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ACVIM Specialty: Ettinger - MS 2023 > Renal > Flashcards

Renal Flashcards

1
Q

Outline the 7 areas to evaluate when trying to distinguish between acute and chronic kidney disease and outline the more advanced methods further.

A
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2
Q

What level of creatinine in abdominal fluid indicates urinary tract rupture?

A

> 2x that of serum

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3
Q

IRIS staging of CKD in dogs and cats.

A

n.b. main difference is for stage 2 (>125mml/L dog, >140mmol/L cat). Otherwise values are essentialy the same

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4
Q

Outline the IRIS AKI Grading criteria

A
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5
Q

Normal GFR values for dog and cat

A
  • Dog: 3.5-4.5ml/min/kg
  • Cat: 2.5-3.4ml/min/kg
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6
Q

4 characteristics for makers that are required to allow GFR measurement

A
  1. Freely filtered at the glomerulus
  2. Not circulate bound to plasma proteins
  3. Not undergo resorption or secretion by renal tubules
  4. Must not alter GFR or cause renal toxicity
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7
Q

What is the definition of urinary clearance vs. plasma clearance?

A

Renal = The rate at which a filtered substance is cleared from a given volume of plasma by the kidneys into the urine. It can be expressed as the amount of substance in the urine appearing per a unit of time.

Plasma = he rate at which a substance is cleared from a given volume of plasma per unit time.

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8
Q

Which feline breed has a higher creatinine?

A

Birmans, n.b. that kittens have a higher creatinine than adults until about 8 weeks of age

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9
Q

What is the role of cystatin C in evaluating GFR?

A

Cystatin C should be reabsorped by the proximal tubules so if elevated concentrations are found in the urine this could be a marker of tubular injury. However, clinical studies in dogs and cats have not been overly promising.

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10
Q

What is the predominant urine protein detected on the dipstick?

A

Albumin

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11
Q

What is the lower limit of detection for a urine protein dipstick?

A

30mg/dL albumin

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12
Q

What are the factors that can lead to false negatives on the urine dipstick vs. false positives?

A
  • False negatives with:
    • Bence-jones proteinuria
    • Dilute urine
    • Acidic urine
  • False positivies with
    • Haematuria
    • Pyuria
    • Concentrated urine
    • Alkaline urine
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13
Q

What is the clinical definition of microalbuminuria?

A

albuin >1mg/dL but <30mg/dL

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14
Q

What are the ‘normal’ limits of UPC in dogs vs. cats and what do these values indicate?

A

Cat > 0.4
Dog >0.5
These indicate a urine albumin of >30mg/dL.
Values ≥0.2 indicate microalbuminuria

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15
Q

How many samples need to be taken to consider UPC abdnormal?

A

≥3 samples taken ≥2 weeks apare

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16
Q

What are the 6 factors that can affect UPC measurement and their actual impact on measurements

A
  • Sample method
    • No difference between cysto, midstream or free-catch
  • Environment
    • Higher in hospital vs. home
  • Haematuria
    • Only gross haematuria (>250 RBC/HPF)
  • Pyuria
    • Minimal
  • Bacturia
    • Minimal as ‘post-renal’ proteinuria is really a result of leakage of proteins from the blood from the inflammation in response to bacteria
  • Day-today variability
    • Can be very high particulary in patients that are markedly proteinuric
    • If UPC <4.0 then day-to-day variability is likely less important
    • If UPC >4.0 then a pooled urine sample is likely to be a good idea
      • Equivolume of urine over 3 measurements
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17
Q

Wat degree of proteinuria should prompt consideration for a renal biopsy

A

UPC >3.5 that is persistent

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18
Q

How long should anti-thrombotic therapy be discontinued prior to renal biopsy?

A

72h

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19
Q

What sample medium should be used when collecting a renal biopsy?

A
  • Post-biopsy handling
    • Put into physiological saline
    • Divide samples:
      • Light microscopy (formalin fixed)
      • Transmission electron microscopy (TEM, gluteraldehyde)
      • Immunoflourescence (Michel’s medium)
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20
Q

What light microscopy stains should be applied to identify the following in renal biopsy specimens:
a) General tissue architechture
b) Collagen
c) Junctions between compartments
d) Glomerular basement membrane to evaluate for immune complex deposition
e) Amyloid

A

a) H&E
b) Masson’s trichrome
c) PAS
d) Jones metanamine silver
e) Congo red

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21
Q

Which IFA markers should be evaluated on a renal biopsy (6)?

