassium wasting

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72
Q

What are the clinical signs of hypokalaemia caused by chronic kidney disease?

A

Inappetence, lethargy, weakness, PUPD

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73
Q

How is hypokalaemia caused by chronic kidney disease managed?

A

Renal diet with/without potassium supplementation

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74
Q

How is hypertension caused by chronic kidney disease assessed?

A

Do a retinal exam
Target = SBP <140mmHg

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75
Q

Describe the anaemia caused by chronic kidney disease.

A
  • Anaemia of chronic disease is common/expected in CKD
  • Usually mild and does not need specific treatment
  • Exacerbated by gastrointestinal haemorrhage and reduced RBC lifespan
  • Reduce GI losses (omeprazole, sucralfate)
  • If PCV <20% and symptomatic for anaemia
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76
Q

What is systemic hypertension due to?

A
  • Increased SNS > increased RAAS > vasoconstriction
  • RAAS > sodium ion retention
  • Volume expansion
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77
Q

What are the causes of secondary hypertension?

A
  • Kidney disease
  • Endocrinopathies
  • Situational hypertension – stress associated
  • Increase intracranial pressure (with bradycardia = Cushing’s reflex)
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78
Q

What are the consequences of systemic hypertension?

A
  • Ocular – hypertensive retinopathy, acute blindness
  • Renal - increased risk of progression of CKD
  • Cardiac – pressure overload causes left ventricular concentric hypertrophy
  • Neurological
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79
Q

What is the normal systemic blood pressure?

A
  • SBP 120-140mmHg
  • Sight/deerhounds 10-20mmHg higher – this appears to be in-hospital situational hypertension
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80
Q

Define the values for hypertension.

A

Pre-hypertensive = 140-159 mmHg, low risk of future target organ damage/TOD

Hypertensive = 160-179mmHg, moderate risk of future TOD

Severely hypertensive = over 180mmHg, high risk of future TOD

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81
Q

How is cuff for blood pressure measurement selected?

A

Cuff width is 40% the circumference of the limb and placed as close to cardiac height as possible

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82
Q

When should hypertension be treated?

A
  • SBP ≥180mmHg = treat
  • SBP ≥160mmHg with evidence of target organ damage = treat
  • Sustained (>1 visit) SBP ≥160mmHg
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83
Q

What are the signs of hypotension the owner should be made aware of?

A

Lethargy, weakness, ataxia/syncope – and reassess immediately

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84
Q

Which medications can be used to manage reduce renal blood flow for hypertension management?

A
  • Amlodipine is 1st choice in cats – calcium blocker that causes vasodilation in peripheral arteries
  • Benazepril is first choice in dogs – ace inhibitor
  • Telmisartan – angiotensin receptor blocker
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85
Q

What is proteinuric kidney disease?

A
  • Proteinuric kidney disease is the most common type of CKD in dogs, rare in feline renal disease
  • Proteinuria accelerates progression of renal disease
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86
Q

How is proteinuria diagnosed?

A

Dipstix – qualitative

Urine protein:creatinine ration – quantitative

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87
Q

How is proteinuria diagnosed from protein:creatinine ratio?

A
  • Normal < 0.2
  • Borderline 0.2-0.4/0.5
  • Proteinuric – > 0.4 in cat, > 0.6 in dog
  • Severely proteinuric >2
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88
Q

What are the pre-renal causes of increased urine protein?

A
  • Increased blood proteins – hyperglobulinaemia, haemo/myoglobinaemia
  • Functional – pyrexia, post-exercise, seizure
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89
Q

What are the renal causes of increased urine protein?

A

Intrinsic renal disease
- PLN
- Glomerular disease - increased permeability to albumin > proteinuria
- Tubular disease

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90
Q

What are the post-renal causes of increased urine protein?

A
  • Urinary tract (ureteric, bladder, prostatic, urethral) - inflammatory or neoplastic disease, urinary tract haemorrhage
  • Reproductive tract disease
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91
Q

Does glomerular disease result in azotaemia?

A

They are not necessarily azotaemic and may retain urine concentrating ability – it is glomerular, not tubular disease

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92
Q

What are the consequences of nephrotic syndrome?

A
  • Progressive proteinuria > hypoalbuminaemia > effusions/oedema
  • Hypercoagulability > exacerbates/accelerates glomerular nephropathy
  • Hypercholesterolaemia
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93
Q

What are some causes of primary glomerular disease?

A
  • Inherited/familial glomerular disease – developmental collagen defects
  • Idiosyncratic disease
  • Autoimmunity
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94
Q

What are some causes of secondary glomerular disease?

A

Secondary > Immune complex formation/deposition or amyloid deposition

  • Inflammatory (sterile, infectious)
  • Neoplastic disease
  • Drug/toxin exposure
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95
Q

What is amyloidosis?

A
  • Chronic inflammatory disease (elsewhere in the body) > production of serum amyloid A (SAA)
  • AA is deposited in tissue – kidneys, liver, other organs
  • Polymerises and forms β-pleated sheet – insoluble
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96
Q

What is renal amyloidosis?

A
  • Causes marked proteinuria
  • Typically glomerular deposition
  • Familial Shar-pei Fever (FSF) believed to be the inflammatory trigger – treat FSF episodes with NSAIDs
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97
Q

How do I find out what type of glomerular disease a patient has?

A
  • Evaluating for a possible underlying trigger of the glomerulonephritis/amyloidosis. Primary vs. secondary/reactive glomerular pathology
  • Renal biopsy
  • Histopathology alone inadequate
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98
Q

When is renal biopsy used?

A
  • Not appropriate disease if secondary disease or end-stage
  • Use in primary cases (no trigger), without familial cause, not responding to ‘standard’ therapy
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98
Q

How is proteinuria treated?

A
  • Angiotensin receptor blocker (first line therapy)
  • Angiotensin converting enzyme inhibitor (second line therapy)
  • Significantly decreases proteinuria and delays onset and progression of azotaemia
  • Monitor every 2 weeks (3 months once stable) - aim UPC < 0.5 or <50% from baseline, creatinine, albumin, sodium, potassium, Blood pressure
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99
Q

What might be the adverse events of treating proteinuria?

A

Worsening azotaemia, hypotension, hyperkalaemia

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100
Q

What are the adjunctive therapies used in all glomerular patients?

A
  • Renal diet
  • Omega-3 PUFAs
  • Anti-platelet therapy (e.g. clopidogrel or aspirin)
  • Oedema management; light exercise
  • Manage hypertension
  • Monitor/manage otherwise as per IRIS guidelines (glomerular disease is a form of CKD)
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101
Q

What is the prognosis of glomerular disease?

A
  • Highly variable, depending on subtype – poor in those presenting with azotaemia and nephrotic syndrome, <2 months
  • Slow progression with survivals of a number of years
  • Spontaneous resolution/remission also reported
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102
Q

What are the features of nephrotic syndrome?

A

Proteinuria, hypalbuminaemia, effusions, hypercholesterolaemia

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103
Q

What is the class of the first line drug for treating proteinuria?

A

Angiotensin receptor blocker

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104
Q

What are 2 tubular disorders?

A

Glucosuria in the absence of hyperglycaemia > osmotic diuresis > PUPD. If normal in blood, is not DM

Fanconi syndrome - hereditary or acquired (copper hepatopathy, leptospirosis, Chinese jerky treats)

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105
Q

What are the clinical signs of lower urinary tract disease?