A

IgG
IgA
IgM
C1q
C3
Lamda and kappa light chains

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22
Q

What are the main risk factors for the development of complications during/following renal biopsy

A

<5kg size
Severe azotaemia (Cr. >442mmol/L)
Haemostatic disorders

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23
Q

What are the components of nephrotic syndrome

A
  • Proteinuria
  • Hypoalbuminaemia
  • Hypercholesterolaemia
  • Peripheral oedema or cavitary effusion
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24
Q

What endogenous (2) and exogenous (3) factors can impact on USG and approximate increases with these

A
  • Severe proteinura
    • 1g per dL increases USG by 0.003 - 0.005
  • Severe glycosuria
    • 1g per dL increases USG by 0.004 - 0.005 (urine dipstick is about 100mg per increment so only 0.1g => very little effect)
  • Colloids
  • Manitol
  • Iohexol
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25
Q

Which antibiotic classess can cause false positives on urine dipstic measurements?

A

Fluroquinolones (part. ciprofloxacin) (glucose oxidase methods)
Penicillins and cephalosporins (copper sulfate methods)

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26
Q

Equation for calculation of FE of electrolytes

A
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27
Q

What is the distribution of uinary epithelial cells in the urinary tract

A

Squamous = urethra or vagina
Transitional = all the way from the renal pelvis to the urethra

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28
Q

What does this picture indicate?

A

Granular cast

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29
Q

What does this picture indicate?

A

Waxy cast - later stage of granular cast

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30
Q

What ketones are detected on the urine dipstick?

A

Acetone and acetoacetic acid (NOT BHB)

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31
Q

What can cause ketonuria in animals, other than DKA

A

Prolonged fasting
Low carbohydrate diet in cats

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32
Q

What is a relatively specific feature of renal lymphoma on ultrasonography?

A

Hypoechoic subcapsular thickening, this can mimic peri-renal fluid

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33
Q

What are perinephric pseudocyts and with what disease are they associated?

A

Fluid filled sacs without an epithelial lining (as would be the case for a true cyst). They are associated with CKD in cats.

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34
Q

Most common nephrotoxins in dogs vs. cats

A

Dogs: Ethylene glycol, NSAIDS, Cholecalciferol, aminoglycosides
Cats: Ethylene glycol, cholecalciferol, lillies

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35
Q

What are the four phases of AKI?

A
  1. Initiation
  2. Extension - hypoxia and inflammation promote ATP depletion, impairement of NA/KATPase and cellular swelling
  3. Maintenance
  4. Recovery
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36
Q

How can FE sodium help in determining the cause of an AKI

A

FE <1% indicates a pre-renal component only as in this scenario the body is trying to conserve sodium and water.

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37
Q

Which antibiotics are directly nephrotoxic?

A

Aminoglycosides
Expired tratracyclines - causes a fanconi-like syndrome
Sulfonamides - intra-tubular crystal formation

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38
Q

What is the mechansm of action of fendolopam?

A

It is a D1 agonist. D1 agonism will dilate renal arteries and therefore increase renal blood flow, theoretically, inhibit ANG II and ADH. It does not have any D2 or adrenergic effects

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39
Q

What is the amount of insensible loss from the respiratory tract in dogs?

A

22ml/kg/d

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40
Q

Outline how to approach fluid therapy for a patient with AKI. Include how you would approach the oliguric or anuric scenario

A
  1. Assess and correct hypovolaemia within the first 6 hours
  2. Rehydrate the animal using nomal calculation
    - Subtract any fluid boluses from 1
    - If not clinically dehydrated and not overydrated then assume a 5% dehydration rate
  3. Once hypovolaemia and hydration have been corrected then use ins and outs:
    - 1. Add 22ml/kg/d for insensible losses
    - 2. Add in urinary losses
    - 3. Add in any ongoing losses
    Anuric patients: only administer insensible losses
    Overhydrated patients: withold fluids until euvolaemic
    Overhydrated anuric/oliguric patients should ideally have dialysis
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41
Q

When to use frusemide in AKI?