A

Similar regardless of aetiology:

  • Dysuria
  • Stranguria
  • Vocalisation, licking prepuce, inappetence, lethargy
  • Haematuria
  • Pollakirua – increased pollakiuria
  • Periuria – voiding in inappropriate places
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106
Q

What are the differential diagnoses for lower urinary tract disease in cats?

A
  • Urethral plus
  • Urethral spasm
  • Behavioural
  • Urolithiasis
  • Bacterial UTI
  • Stricture (congenital)

Rare - neurological, neoplasia, prostatic

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107
Q

What are the differential diagnoses for lower urinary tract disease in dogs?

A
  • Bacterial UTI – prone to ascending infections due to short wide urethra
  • Prostatic disease
  • Urolithiasis
  • Transitional cell carcinoma

Rare:
- Urethritis
- Cyclophosphamide induced sterile haemorrhagic cystitis
- Stricture (congenital)
- Neurological

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108
Q

When is a neurological examination indicated for lower urinary tract disease?

A

If hindlimb ataxia, difficulty posturing, dribbling urine

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109
Q

What is the presentation of urinary obstruction?

A
  • Unproductive urination attempts
  • Tense, usually large painful bladder
  • Not palpable? Ruptured? AFAST
  • Associated complications
  • Bradydysrhythmias – life-threatening hyperkalaemia
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110
Q

How is urinary obstruction diagnosed from basic urinalysis?

A
  • Submaximally concentrated – appropriate vs. pathological
  • Dipstix analysis
  • Urine biochemistry – expect some proteinuria due to LUT inflammation
  • Crystals – true vs. storage artefact. normal vs. abnormal (plain tube). Can be normal alone, abnormal if with stones
  • Bacteria – asymptomatic bacteriuria vs. urinary tract infection
  • Cytology – inflammatory, neoplastic cells
  • Culture
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111
Q

How is urinary obstruction diagnosed from ultrasounds?

A
  • For cystocentesis
  • Bladder wall morphology
  • Prostatic parenchyma
  • Uroliths
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112
Q

How is urinary obstruction diagnosed from radiography?

A

Plain – uroliths (radio-opaque), prostato/lymphadenomegaly

Contrast, double contrast – uroliths (radiolucent), masses, polyps, strictures

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113
Q

What further diagnostics could be used to diagnose urinary obstruction?

A
  • Haematology, serum biochemistry – underlying systemic disease?
  • Free abdominal fluid? – analyse
  • Prostatic wash/suction
  • Bladder suction biopsy
  • Cystoscopy
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114
Q

How might urine samples be collected?

A
  • Cystocentesis – preferred method for culture
  • Catheterisation - can culture, although less sterile than cystocentesis
  • Analyse fresh from free catch or litter trays – appropriate for USG, biochemistry, UPC, sediment exam, cytology
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115
Q

What are the predisposing factors for UTIs?

A
  • Indwelling urinary catheter – risk for infection, do not treat while catheter is in situ, will only create resistant infection
  • Structural urinary tract disease
  • Abnormal voiding
  • Sub-maximally concentrated urine
  • Immunosuppression/systemic disease
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116
Q

How are UTIs treated in dogs?

A

Ideally treat based on culture and sensitivity. Ideally NSAIDs only pending results. Amoxicillin or trimethoprim sulphonamide. 3-5 day course

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117
Q

What are the considerations for UTI management?

A
  • Fresh water access
  • Enable frequent voiding
  • Keep vulva, prepuce clean and free from urine scald – UTIs are typically due to ascending infections if alkaline pH, consider evaluating for struvite uroliths
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118
Q

What are the possible complications of UTIs?

A
  • Struvite uroliths – urease producing bacteria (Staphylococcus, Proteus)
  • Pyelonephritis
  • Polypoid cystitis
  • Emphysematous cystitis
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119
Q

When might UTIs be complicated?

A

Recurrent bacterial cystitis, cats?, male dogs?, predisposing factors

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120
Q

How are complicated UTIs managed?

A
  • Evaluate for and treat underlying cause
  • Base treatment on culture and sensitivity
  • Prostatic – only TMPS, fluoroquinolones and doxycycline will penetrate, 3-6 weeks. Neuter entire male dogs 1-2 weeks into treatment
  • Pyelonephritis – treat pending c&s – Quinolone, 7-14 days
  • Re-culture - 1 week into treatment to demonstrate control and1-2 weeks after stopping treatment
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121
Q

Which cats are susceptible to feline idiopathic cystitis?

A
  • Neuroendocrine modulation – adjusted sensory nerve function, abnormalities of the CNS stress response
  • GAG layer hypofunction
  • Environmental stress manifests as FLUTD
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122
Q

What is the presentation of non-obstructed feline idiopathic cystitis?

A
  • Signs of LUTD
  • Still able to void
  • Often self-limiting
  • May experience recurrent episodes
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123
Q

What is the presentation of obstructed feline idiopathic cystitis?

A
  • Urethral spasm or plug
  • Unproductive attempts to urinate
  • Emergency
  • More common in males (non-obstructive equi-prevalent)
  • High recurrence rates
  • > 40% experience a recurrence within 6 12 months
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124
Q

What should never be done in feline idiopathic cystitis?

A

Never attempt to express their bladder

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125
Q

How is feline idiopathic cystitis managed?

A
  • FLUTD signs, young cat, first episode, non-obstructed – manage medically
  • Obstructed – alleviate obstruction then manage medically
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126
Q

What is the presentation of urethral obstruction?

A
  • Back pressure on kidneys > post renal azotaemia
  • Hyperkalaemia
  • Painful bladder
  • Agitated/painful vs. depressed
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127
Q

What is the emergency management for hyperkalaemia as the result of obstruction?

A
  • Definitive correction requires alleviation of obstruction – urinary catheterisation
  • Hyperkalaemia needs addressing first
  • Bladder decompression rarely required in the interim
  • Analgesia (opioids) during stabilisation, pending GA
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128
Q

How is urinary catheterisation done?

A
  1. Rectal examination
  2. Use a drape
  3. Examine penis for plugs, stones, trauma
  4. Straighten penis and advance the catheter using flushing
  5. Do not force, if not advancing easily, flush to alleviate obstruction
  6. Leave it in situ for 24-48 hours to provide sufficient analgesia and drugs to alleviate spasm – stitch in
  7. Submit urine for full analysis
  8. Flush bladder until clear
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129
Q

How do you care for a urinary catheter post catheterisation?

A
  • Closed, clean system – wear gloves for handling, keep bag off the floor
  • Change bag daily
  • Avoid antibiotics
  • Tape collection system to tail to avoid pulling
  • Buster collar
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130
Q

What should be monitored post catheterisation?

A
  • Monitor urine output
  • Monitor hydration/volaemic status
  • Monitor electrolytes – post obstruction diuresis > hypokalaemia
  • Urine sediment/cytology daily for evidence of infection
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131
Q

Which analgesics are used for cats with lower urinary disease?

A
  • Opioids – buprenorphine
  • NSAIDs – consider contraindications
  • Gabapentin – useful in severely affected cases, anxiolytic
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132
Q

How is feline idiopathic cystitis managed by environmental modification?

A
  • Alleviate predisposing stressor
  • Address negative cat-cat interactions
  • Plentiful clean/varied toileting stations
  • Feliway
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133
Q

How is urinary health promoted in feline urinary cystitis?