A

Only if there are clinical signs of volume overload as it has actually been associated with worse outcome.s

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42
Q

What is the lower end of blood pressure that is tolerable for renal autoregulation?

A

60 - 80 MAP or 80 - 100mmHg systolic

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43
Q

What are the definitions of oliguria?

A

In a well hydrated pet <1ml/kg/h is relative oliguria and 1 - 2 ml/kg/h would be considered relative oliguria in a patient receiving aggressive fluid therapy.

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44
Q

Antidotes for ethylene glycol toxicity?

A

4-methylpyrazole or ethanol given within 8 hours of exposure

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45
Q

Aminoglycoside antidotes

A

Tircacillin
Cabenicillin

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46
Q

What hypothesis is applicable to the progression of CKD in dogs and cats?

A

The trade off hypothesis

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47
Q

What canine breeds MAY CKD be more likely in?

A

Cocker spaniels and CKCS

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48
Q

Compare and contrast the differences in primary histopathologic findings in CKD between dogs and cats

A

Chronic tubulointerstitial nephritis is the most common in both dogs and cats and the second most common is glomerulonephropathy with an increased prevalence in dogs. The third most common cause in dogs is amyloidosis and lymphoma in cats.

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49
Q

Compare and contrast negative prognostic factors for CKD in dogs vs. cats

A

Factors in both:
- IRIS Stage
- Proteinuria

Dogs only:
- Feeding a renal diet
- Hypertension
- Decreased BCS

Cats only:
- Serum phosphorus
- Anaemia

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50
Q

Which species is uraemic gastropathy more common in?

A

Dogs

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51
Q

Explain the pathophysiology of renal secondary hyperparathyroidism

A
  1. PO4 is increased due to declining GFR –> increased PTH
  2. FGF23 increases in response to increased phosphorus –> inhibition of 1-alpha hydroxylase leading to reduced vitamin D –> increased PTH
  3. Uraemia also inhibits calcitriols negative feedback on the parathyroid gland
  4. Net result is a reduced resorption of calcium from the gastrointestinal tract
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52
Q

What alterations in CKD may predispose to a metabolic acidosis?

A

Decreased ability of renal tubular cells to synthesise ammonia (from glutamine)
Decreased ability to secrete hydrogen ions
Decreased excretion of phosphate buffers

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53
Q

In addition to RSHP what mechanisms may reduce total calcium in CKD?

A

Increased inorganic ions such as citrate, phosphate and sulfates may occur in the blood

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54
Q

Targets for phosphate restriction in CKD

A
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55
Q

How long after starting a phosphate restricted diet or phosphate binder can serum phosphate be re-evaluated?

A

4 - 6 weeks after a change

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56
Q

What are the four agents that can bind dietary phosphates, their risks and administration considerations, if applicable.

A

Aluminium hydroxide - risks of neuromuscular toxicity and microcytosis
Calcium containing - likely to increase calcium, do not give alongside calcitriol
Lanthanum - few side effects
Sevalamer - can cause metabolic acidosis and hypercalcaemia (from the acidosis maybe?)

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57
Q

Treatment for metabolic acidosis due to CKD?

A

Renal diet
Potassium citrate
Sodium HCO3

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58
Q

What percetage of CKD dogs and cats treated with EPO will develop EPO antibodies?

A

25 - 30% cats and 50% dogs

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59
Q

When can the use of calcitriol therapy be considered and what conditions apply to its use?

A

Theory - it may reduce PTH levels (although this has not been proven to be prognostic)
There is no evidence for its use in cats
There is some evidence to suggest its use in dogs in stage ≥III CKD with evidence fo improved mortality
Do not use if there are alterations in serum phosphorus or calcium as it will lead to absorption of BOTH of these in the GIT.

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60
Q

What is the most important determinant of passage of substances across the glomerulus?

A

Size - 60 - 70kDa is the upper limit
Other factor is charge selectivity (negative charges are resisted by the BM)

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61
Q

Which breeds of dog seem to be predisposed to glomerular disease in general?

A

Labradors and golden retrievers

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62
Q

What combination of azotaemia and concentrating ability of the urine is a hallmark of glomerular disease?

A

Renal azotaemia with intact concentrating ability is suggestive of glomerular disease (as if you think about it the glomerulus has nothing to do with concentrating ability).

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63
Q

What are the four components of nephrotic syndrome

A

Hypoalbuminaemia
Proteinuria
Hypercholesterolaemia
Oedema formation

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64
Q

Outline the classification of glomerular diseases in dogs/cats

A

Main categories:
- Glomerulosclerosis (incl. FSGS and Global)
- Immune complex glomerulonephritis (membranous, membranoproliferative, lupus, proliferative, cresentric, IgA)
- Amyloidosis
- Hereditary nephritis
- Mimimal change glomerulopathy

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65
Q

What are the most common forms of glomerular disease?

A

ICGN (around 50% cases historically), glomeruloschlerosis and amyloiodosis

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66
Q

What glomerular disease is associated with lyme borreliosis?

A

Membranoproliferative glomerulonephritis

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67
Q

What findings suggest a primary vs. secondary ICGN?

A

Complement and Ig binding to the endothelial side is more suggestive of a secondary disease process wheras binding on the urinary side may suggest more of a primary process (e.g. membranous nephritis)

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68
Q

Which ICGN seems to be more of a primary disease?

A

Membranous nephritis - this is the most common glomerular disease in cats and often presents with quite severe proteinuria.

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69
Q

Compare and contrast the renal biopsy findings that may be found in MPGN, MN, proliferative nephritis and IgA nephropathy?

A

MPGN - predominance of immune stuff on the endothelial side. Capillaries are thickened and the mesangium is hypercellular

MN - subepithelial immune complex deposition.

Proliferative - immune complexes found in most places and there is generalised proliferation of the mesangium and capillaries

IgA - predominance of IgA reactivity with lower positivity of other immune complexes.

70
Q

What is the pathomechanism of hereditrary nephritis?

A

This is characterised by a defect in the GBM collagen type IV

71
Q

What is the histologic findings that indicated minimal change disease?

A

Effacement of podocyte foot processes

72
Q

which of FGSC and GS are the end stage of a glomerular insult vs. a potentially primary glomerular disease?

A

GS is end-stage
FSGS is considered a primary glomerulopathy

73
Q

Which breed is predisposed to MPGN?

A

Burnese moutain dogs
Labradors and GR that have lyme disease

74
Q

What percentage of Shar-Pei’s have glomerular amyloidosis and what percentage are proteinuric?

A

64% have glomerular involvment. 25 - 43% are proteinuric (as it predominanly affects the medulla)

75
Q

Outline the pathogenesis of renal amyloidosis

A

SAA is produced in hepatocytes due to macrophage-derived cytokines. (e.g. Il-6 in Shar=Pei).

76
Q

At what stage of disease in renal amyloidosis may colchicine still be effective?

A

When there is no azotaemia or hypoalbuminaemia it can still result in reversal of proteinuria

77
Q

What percentage of Shar-Pei’s will develop renal amyloidosis?

A

23%

78
Q

Which breed is predisposed to fanconi syndrome?

A

Basenji’s

79
Q

What drugs/disorders has aquired fanconi syndrome been associated with?

A

Gentamycin
Primary hypoparathyroidism
Chicken Jerkey treats
Chlorambucil

80
Q

What is the cause of proximal (type II) RTA?

A

Deficiency in the basolateral Na/HCO3 exchanger

81
Q

Gene responsible for cystinuria in:
a) Newfoundland, Labrador and Australian Cattle dogs
b) Miniature pinchner

A

a) Slc3A1
b) Slc7a9

Just putting that Dalmations urate issue is Slc2A9 here as I always get confused between these.

82
Q

What is the mechanism of action of 2-MPG?

A

Tiopronin - this forms cystine-thiol compound rather than a cystine-cystine compound increasing the solubility of cystine to allow excretion.

83
Q

What alternative drug to tiopronin can be used in cystinuria?

A

D-penicillamine

84
Q

What breeds are bredisposed to hyperuricosuria?

A

Dalmations
English bull terrier
Russian Terrier

85
Q

What is the genetic mutation responsible for hyperuricosuria?

A

SLC2A9

86
Q

What is the Gonto protocol?

A

This is a facebook thing that aims to reverse the hyperchloraemic metabolic acidosis that can occur with Fanconi syndrome and is often pushed by Basenji groups, however there is no evidence for its eficacy.

87
Q

How can proximal and distal renal tubular acidosis be distinguished?