A
  • Encourage water intake – dilute inflammatory mediators/noxious substances in urine
  • Wet diets
  • Urinary diets
  • Avoid obesity
  • GAG supplementation - GAG protects against noxious substances in urine
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134
Q

What are the antispasmodics used in feline idiopathic cystitis, commonly used in post-obstruction?

A

Prazosin – α1 blocker, smooth muscle relaxant, may cause hypotension

Dantrolene – skeletal muscle relaxant, (external urethral sphincter)

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135
Q

What are the functions of the kidney?

A
  • Homeostasis – acid-base balance, water and electrolyte balance
  • Endocrine – renin-aldosterone, erythropoietin, vitamin D activation
  • Formational of urine – elimination of metabolic waste
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136
Q

How are pig kidneys different to dog kidneys?

A

Pig kidney also similar but has papillae rather than a renal crest

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137
Q

How is the cat kidney different from a dog’s?

A

Cat has a single papillae but looks like a renal crest. In some cats, the cortex is pale tan-cream owing to lipid storage – normal, looks paler than you might expect. Cats also have stellate veins

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138
Q

How are bovine kidneys different to dog kidneys?

A
  • Multiple lobes
  • No renal pelvis
  • After passing through the renal hilus, the ureter branches and forms a funnel-shaped calyx around each of the renal papillae
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139
Q

What are kidney structural components and how are they linked?

A

Interdependent. Irreversible damage to 1 components will result in impaired function of other components

Vasculature
Glomeruli
Interstitium
Tubules

140
Q

Explain the vasculature of the kidney.

A

Renal arteries branch to interlobular arteries and arch into the arcuate arteries at the corticomedullary junction. These then extend into interlobular arteries (end arteries) in to the cortex.

141
Q

Explain the vasculature of the nephron.

A

Arcuate artery > interlobular artery > afferent glomerular arteriole > glomerular capillaries > efferent glomerular arteriole. Often goes artery to veins but in the kidney is back to arteries

142
Q

If there is a change in the amount of blood being delivered to the glomerulus or passing through the glomerulus, what will happen to the blood flow within the peritubular capillaries surrounding the tubules?

A

Is changed in the same way. Such as glomerular disease causing decreased peritubular capillary perfusion ay result in tubular atrophy of if severe enough will result in necrosis of the tubular cells.

143
Q

Describe the structure of the glomerular filtration barrier.

A
  1. Podocytes – interdigitate and foot processes create filtration slits
  2. Glomerular basement membrane permeable to water and small solutes – is charged and doesn’t allow large molecules
  3. Capillary endothelium is fenestrated – always more fluid to pass through it than most endothelia.
144
Q

Describe the constituents of the ultrafiltrate.

A

The ultrafiltrate from plasma (primary urine) contains water, salts, ions, glucose. It is largely devoid of proteins as the glomerular filtration barrier excludes high molecular weight proteins. Ultrafiltrate (primary urine) flows through the filtration slits into the uriniferous space

145
Q

If injury to the glomerular filtration barrier causes increased permeability, what plasma component is most likely to start to appear in the urine?

A

Proteins. Glomerular disorders often result in proteinuria. However, protein in urine can also originate from other causes and sites within the urinary tract.

146
Q

What are the functions of the nephron tubules?

A
  • Reabsorption of components of the glomerular filtrate - 99% of the water in the glomerular filtrate, requires energy from Na pumps. Active transport may become saturated – glucose reabsorption
  • Excretion of substance – H+ and bicarbonate for acid-base regulation
  • Tubular function, such as reabsorption and excretion, requires close apposition of tubules and peritubular capillaries
147
Q

What is in the renal interstitium?

A

Normally the renal interstitium is relatively sparse – there is little material separating the tubules, blood vessels and renal corpuscle.

148
Q

Pathological changes can result in expansion of the interstitium. Considering various general pathological processes, what could enter or be deposited in the interstitium during these processes to cause expansion of the interstitium?

A

Fluid – oedema, haemorrhage
Cells – inflammatory cells, neoplastic cells
Connective tissue – increased collagen
Other substances – calcium and amyloid

149
Q

What are the routes of entry of aetiological agents to the urinary tract?

A
  • Haematogenous (blood-borne) into the tissues
  • Glomerular filtrate/urine – aetiological agents (infectious agents or toxins) entering the glomerular filtrate or urine as it travels through the urinary tract can then contact the luminal surface of tubules, ureters, bladder or the urethra
  • Some infections may ascend the urinary tract – from externally via the urethral entrance, or from a site of infection within the urinary tract
  • Direct penetrating injury – cystocentesis
150
Q

What are the causes of renal vascular disease?

A
  • Obstruction - embolism, thrombosis
  • Vascular injury and inflammation (vasculitis)
  • Compression of blood vessels
  • Loss of autoregulation of renal perfusion
151
Q

What is the result of renal vascular disease?

A
  • Ischaemia, infarctions, necrosis, atrophy
  • Haemorrhages
  • Inflammation
152
Q

Which infarction locations in the kidney vasculature are most common?

A

Most common – interlobular or smaller vessel infarction. Causes localised infarction of a segment of the cortex

Less common – arcuate or interlobar artery infarction. Causes localised infarction of a segment of the cortex and medulla

Uncommon – renal artery infarction. Causes total or subtotal infarction of the kidney

153
Q

List 2 cardiac diseases that may cause secondary renal infarction.

A
  • Hypertrophic cardiomyopathy in cats with cardiac thrombus formation and thromboembolism (usually sterile)
  • Endocarditis affecting the LHS heart, especially left AV valve or aortic valve
154
Q
A
155
Q

What are 3 causes of renal vascular injury and vasculitis?

A
  • Thromboembolism – sterile or septic
  • Bacteraemia, viraemia
  • Feline infectious peritonitis
156
Q

What is the effect of septic emboli on the kidney?

A

Suppurative/purulent nephritis or abscesses

157
Q

What are 4 infectious agents that could cause renal vascular injury and vasculitis?

A
  • Porcine erysipelas infection with extensive renal haemorrhages
  • African swine fever – the renal capsule has been stripped from the cortex surface revealing multiple cortical haemorrhages
  • Canine herpesvirus infection – in a 2-3 week old puppy with widespread renal cortical haemorrhages, associated with areas of necrosis observed microscopically
  • Feline infectious peritonitis – vasculitis and multifocal pyogranulomatous nephritis
158
Q

What is the result of downstream obstructive disease?

A
  • Impaired urine flow in ureter
  • Increased ureter and renal pelvis pressure
  • Pressure atrophy of renal medullary parenchyma via by compression of the vasculature and dilation of the ureter
  • Atrophy may progress to cortical parenchyma
  • Hydronephrosis and hydroureter is the result
159
Q

Describe the normal autoregulation of renal perfusion.

A
  1. Renal hypotension
  2. Ischaemia
  3. Prostaglandin production (PGE2) in the medulla
  4. Vasodilation of afferent arterioles in juxtamedullary nephrons
  5. Maintains perfusion of inner cortex and medulla
160
Q

What are 3 causes of renal medullary/papillary necrosis/atrophy?

A
  • Compression of the vasculature – urinary obstruction, medullary amyloidosis
  • Loss of autoregulation of renal perfusion
  • Pyelonephritis
161
Q

What are the potential functional effects of glomerular injury?