A

Proximal - hyperchloraemic acidosis with an acidic pH, HCO3 therapy can be used but requires more than distal RTA and FE of HCO3 will be increased (>15%). You may also see other proximal tubular defects or damage on UA/bloods. Ammonium chloride administration will remain acidic.
Distal - hyperchloraemic metabolic acidosis with an alkaline pH, alkali therapy is more effective and FE of HCO3 is <15%. Ammonium chloride administration urine will remain alkaline.

88
Q

What light microscopy findings are suggestive of renal dysplasia

A

The demonstration of immature renal structures which may be accompanied by the presence of hyperplastic normal nephrons and secondary changes such as intestitial nephritis

89
Q

What is the mode of inheritance of hereditary nephritis in the following breeds?
a) Samoyed
b) English Cocker Spaniel
c) Bull Terriers and Dalmatians

A

a) X - linked SNP in COL4A5 gene
b) Autosomal recesive trait associated with a SNP in COL4A5
c) Autosomal dominant trait

90
Q

What is the clinical course of hereditary nephritis in Samoyeds?

A

In males it is usually rapidly progressive with death occuring within 1 year. Females have a more prolonged clinical course

91
Q

In which breeds is hereditary nephritis more rapidly progressive vs. less rapidly progressive?

A

More rapid in Samoyeds (particularly males), English Cocker Spaniels and is slower in Bull terriers and dalmatians

92
Q

Which breeds of hereditary nephritis can IHC be used to diagnose the condition?

A

This can be used in Samoyeds (probably english cocker spaniels) but NOT bull terriers and dalmatians

93
Q

What genetic renal disease do soft-coated wheaten terriers get and what is the genetic basis?

A

Podocytopathy and glomerulosclerosis
Complex inheritance pattern associated with NPHS1 and KIRREL2 gene

94
Q

What canine brreds are predisposed to PKD? What is the genetic basis

A

Bull Terriers, WHWT and Cairn Terriers
Bull Terriers have an autosomal dominant mutation in PKD1 gene

95
Q

What is genetic basis for PKD in cats?

A

Exon 29 in the PDK1 gene

96
Q

What is telangiectaia and in what breed has this been reported?

A

It results in periodic gross haematuria and has been described in the Welsh Corgi

97
Q

What breed has reflux nephropathy been described in?

A

Boxers

98
Q

What is the genetic basis for cystadenocarcinoma in GSD?

A

Autosomal dominant with BHD gene mutation

99
Q

What calcium-phosphate ratio increases the risk of soft tissue mineralisation?

A

CaPO above 70mg2/dL2 = >5.6mmol/L is the value that likely increases the risk of soft tissue mineralisation.

100
Q

Normal ureteral diameters in the dog and cat

A

Dog ≤2.7mm
Cat 0.3 -0.4mm

101
Q

What is the role of the following receptors in the ureter?
a) alpha 1
b) alpha2
c) beta
d) Cholinergic

A

a & b stimulate contration of the ureter and alpha 1 fibres predominate
c) relaxes
d) relaxes

102
Q

Why is dissolution of a ureteric stone not appropriate even if struvite is suspected?

A

Because the stone will not be continuously bathed by urine therefore eliminating the infection is troublesome.

103
Q

Why is shock-wave lithotripsy not useful in cats with ureteric obstruction?

A

Cats kidneys are more prone to damage from the shockwaves
The shockwaves will create fragments but given that these can stll be 1 - 2mm in size, these will still not pass down the ureter.

104
Q

What is the most common reason for formation of a vaginoureteral fistula?

A

Accidental ligation of the ureter to the vaginal stump

105
Q

Differences between UTI prevalence/types in dogs and cats?

A

Dogs: > 60% are gram negative infections with the majority being E. coli
Cats: 50:50 between gram negative and gram positive. Most common is E. coli followed by Enterococcus spp.

106
Q

What are the factors to consider when trying to predict urinary stone compostion?