A
  • Damage to components of the glomerular filtration barrier = proteinuria and protein losing nephropathy
  • Impaired glomerular blood flow = impaired ultrafiltrate formation = impaired peritubular perfusion causing reduced nephron function
  • Severe or persistent injury = glomerular tuft atrophy or sclerosis (glomerulosclerosis) = loss of nephron function
162
Q

What are the causes of glomerular injury?

A
  • Entrapment of thromboemboli
  • Infectious agents
  • Deposition of substances in glomeruli - immune complexes, amyloid
163
Q

What does glomerulonephritis imply?

A

Primary glomerular disease and secondary changes in other components of the nephron (tubulo-interstitial, vasculature)

164
Q

What is the effect of suppurative glomerulitis/embolic nephritis?

A

Bacteraemia with bacteria lodging in glomerular capillaries with/without interstitial capillaries. Causes formation of microabscesses.

165
Q

What are the most common causes of glomerulonephritis?

A

Most common is deposition of immune complexes

Can be associated with some infectious and neoplastic diseases

166
Q

What glomerular pathology may arise due to glomerulonephritis?

A
  • Thickening of glomerular basement membrane
  • Proliferation of glomerular cells (mesangial and/or endothelial)
  • Inflammatory cell infiltrates
167
Q

What are the consequences of glomerulonephritis?

A
  • Damage to glomerular filtration barrier (increased permeability)
  • Proteinuria
  • Interstitial fibrosis
  • Reduced nephron function
168
Q

Why might glomerular disease be difficult to detect grossly?

A

Finely granular appearance of the capsular and cortical surfaces

169
Q

What happens in glomerular amyloidosis?

A
  • May be associated with chronic inflammatory diseases or neoplastic diseases
  • Renal amyloid deposition most commonly affects the glomeruli and can cause progressive proteinuria and renal insufficiency
  • Less commonly amyloid is deposited in the renal medulla, especially in cats and Shar-Pei dogs
170
Q

What are the causes of tubular damage?

A

Nephrotoxins
Ischaemia
Infectious agents

171
Q

What are the possible nephrotoxins that could cause tubular damage?

A
  • Drugs – NSAIDs, aminogycosides, tetracyclins, sulphonamides, cisplatin
  • Oxalates – antifreeze (ethylene glycol)
  • Heavy metals
  • Microorganism/plant toxins – bacterial, fungal, oak, raisins/grapes (dogs), lilies (cats)
  • Pigments – haemoglobin, myoglobin
  • Hypercalcaemia
172
Q

What are the possible tubular epithelial responses to injury?

A

Atrophy
Degeneration
Necrosis/apoptosis
Regeneration

173
Q

What is the histological appearance of necrotic tubular epithelium?

A

Necrotic staining is dark pink

174
Q

What are the functional consequences of acute tubular degeneration and necrosis?

A
  • Intratubular obstruction by sloughed necrotic epithelium
  • Increased tubular permeability allows leakage of filtrate out of tubules
  • Vasoconstriction from tubuloglomerular feedback mechanisms
  • Acute decrease in glomerular filtration rate and renal function > oliguria or anuria (decrease or absence of urine production)
175
Q

What is the pathogenesis of ethylene glycol/antifreeze poisoning?

A
  1. Ethylene glycol ingestion – minimum lethal dose is 1.5ml/kg in cats, 6.6ml/kg in dogs
  2. Most excreted unchanged, some metabolised
  3. Metabolised into nephrotoxic metabolites causing acute tubular injury, other metabolites including lactic acid and oxalate
  4. Oxalate precipitates in tubules and causes tubular obstruction when they crystallise
176
Q

How do tubules regenerate following tubular degeneration and necrosis to restored function?

A
  1. Tubular injury, such as nephrotoxic injury
  2. Degeneration and necrosis of tubular epithelial cells
  3. Sloughing of necrotic epithelial cells, the basement membrane is intact
  4. Early regeneration commences within 3 days of insult
  5. Epithelial regeneration – limited functional capability, polyuria
  6. Maturation of epithelium and restoration of function may take 3-8 weeks
177
Q

How do tubules regenerate following tubular degeneration and necrosis to atrophy?

A
  1. Tubular injury, such as severe ischaemic injury
  2. Degeneration and necrosis of tubular epithelial cells and disruption of the tubular basement membrane (tubulorrhexis)
  3. Sloughing of necrotic cells – activation of macrophages and fibroblasts
  4. Fibrosis and tubular atrophy
178
Q

What is interstitial injury?

A

Often occurs in conjunction with injury to glomeruli tubules (tubulointerstitial nephritis) and vascular components of the kidney

179
Q

What are the causes of interstitial injury?

A

Toxins

Infectious agents – route of entry may be haematogenous, via tubules or ascending infection of the urinary tract

180
Q

Which infectious agents could cause interstitial injury?

A
  • Leptospira
  • Encephalitozoon cuniculi
  • Malignant catarrhal fever
  • Equine infectious anaemia
  • Leishmania
  • FIP
  • Haematogenous (embolic nephritis) or ascending (pyelonephritis) bacterial infections
181
Q

What are some responses to interstitial injury

A

Oedema
Inflammation
Fibrosis

182
Q

What is the post mortem appearance of interstitial nephritis?

A

Pitted, undulated, colour change, can have whiter areas of fibrosis, mottled, browner areas between, some area of the cortex look thinner from atrophy

183
Q

What causes pyelonephritis?

A
  • Bacteria ascend from lower urinary tract infection
  • Predisposing factors include conditions that encourage vesicoureteral reflux of urine from the urinary bladder into the ureters
  • Can resemble infarcts
184
Q

What is characteristic about horse kidneys?

A

Produce mucus in their renal pelvis - do not confuse with pathology

185
Q

What are simple renal cysts?

A
  • Most common in pigs and calves
  • One or more cysts, unilateral or bilateral
  • Usually incidental
186
Q

What is an ectopic ureter? What is the consequence of ectopic ureters?

A

Ectopic ureter emptying into the bladder neck or urethra or other sites (rectum, vagina, etc)

Causes constant urine dribbling and incontinence

187
Q

What does ectopic ureters predispose?

A

Predisposes to ascending infection or obstruction

188
Q

What are the predisposing factors of cystitis?

A
  • Female
  • Local infections - metritis, prostatitis
  • Obstructive urinary diseases/urinary stasis
  • Trauma to the bladder urothelium - catheterisation, urolithiasis
  • Diabetes mellitus (glucose encourages bacterial growth)
189
Q

What is the result of chronic cystitis?

A

Mucosal thickening

190
Q

What is polypoid cystitis?

A

Polyps of fibrous tissue and chronic inflammatory cells

191
Q

What is follicular cystitis?

A

Nodular proliferation of lymphoid tissue. May have concurrent urolithiasis

192
Q

What are the possible renal neoplasias?

A

Epithelial most common – mostly renal carcinomas
Lymphoma
Undifferentiated sarcomas
Fibroma/fibrosarcoms
Haemangioma/haemangiosarcoma
Embryonal tumours (nephroblastoma)

Renal secondary tumours are more common than primary

193
Q

What are the neoplasias that effect that urinary bladder?

A

Epithelial 90%
- Urothelial carcinoma (transitional cell carcinoma) – most common
- Papilloma (may be multiple)

Leiomyoma/Leiomyosarcoma

Rhabdomyosarcoma in young dogs

194
Q

What are the characteristics of transitional cell carcinomas?

A
  • Often at the bladder trigone
  • Invasive and often metastasised by time of clinical diagnosis 40% to local lymph node and lung
195
Q

How is polyuria differentiated from pollakiuria/increased frequency of urination in horses?

A
  • Measure water intake over 24 hours
  • Polydipsia = intake more than 100ml/kg/day (> 50l / 500kg horse)
196
Q

What extra steps to clinical examination are used for horses with urinary issues?

A
  • Rectal to feel the bladder - size, wall thickness, uroliths, masses
  • Rectal to feel caudal pole of left kidney
  • Examine penis – sedate with alpha-2 butorphanol plus ACP
  • Pass the urine catheter if suspect an obstruction
197
Q

What does leukocytosis on haematology from a horse with urinary issues indicate?

A

Inflammation or infection

198
Q

What does anaemia on haematology from a horse with urinary issues indicate?

A

Chronic disease, chronic renal failure (EPO)

199
Q

What is done on urinalysis for a horse with urinary issues?

A
  • If pigmenturia, note timing and duration of passage of discoloured urine
  • Urine specific gravity
  • Reagent strip analysis
  • Sediment analysis
  • (Enzymuria)
  • USG
200
Q

What is normal USG in horses?

A

Isosthenuria (1.008-1.014). Adult normally concentrated, foal dilute

  • Urine that is more dilute than serum = hyposthenuric (< 1.008)
  • Urine more concentrated than serum (> 1.014)
201
Q

What can you diagnose in horses with urinary issues with ultrasonography?

A

Uroliths in kidneys or bladder
Architecture and size of kidneys

202
Q

What is cystoscopy used for in horses with urinary issues?

A
  • Investigate abnormal urination
  • Examine urethra, bladder, watch (can sample) urine coming from ureters (may identify a unilateral renal problem
203
Q

What other tests can be done to investigate horses with urinary issues?

A
  • Water deprivation and anti-diuretic hormone challenge tests
  • Renal biopsy
204
Q

What is patent urachus in foals?

A
  • Urine passes from bladder to allantoic cavity via urachus
  • Normally, urachus closes at time of parturition
  • Congenital patent urachus – failure to close at birth
  • Drip urine from the umbilicus
205
Q

How is patent urachus in foals treated?

A
  • Congenital – prophylactic antibiotics, close with time
  • Acquired – ultrasound to assess infection, investigate and treat sepsis and failure of passive transfer
  • Surgical removal?
206
Q

What are the pre-renal failure causes of acute kidney injury in horses?

A
  • Decreased renal perfusion without associated cell injury
  • From conditions causing decreased cardiac output/increased renal vascular resistance
  • Such as, diarrhoea, endotoxaemia, septic shock, with/without use of NSAIDs in these cases
207
Q

What are the clinical signs of acute kidney injury in horses?

A
  • Often oliguria in adults, anuria in foals
  • Will become polyuric unless significant renal damage where stay oliguric and so retain fluid – get oedema, soft faeces
208
Q

How is acute kidney injury in horses diagnosed?

A
  • Azotaemia
  • Urine specific gravity
  • Casts – show damage
  • Rule in/out prerenal and postrenal causes, if not is intrarenal
  • If intrarenal, ultrasound, biopsy?
209
Q

How is acute kidney injury in horses treated?

A
  • Reverse underlying cause
  • Correct fluid and electrolyte imbalances
  • If insufficient response dopamine infusion to improve renal blood flow
  • Diuretics?
  • Stop aminoglycosides where possible
210
Q

What does prognosis of acute kidney injury in horses depend on?

A
  • Underlying cause
  • Duration
  • Response to treatment
  • Development of complications like thrombophlebitis, laminitis
211
Q

What are the causes of chronic interstitial nephritis in horses?

A

Acute tubular necrosis after ischaemia
Endotoxaemia
Sepsis
Ascending infection
Exposure to nephrotoxic compounds

212
Q

What are the clinical signs of uraemic syndrome from chronic kidney disease in horses?

A

Lethargy (anaemia)
Anorexia
Weight loss
PU/PD
Dental tartar

213
Q

How is chronic kidney disease in horses treated?

A
  • Persistent isosthenuria, azotaemia and clinical signs
  • Urea:Cr > 10:1
  • Often further non-specific abnormalities, such as anaemia
  • If hypercalcaemic think RF
  • May see/feel changes on ultrasonography/rectal
214
Q

How is chronic kidney injury in horses treated?

A
  • Peritoneal/haemo dialysis only for valuable breeding animals
  • Palliative efforts to minimise further loss of renal function, monitor closely to PTS before develop uraemic decompensation
  • Free access to water
  • Palatable diet to encourage appetite and minimise weight loss
215
Q

What is the treatment for urinary tract infections in horses?

A
  • Systemic antibiotics
  • Base on culture and sensitivity
  • Usually TMPS effective (anyway) as get high concentration in urine
  • 1 week usually enough
  • 4-6 weeks if recurrent
216
Q

How is pyelonephritis diagnosed in horses?

A
  • Look for underlying cause
  • Ultrasound
  • Urine and ureteral sample
217
Q

How is pyelonephritis treated in horses?

A
  • Prolonged course appropriate antibiotics
  • Even unilateral nephrectomy
218
Q

Are uroliths more common in males or mares and why?

A

Males (shorter, wider urethra makes it easier for mares to pass small calculi)

219
Q

What are the 2 stages needed for calculus formation for urolithiasis formation in horses?

A

Nucleation of urine crystals
- Supersaturation of urine
- Prolonged urine retention
- Genetic variation in ion excretion rates

Crystal growth – once started to grow around a nidus, equine urine is very alkaline, favouring crystallisation

220
Q

Distinguish type 1 and 2 urolithiasis in horses.

A

Type 1 – more than 90%, yellow, spiculated, easily fragment

Type 2 – grey, smooth

221
Q

When does nephrolithiasis and uterolithiasis lead to acute/chronic renal failure in horses?

A
  • Usually asymptomatic until bilateral obstructive disease leads to ARF/CRF
  • When clinical signs are present they are non-specific associated with uraemia rather than obstructive disease
222
Q

When and how are horses treated for nephrolithiasis and uterolithiasis?

A
  • Most are in CRF by diagnosis so few amenable to treatment
  • Unilateral, nephrectomy
  • Lithotripsy?
223
Q

What are the clinical signs of cystic caliculi in horses?

A
  • Dysuria
  • Haematuria
  • Stranguria
  • Incontinence
  • Especially at/after exercise
224
Q

How are cystic caliculi treated in horses? What are the advantages and disadvantages of each?

A

Laparocystotomy:
- Recovery as for colic surgery
- But low long term complications

Perineal urethrotomy
- Small stones or need to break up
- Standing
- But actually more complications

225
Q

What are the consequences of cystic caliculi in horses when they cause a blockage?

A
  • Colic, ARF (postrenal), risk of rupture
  • Repeated temporary blockage, CRF (postrenal)
  • Perineal urethrotomy
226
Q

How should owners be advised about avoiding recurrence of cystic caliculi?

A
  • Lowish recurrence rate
  • Can’t acidify urine
  • No supplementary electrolytes
  • No alfalfa/lucerne
  • Check for UTI
227
Q

What is pigmenturia in horses?

A
  • Urine may contain an oxidising agent that can cause it to turn red/brown after exposure to shavings/snow
  • Blood, haemoglobin, myoglobin
228
Q

How is pigmenturia in horses diagnosed?