A
  • Radiogarphic appearance
  • Stone prevalence
  • Signalment
  • Urine pH
    (sediment)
107
Q
A

Calcium oxalate monohydrate crystal

108
Q

Calcium oxalate monohydrate crystal

A
109
Q
A

Calcium oxalate dihydrate crystal

110
Q

Calcium oxalate dihydrate crystal

A
111
Q

Radiographic appearance of calcium oxalate monohydrate vs. dihydrate

A

Monohydrate tend to be small round-to-bosselated. Whereas dihydrate can have a star/rosette shaped appearance (see picture)

112
Q
A

Calcium carbonate crystal

113
Q

Calcium carbonate crystal

A
114
Q

Struvite crystals

A
115
Q
A

Struvite crystals

116
Q
A

Urate crystals

117
Q

Urate crystals

A
118
Q

What stone is this likely to be?

A

Urate

119
Q
A

Cystine crystals

120
Q

Cystine crystals

A
121
Q
A

Silica crystals

122
Q

Silica crystals

A
123
Q

What is the recurrance rate of CaOx crystals?

A

50% recurrance within 2 years

124
Q

Treatment/prevention of CaOx

A
  1. USG < 1.020
  2. Avoid urinary acidification
    • Consider potassium citrate
  3. Hydrochlorathiazie
125
Q

Which diets are suitable for CaOx prevention, which ones acify?

A

Hills u/d (only one that alkalanises the urine)
Hills w/d
Hills c/d multicare
RC SO

126
Q

Diets suitable for struvite prevention?

A

Hills c/d multicare
Royal canin SO

127
Q

What urine pH do urate stones form in?

A

Acidic urine

128
Q

What is the maximum size of stone that is amenable to voiding retrohydropropulsion?

A

<4mm stones, female animls only

129
Q

What are the most common compound uroliths?

A
  1. Calcium oxalate inner with outer struvite (CaOcx the primary stone with ifection resulting in struvite)
  2. Inner struvite with outer calcium phosphate carbonate (infection associated)
130
Q

Purine synthesis pathway

A
131
Q

Which feline breeds are urate stones most frequenty found in?

A

Egyptian mau (82%)
Birman (27%)
Siaese (13%)

132
Q

Outline the nervous control of the bladder

A

The hypogastric nerve provides sympathetic innervation to the detrusor muscle (beta) and to the internal ureathral sphincter (beta3 - inhibitory and alpha1 - stimulatory).

The pelvic nerve provides muscarinic inntevation to the detrusor muscle which allows the bladder to contract.

Somatic innervation is provide through nicotinic receptors which affect the external urethral sphincter.

133
Q

What is the efferent stimulation for urinary voiding?

A

Parasymathetic stimulation due to bladder wall stretch travels via the pelvic nerve up to the pontine micturition centre. Voluntary inputs from the cortex will then allow or refute voiding.

134
Q

What are the main disorders of storage of urine (i.e. will result in incontinance)?

A

USMI
LMN bladder
Detrusor hyperreflexia

135
Q

What conditions predispose to USMI signs?

A

Short urethra
Pelvic bladder
Recesserd vulva

136
Q

How would a dog with USMI present in contrast to a behavioural cause of ‘incontinance’ or reflex dysnergia?

A

USMI is associated with unconcious incontinance. In male dogs the bladder should be empty following voiding otherwise dysnergia remains a differential.

137
Q

What is the effect of estrogens in USMI?

A

Oestrogens promote the expression of alpha receptors in the internal urethral sphincter.

138
Q

What is the response rate of male dogs vs. female dogs to PPA with USMI?

A

Females response in 75 - 90% cases wherase in males response rates of more like 43% are noted. Neutered males may benefit from testosterone cyprionate.

139
Q

What drug can be used to help with LMN bladders?

A

Bethanacol - this is a parasympatheticomimetic so can help with urine voiding.

140
Q

What medical options are there for the management of detrusor hyperreflexia?

A

Oxybutynin and imipramine

Oxybutynin is an antispasmodic with anti-muscarinic effects
Imipramine is a TCA

141
Q

What are the main disorders of abnormal bladder emptying?

A

Detrusor atony
Detrusor urethral dyssenergy
Dysautonomia

142
Q

What are the treatment options for detrusor atony?

A

Keeping the bladder empty for several weeks

Bethanacol

143
Q

Which breed is predisposed to BPH?

A

Scottish terriers

144
Q

What are the main hormones involved in the development of BPH?

A

DHT - promoted growth of glandular and ductal cells

Estradiol (17 beta) = causes cellular metaplasia

n.b. metaplasia = the replacement of one differentiated somatic cell for another in tissue

145
Q

What medical treatment is most appropriate for dogs with BPH that you want to keep fertile?