A
  • See red cells under microscope
  • Dipstick can’t differentiate Hb and Mb, there’s a complex test but can tell from history/muscle enzymes
229
Q

What does pigmenturia with myoglobin in horses mean?

A

Myopathy

230
Q

What does pigmenturia with haemoglobin in horses mean?

A

Haemolysis

231
Q

What does pigmenturia with haematuria in horses mean?

A
  • Throughout urination – haemorrhage from kidneys, ureters or bladder
  • Beginning of urination – distal urethra
  • End urination – proximal urethra
232
Q

What are the clinical signs of urethral rents in horses?

A
  • Haemospermia/haematuria
  • Haematuria at end urination
233
Q

How are urethral rents in horses diagnosed and treated?

A

Endoscopy

If > 1 month anaemia, temporary perineal urethotomy

234
Q

What are the causes of PUPD in horses?

A
  • Renal failure (isosthenuria, azotaemia)
  • PPID
  • Primary/pyschogenic polydipsia
  • (Central/nephrogenic diabetes insipidus)
  • (Diabetes mellitus)
235
Q

What are the clinical signs of penile squamous cell carcinomas in horses?

A
  • Malodourous/swollen sheath
  • Haematuria if distal urethra involved
  • Urinary tract obstruction is uncommon unless tumours are large
236
Q

How is penile squamous cell carcinomas in horses treated?

A
  • Local excision
  • Penile resection
  • But high rate recurrence although slow metastasis (inguinal lymph nodes) – penile resection plus urethrostomy
237
Q

What are the clinical signs of urinary incontinence in horses?

A
  • Signs exacerbated by coughing/exercise
  • Similar signs to urolithiasis, which is more common – so investigate for that
238
Q

What are the causes of urinary incontinence in horses?

A
  • Upper motor neuron (incl. EHV myeloencephalitis), lower motor neuron or myogenic disorders
  • Sabulous urolithiasis (bladder full of sediment)
239
Q

How are anti-proteinuric drugs used for severe proteinuria associated with glomerular disease?

A
  • Need to address underlying glomerular disease but also reduce protein loss
  • Glomerular filtration pressure associated with degree of protein loss
240
Q

How can the renin angiotensin system be manipulated to reduce proteinuria?

A
  • Helps maintain arterial blood pressure
  • Affects glomerular filtration pressure
  • Angiotensin II acts preferentially on glomerular efferent arteriole
  • Maintains glomerular filtration rate (GFR) and transcapillary pressure in glomerulus
241
Q

Does angiotensin II act preferentially on the afferent or efferent glomerular arteriole?

A

Efferent

242
Q

What happens if the effect of angiotensin II is blocked?

A
  • Prevents efferent vasoconstriction (effectively vasodilation)
  • Reduces transcapillary pressure in glomerulus
  • Reduces degree of proteinuria
243
Q

How can the renin-angiotensin pathway be influenced at 2 points to reduce proteinuria?

A
  • Angiotensin converting enzyme inhibitors (ACE-i)
  • Angiotensin receptor blockers (ARB)
244
Q

What are the indications for ACE inhibitors?

A
  • Reduce glomerular pressure and proteinuria
  • Reduce afterload and preload in heart failure
  • Mild reduction in blood pressure (systemic hypertension)
245
Q

What are the ACE inhibitors used in veterinary?

A
  • Benazepril (biliary excretion) - Benefortin, Nelio, Fortekor, Benazecare
  • Fortekor plus – with pimobendan (calcium sensitiser)
  • Cardalis – with spironolactone (potassium sparing compared to furosemide)
246
Q

What are the warnings associated with ACE inhibitors?

A
  • Contraindicated in hypovolaemia, hypotensive states, hyponatraemia and acute kidney injury (AKI)
  • Use with care in azotaemic patient, monitor urea and creatinine
247
Q

What are the indications for angiotensin receptor blockers?

A
  • Reduction of proteinuria associated with chronic kidney disease (CKD)
  • Possibly avoids angiotension converting enzyme (ACE) escape
248
Q

Name an angiotensin receptor blocker.

A

Telmisartan (Semintra)

249
Q

What are the warnings for angiotensin receptor blockers?

A
  • Care with hypotensive and hypovolaemic states again
  • Monitor patients with chronic kidney disease
250
Q

Name an ACE inhibitor and an ARB.

A

Benazepril and telmisartan

251
Q

What are the types of urinary tract pharmacology available in veterinary?

A
  • Anti-proteinuric drugs
  • Diuretics
  • Velagliflozin (feline diabetes mellitus)
  • Drugs affecting bladder (detrusor muscle)
  • Drugs affecting urethral sphincter pressure
252
Q

What is Velagliflozin?

A
  • Alternative to insulin injections
  • Sodium-glucose co-transporter 2 (SGLT-2) inhibitor
253
Q

Describe the action of velagliflozin.

A
  • Blocks SGLT-2 in the proximal tubule, thus blocking around 90% of glucose reabsorption
  • Thus reducing glycosuria and associated clinical signs
254
Q

During bladder emptying the detrusor muscle contracts. Which arm of the ANS controls this?

A

Parasympathetic

255
Q

What is bethanechol?

A
  • Parasympathomimetic
  • Promote function of acetyl choline
  • Used in bladder atony
  • Can be enough to void normal enough without manual intervention or catheters
256
Q

What are the cholingeric side effects of bethanechol using DUMBBELS?

A

Diaphoresis/diarrhoea
Urination
Miosis
Bronchospasm
Bradycardia
Emesis
Lacrimation
Salivation

257
Q

Describe the filling stage of urination.

A
  • Storage of urine under sympathetic control:
  • Internal urethral sphincter (smooth muscle) under sympathetic nervous system control
  • Skeletal muscle of the urethra under voluntary control
  • During filling stage, detrusor muscle relaxes and urethral sphincter remains closed
258
Q

Describe micturition phase of urination.

A
  • The Parasympathetic Nervous System results in contraction of bladder smooth muscle (detrusor muscle)
  • During voiding phase, the detrusor muscle contracts and urethral sphincter opens
259
Q

What is USMI?

A
  • Commonest in spayed bitches
  • Decreased urethral closure pressure
  • Typically leak urine when at rest, lying down or asleep
  • Need to improve urethral sphincter tone
260
Q

Which arm of ANS keeps the internal urethral sphincter closed?

A

Sympathetic (S for storage)

261
Q

Name 3 drug classes that can be used to treat USMI.

A

Alpha-adrenergic agonists
Oestrogens
Testosterone in male dog – can try using for male incontinence

262
Q

Name an alpha-adrenergic agonist used to treat USMI.

A

Phenylpropanolamine

263
Q

Describe phenylpropanolamine.

A
  • Sympathomimetic
  • Can cause side effects associated with this
  • Oral syrup formulation
264
Q

How do oestrogens treat USMI?

A
  • Increase responsiveness of adrenergic receptors
  • Side effects associated with hormone
  • Synergistic with α-Ad agonists
265
Q

What is urethral spasm?

A
  • Seen in cats with feline lower urinary tract disease/FLUTD and dogs with reflex dyssynergia
  • No physical obstruction
  • Functional spasm
266
Q

What is the principle of treating urethral spasm?

A

Try to relax both smooth and skeletal muscle

267
Q

Name 2 drugs to relax smooth muscle in urethral spasm.

A

Prazosin - alpha 1 antag, fast onset

Phenoxybenzamine - alpha 1 antag, slower

268
Q

Name 2 drugs to relax skeletal muscle in urethral spasm.

A

Dantrolene
Diazepam

269
Q

What are the adjunctive treatments used for urethral spasm?

A
  • Analgesia
  • Glycosaminoglycans supplements
  • Stress relief (nutraceuticals, feline pheromone analogues)
  • Water intake
270
Q

How do smooth muscle spasmolytics work?

A
  • Alpha-adrenergic antagonists (eg. prazosin)
  • Also act on vascular smooth muscle leading to vasodilation and hypotension
271
Q

How do skeletal muscle spasmolytics work?

A

Dantrolene – uncouples excitation contraction process

Diazepam
- Enhances GABA activity
- Risk of idiosyncratic hepatic necrosis, (cats)
- Very short half-life in dogs

272
Q

What is the presenting complaint of urinary tract problems in bovine?

A

Abnormal appearance of urine
Abnormal passage of urine

273
Q

What are the urine sample collection options in cows?

A

Wait, stimulate vagina and perineum or urinary catheterisation

274
Q

What are the urine sample collection options in bulls?

A

Massage prepuce or wash with warm water, or urinary catheterisation

275
Q

How are urinary catheters placed in cattle?

A

Go in vaginally, urethral opening on the floor of the vestibule, catch the opening, diverticulum ay catch the catheter, handbreadth in

276
Q

Describe urinalysis used in cattle.

A
  • Colour – leave to settle while you do clinical exam
  • Dipstick or lab submission
  • USG = 1.020 – 1.045
  • pH usually alkaline pH 7-8 – do not panic if acidic, may be on acidifying diet
  • Deposits, such as calculi
  • Culture
277
Q

For which pigmenturia will urine clear if left to stand in cattle?

A

If RBC they will clot and settle out, but this is not the case with haematuria and myoglobinuria

278
Q

What are the causes of haemoglobinuria in cattle?

A

Babesia
Brassica toxicity
Post partum haemoglobinuria
Water intoxication
Bacillary haemoglobinuria
Leptospirosis (non hardjo serovars)
Copper poisoning

279
Q

What are the causes of haematuria in cattle?

A

Cystitis
Pyelonephritis
Urolithiasis
Enzootic haematuria (Bracken poisoning)

280
Q

What is the aetiological agent of redwater?

A

Babesia divergens

281
Q

What is the epidemiology of babesia divergens in cattle?

A
  • Tick infested areas
  • Spring to autumn
  • So shouldn’t be seen in housed cows in winter
  • Non-immune animals at greatest risk – age immunity. Though animals less than 2 years of age are unlikely to suffer form clinical disease
282
Q

What is the pathogenesis of babesia divergens in cattle?

A
  • RBC intracellular parasite – so do a blood smear
  • Replication cycles followed by cell rupture
  • Haemolysis, anaemia, icterus and haemoglobinuria
  • Drops in PCV can be sudden and dramatic – below 25 is abnormal
  • Spiking fever
283
Q

What are the acute clinical signs of babesia divergens in cattle?

A
  • Red urine (does not settle)
  • Very marked pyrexia (to 43ºC) – not fit for human consumption if pyrexic so may help with conversation for who to treat
  • Anaemia, tachycardia and tachypnoea – pale mmbs, dull, depressed, standing off from the group, ataxic, possible diarrhoea and rumen stasis
284
Q

What are the subacute clinical signs of babesia divergens in cattle?

A

Transient dullness (immune animals)

285
Q

How is babesia divergens diagnosed in cattle?

A
  • History, clinical signs and location
  • Identification of the parasite on blood smears
  • PCR
286
Q

How is babesia divergens treated in cattle?

A
  • Imidocarb diproprionate/Imizol
  • Oxytetracycline
  • Blood transfusion if PCV < 15%
  • NSAID
287
Q

Describe the action of Imidocarb diproprionate/Imizol in treatment of babesia divergens in cattle.

A
  • Long withdrawals (21 day milk, 213 day meat)
  • Narrow therapeutic margin so accurate weights are essential because of side effects
  • Cholinergic side effects (tachycardia, muscle tremors and drooling) – transient
288
Q

How is babesia divergens controlled in cattle?

A
  • Tick control
  • Preventative use of Imidocarb diproprionate
  • Graze calves (resistant) on affected land to build natural immunity into adulthood
289
Q

Which groups of animals would be at risk of clinical disease due to Babesia?

A

Brought in cows in a herd and putting on marginal grazing

290
Q

What are brassicas?

A

Rape and kale – some farmers use as autumn feed and when digested has a haemolytic factor in the rumen produced. Brassica poisoning – rare but important differential for babesia

291
Q

What is the pathogenesis of brassica poisoning in cattle?

A
  • Toxin converted to haemolytic factor in rumen
  • Hamolysis, icterus, anaemia and haemoglobinuria
292
Q

What are the clinical signs of brassica poisoning in cattle?

A

Peracute – collapse and death

Acute – haemoglobinuria, dullness, weakness and anaemia 1-2 weeks after grazing

Chronic and subclinical forms

293
Q

How is brassica poisoning diagnosed in cattle?

A
  • Clinical signs (non-pyrexic) and history
  • Heinz-body anaemia
294
Q

How is brassica poisoning treated in cattle?

A

Blood transfusion

295
Q

How is brassica poisoning prevented in cattle?

A
  • Strip grazing, strict intakes
  • Buffer feeding
296
Q

What are the causes of stranguria in cattle?

A
  • Vaginitis, cystitis, pyelonephritis
  • Urolithiasis (partial obstruction)
  • Other causes of tenesmus
297
Q

What are the causes of anuria in cattle?

A

Urolithiasis

298
Q

What are the causes of polyuria in cattle?

A
  • End stage pyelonephritis
  • Chronic renal failure
  • Oak poisoning
299
Q

What are the causes of dysuria in cattle?

A
  • Urethritis
  • Vaginitis
  • Cystitis
  • Balanoposthitis
300
Q

What are the causes of oliguria in cattle?

A
  • Pre renal – shock, hypovolaemia, dehydration
  • Renal – acute nephrosis
  • Post-renal – urethral obstruction
301
Q

What are the aetiological agents of cystitis in cattle?

A

Ascending infection of C.renale, E,coli, proteus valgaris

302
Q

What are signs of straining to urinate in cattle?

A

Arching back, tail raised, squatting position

303
Q

What is the incidence of cystitis in cattle?

A
  • Mostly sporadic
  • Often post-partum
  • May be association with pyelonephritis
  • Females > male
304
Q

What are the clinical signs of cystitis in cattle?

A
  • Haematuria with/without pyuria
  • Stranguria and dysuria
  • Mild pyrexia
  • Pain on urinating
  • Arching of back
  • Weight loss
  • Possible bladder thickening per rectum
305
Q

How is cystitis in cattle treated?

A
  • Antibiotics
  • NSAIDs
  • Encourage water intake
306
Q

What antibiotic would be appropriate for the treatment of cystitis in cattle?

A

Mixed infection – amoxicillin

307
Q

What NSAID would be appropriate for the treatment of cystitis in cattle?

A

Meloxicam

308
Q

What is the aetiological agent causing polynephritis in cattle?

A

Corynebacterium renale ascending infection

309
Q

What is the epidemiology of polynephritis in cattle?

A
  • Contagious, sporadic disease of cows
  • Venereal spread, requires a male for spread
310
Q

What are the clinical signs of polynephritis in cattle?