A

Finasteride - this is 5a reductase inhibitor which prevents the conversion of testosterone to DHT. Therefore it will reduce prostatic size without affecting fertility or behaviour.

146
Q

Most common bacteria implicated in bacterial prostatitis

A

E. coli, staphylococcus, klebsiella, proteus……

147
Q

Clinical presentation of acute bacterial prostatitis

A

Usualy systemically unwell with caudal abdominal pain, stranguria may be in the history and they may also have a stiff or stilted hindlimb gait.

148
Q

Why should castration be avoided in the acute stages of acute bacterial prostatitis?

A

It can result in scirrhous spermatic cord happening

149
Q

What are the treament options for a prostatic abscess?

A
  • AUS guided drainage or surgical drainage and omentalisation
  • Treatment with antimicrobials
  • Castration or other medical therapies to reduce prostatic size
150
Q

What are paraprostatic cysts?

A

Cysts that form outside of the prostatic parenchyma from remnants of the uterus masculinis.

151
Q

How could paraprostatic cysts present?

A

Potentially could get referred for a cuadal abdominal mass. They can cause problems with defecation.

152
Q

What are the most common metastatic sites for prostatic neoplasms?

A

Local lymph nodes, lung and bone. Also can be in the bladder and pelvic musculature.

153
Q

Treatment of choice for prostatic neoplasia?

A

NSAIDs and cisplatin
Consider bisphosphonated for bone pain.

154
Q

Practical considerations for blood pressure measurement
a) size of cuff
b) number of measurements

A

a) 30 - 40% of limb circumference
b) 5 - 7 consistent measurements

155
Q

How much higher do sighthounds blood pressures measure?

A

10 - 20mmHg

156
Q

How much is blood pressure expected to increase with age?

A

1 - 3mmHg/year - dogs only

157
Q

What are the screening guidelines for healthy animals with regards to systemic hypertension?

A

Routine screening for hypertension is not reccomended. However, screening for diseases that could be associated with hypertension can be considered for animals ≥9 years old

158
Q

Categories of hypertension based on most recent consensus guidelines

A

Normotensive < 140 mmHg
Pre-hypertensive 140 - 159 mmHg
Hypertensive 160 - 179 mHg
Severe hypertension ≥180 mHg

159
Q

Approach to diagnosis of hypertension

A
160
Q

Approach to management of hypertension

A
161
Q

What are the goals generally, of anti-hypertensive treatment

A

Ideally <140mmHg but otherwise reduce category of risk by 1 category
< 160mmHg is a minimum goal
Avoid <120mHg

162
Q

When should dogs be given combination therapy for hypertension?

A

If BP > 200mmHg

163
Q

Treatment reccomendation for amlodipine in cats with hypertension

A

0.625mg if <200mmHg
1.25mg if >200mmHgW

164
Q

What is the clinical scenario in which acute hypertensive management should be emplyed?

A

Patients with acute hypertension (>180 mmHg) with signs of intra-cranial target organ damage

165
Q

What is the treatment goal for hypertensive emergencies?

A

Reduction of blood pressure by 10% in the first hour and then 15% over the following several hours. Acute reductions are likely to be detrimental as often the cause will not be acute and there will be some compensatory mechanisms that will have occured.

166
Q

What is the treatment of choice for acute hypertensive crises and how should it be monitored?

A

Fenoldopam, delivered via a CRI and titrated to effect every 10 minutes.

167
Q

When, after managing a hypertensive crisis, can oral agents be considered?

A

After 12 - 24 hours and the parenteral medication can be titrated down as the oral medication takes effect.

168
Q

What blood pressure reading does doppler measurement correlate best to in dogs and cats?

A

In both it is generally more likely to equate to the systolic blood pressure but in cats it is thought to be closer to MAP

169
Q

Following ureteric obstruction, what percentage of reduction is expected to be permanent after the following periods of time:
- 7 days
- 14 days
- 40 days

A
  • 35%
  • 54%
  • 100%
170
Q

How should ureteric obstructions be managed in dogs according to consensus reccomendations

A

Ureteral stenting

171
Q

What size of urolith can SWL be considered for?

A

<1.5cm stones

ACVIM Specialty: Ettinger - MS 2023 (12 decks)

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