A
  • Weight loss and reduced milk yield over weeks
  • Stranguria, haematuria and pyuria
  • Frequent painful urination
  • Arched back
  • Intermittent pyrexia
  • Fluctuating appetite
311
Q

How polynephritis diagnosed from rectal examination in cattle?

A
  • Kidneys becomes grossly enlarged with a loss of lobulation – only left is palpable
  • Ureters thickened and calcified
  • Bladder all and mucosa thickened
312
Q

How polynephritis diagnosed from urinalysis in cattle?

A
  • Dipstick – blood, protein +++, pH 8-9
  • Smear – bacteria, WBC, epithelial cells
  • Culture
313
Q

How is polynephritis treated in cattle?

A
  • Prognosis guarded, depends on duration of infection
  • High doses of procaine penicillin BID for 10-14 days
314
Q

How is polynephritis prevented in cattle?

A
  • Isolate affected cattle
  • Hygiene at calving/AI
  • Consider the possibility of carrier bull
315
Q

What antibiotic is cleared by the kidney and appropriate for a gram +ve organism e.g. Corynebacterium renale?

A

Penicillin

316
Q

What is the aetiology of urolithiasis in cattle?

A
  • Calculi – small stones of Ca or Mg ammonium phosphate, form in bladder
  • Obstruction of the urethra at sigmoid flexure (bulls) or vermiform appendage (rams)
317
Q

What are the risk factors for urolithiasis in cattle?

A
  • Often pet animals that have been castrated and are being fed inappropriately
  • Castrated males
  • Excessive body condition
  • Calves on milk substitute
  • High levels of concentrates
318
Q

What are the clinical signs of urolithiasis in cattle?

A
  • Stranguria, oliguria, anuria
  • Mild to severe colic, paddling hind limbs
  • Calculi on preputial hair
  • With/without bladder rupture, uroperitoneum and abdominal distension
  • With/without urethral rupture and sloughing of subcutaneous tissues
319
Q

How is urolithiasis diagnosed in cattle?

A

Clinical signs

Rectal exam
- Pulsations of urethra in ischial arch region
- Distended bladder (unless ruptured)

320
Q

How is urolithiasis in cattle treated medically?

A
  • Butyscopolamine (Buscopan) to relieve smooth muscle spasm
  • Urethral catheterisation with/without retrograde hydropulsion
  • Intravenous fluid therapy – diuresis, management of azotaemia
321
Q

How is urolithiasis treated in rams?

A

Remove vermiform appendage

322
Q

How is urolithiasis treated surgically in cattle?

A

Sub-ischial urethrostomy

323
Q

How is urolithiasis in cattle prevented?

A
  • Ensure correct Ca: P ratio in diet
  • Avoid excessive dietary magnesium in milk-fed calves
  • Manage body condition – especially in old castrated males
  • Oral ammonium chloride to aid crystal dissolution
  • Ensure free access to drinking water
324
Q

What is the aetiology of bladder paralysis in cattle?

A
  • Dystocia, intrapelvic sacral nerve injury
  • Crushing of sacrum and tail head, vertebral damage
325
Q

What are the clinical signs of bladder paralysis in cattle?

A
  • Dribbling urine
  • Voiding small amounts
  • Urine scalding
326
Q

Distinguish uroliths and crystals.

A

Urolith – urinary stone, macroscopic. Organised crystal aggregates of minerals in small amounts of organic matrix

Crystal – microscopic mineral precipitate

Crystalluria and uroliths may happens separately or together, not necessarily the same constituents.

327
Q

What promotes crystal formation?

A
  • Concentration of a compound in the urine
  • USG
  • Urine pH
  • Urine stasis
328
Q

How do uroliths form?

A

Uroliths may form homogenously/pure or heterogeneously – less supersaturating is required to promote heterogeneously

329
Q

What happens are urine saturation concentration with a given compound increases?

A

Urine subsaturated with no crystals > solubility product, urine saturated with a compound > urine supersaturated > formation product, crystals form > urolith formation can occur

330
Q

When do uroliths require treatment?

A
  • Local inflammation
  • Secondary infections
  • Obstructions
331
Q

When may uroliths not require treatment?

A

Asymptomatic non-dissolvable uroliths without obstruction risk

332
Q

What can cause ureteroliths and cystoliths?

A

Urethroliths cause obstructions and unproductive urination

Cystoliths cause cystitis signs with/without bacterial cystitis

333
Q

What are the clinical signs of nephroliths?

A
  • Abdominal pain, anorexia/inappetence, lethargy
  • With/without pyelonephritis
  • May also be asymptomatic
334
Q

How may ureteroliths present?

A

May present like AKI or CKD, so image every patient with a renal/post-renal azotaemia

335
Q

What are the treatment options urethal uroliths causing obstruction?

A

Retropulsion of stone into the bladder, much easier to remove stone from the bladder so we can then remove from the bladder if necessary

Urethrotomy is absolute last resort and rarely needed, seek referral/advice if retropulsion not possible, often get stricture at this site

336
Q

What are the treatment options ureteral uroliths causing obstruction?

A

Intervention/bypass at referral, artificial silicon ureter

337
Q

How are cystoliths not causing obstruction addressed?

A
  • Amenable to dissolution – medial therapy
  • Not amenable to dissolution – cystotomy vs. minimally invasive techniques e.g. voiding urohydropulsion/laser lithotripsy
338
Q

How are nephroliths not causing obstruction addressed?

A
  • Dissolution of nephroliths is possible
  • If symptomatic and dissolution not possible – seek referral
339
Q

For a stone in situ, what 3 things are used to determine its composition?

A

Radiographic appearance, urine pH and crystals in the urine.

340
Q

Describe the radiolucency of stones.

A

Moderately-markedly radiopaque = calcium oxalate, struvite

Moderately radiolucent = urate

341
Q

When can stones in situ be visualised on radiographs?

A
  • Uroliths need to be >2-3mm to visualise on radiographs
  • Plain – radiopaque uroliths
  • Contrast/double contrast – radiolucent uroliths
342
Q

How can stones in situ be visualised on ultrasonography?

A
  • Can visualise radio-opaque and radio-lucent uroliths
  • Useful for evaluating renal pelvic dilation – used as an indicator of ureteric obstruction
343
Q

How is urinalysis used to determine the composition of a stone in situ?

A
  • USG – concentrated urine
  • pH – may guide likely stone type
  • Protein – often increased, urothelial inflammation
  • Blood? Inflammatory cells? Direct urothelial inflammation from urolith with/without concurrent urinary infection
  • Sediment exam – crystalluria? Analyse fresh, may not be concordant with the urolith
  • Culture
344
Q

Describe the pH of uroliths.

A

Acidic pH = urate
Acidic to neutral pH = calcium oxalate
Alkaline pH = struvite

345
Q

What are the general principles of urolith management?

A
  • Dilute urine = supersaturation not possible. Increase water intake, target USG
  • Encourage voiding
  • Avoid obesity
  • Specific management will depend upon stone type
346
Q

What are the uroliths that are most common in dogs?

A
  • Struvite most common – infection associated
  • Calcium oxalate
  • Urate
  • Cystoliths (bladder) and urethroliths (urethra) most common sites
347
Q

What are the uroliths that are most common in cats?

A
  • Struvite most common – calcium oxalate most common in upper urinary tract
  • Increased incidence of ureteroliths and nephroliths. Therefore may present as AKI with/without CKD

CVSOH 4 (25 decks)

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