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Cat & Dog > Urology > Flashcards

Urology Flashcards

1
Q

What is the normal water consumption for a dog vs a cat?

A

Dog: 50-100mL/kg/day
Cat: 30-50ml/kg/day

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2
Q

What is the normal urine production for a dog vs a cat?

A

Dog: 50ml/kg/day
Cat: 25-50ml/kg/day

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3
Q

List 3 general clinical signs that can be associated with an upper urinary tract infection

A
  1. Inability to concentrate urine (with PUPD)
  2. Failure to produce urine
  3. Systemically unwell (pyrexia, anorexia)
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4
Q

Define polyuria

A

Producing more than 2 ml/kg/hour of urine

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5
Q

Define anuria

A

Producing less than 0.25 ml/kg/hour of urine

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6
Q

Define oliguria

A

Producing less than 1 ml/kg/hour of urine

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7
Q

Define uraemia

A

The group of clinical signs associated with nephron loss

Uraemia is the clinical signs of azotaemia

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8
Q

List 5 classical clinical signs that present as uraemia

A
  1. Urine smelling breath
  2. Oral ulceration
  3. Anorexia
  4. Vomiting
  5. Neurological signs
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9
Q

List 2 general clinical signs that can be associated with a lower urinary tract infection

A
  1. Inability to store urine
  2. Inability to void urine
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10
Q

List the clinical terms associated with an inability to store urine

A
  1. Incontinence
  2. Pollakiuria
  3. Periuria
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11
Q

List the clinical terms associated with the inability to void urine

A
  1. Dysuria
  2. Stranguria
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12
Q

What are some general things you want to obtain from a Hx when presented with an animal with urinary issues?

A
  1. Quatifiy the polydipsia (is it true/how much/was there a change in diet)
  2. Establish a urination pattern (volume, frequency, discomfort, location)
  3. Is there discolouration or an odour
  4. Is the animal aware
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13
Q

What does a urine protein to creatinine ratio tell us?

A

How much protein is in the urine irrespective of the urine concentration

Dipstick protein can be unreliable because it doesn’t consider {}

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14
Q

What is a normal UP:C ratio for dogs and cats

A

Dogs: less than 0.5
Cats: less than 0.4

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15
Q

What does a UP:C ratio of more than 2 tell us?

A

There is a problem in the glomerulus and protein is leaking out

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16
Q

What does a specific gravity tell us?

A

The concentration of the urine (how much pee weighs compared to the same amount of water)

Key indicator of kidney function

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17
Q

Define hyposthenuria

A

When the urine is dilute compared to plasma concentration (less than 1.007 SG)

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18
Q

Define isothenuria

A

When the urine is the same concentration as plasma (1.008-1.012 SG)

Means the kidneys are doing nothing (kidney disease)

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19
Q

Define hypersthenuria

A

When the urine is more concentrated than the plasma (more than 1.013 SG)

This is what we want bc it means the kidneys are filtering

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20
Q

What is a normal SG for a dog?

A

~1.030

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21
Q

What is normal SG for a cat?

A

~1.035

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22
Q

Define azotaemia

A

Elevated blood levels of nitrogenous waste products (creatine and urea)

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23
Q

Describe where urea comes from in the body

A

When you eat a high protein meal, protein is broken down into ammonia in the GI tract, then it goes to the liver where it is converted to urea. Most of the urea is peed out, but some is kept by the kidney to make it concentrated (contributes to tonicity)

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24
Q

What does a high urea with a normal creatinine indicate?

A

A GI bleed
(stomach is digesting blood as if it was from a high protein meal, converting ammonia to urea)

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25
Q

What does a low urea with a normal creatinine indicate?

A

The animal hasn’t been eating

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26
Q

What is the gold standard parameter for assessing GFR?

A

Blood creatinine

Its released from the muscle into the blood and filtered right away

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27
Q

What happens to the kidneys in a pre-renal azotaemia?

A

The kidneys are not getting enough blood for them to filter it

Ex. animal is haemorrhaging, hypovolaemic, dehydrated

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28
Q

What does the USG look like for pre-renal azotaemia?

A

Usually high (greater than 1.030)

Kidneys are concentrating urine to reduce water losses

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29
Q

What happens to the kidneys in a renal azotaemia?

A

The blood reaches the kidneys but they’re not working

Ex. AKI, CKD

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30
Q

What does the USG look like for a renal azotaemia?

A

Isothenuric (1.007-1.012)

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31
Q

What happens to the kidneys in post renal azotaemia?

A

Theres a block somewhere past the kidneys, so the body can’t expel the urine causing a back up of pressure, and then the kidneys will stop filtering (bc it can’t go anywhere)

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32
Q

What does the USG look like for a post renal azotaemia?

A

Variable - not a good indicator

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33
Q

How much of kidney function do you have to lose before the kidneys can’t filter anymore?

A

2/3

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34
Q

What does SDMA test for?

A

Can detect CKD with only 25% of function lost, irrespective of muscle mass

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35
Q

Why is SDMA a better indicator for CKD than creatinine?

A

Creatinine is dependent on muscle mass, so it is not always reliable in thin animals

Can be falsly low, just bc they’re skinny

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36
Q

Which section of the kidney can you biopsy?

A

The cortex (not the medulla)

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37
Q

What condition would be an indication for doing a renal biopsy?

A

Protein losing nephropathies (there’s lots of cons, so we want to avoid doing it if we can)

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38
Q

How is chronic kidney disease classified?

A

It is irreversible and progressive, and present for at least 3 months

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39
Q

List 5 conditions/causes that can progress to CKD?

A
  1. Metabolic dysfunction
  2. AKI
  3. Hypoperfusion
  4. Infection
  5. Drugs/toxins
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40
Q

Describe the progression to CKD

A

Inflammation in the kidney causes fibrosis (inflammatory cells promote fibrosis), decreasing functional nephron numbers, thus reducing GFR

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41
Q

What are 6 clinical signs of CKD?

Briefly explain why these signs are present

A
  1. PU with compensatory PD (loss of concentrating ability, urine volume increases)
  2. Anorexia (urea and PTH suppress appetite)
  3. Weight loss (decreased intake and protein loss)
  4. Vomiting (uraemic gastritis)
  5. Muscle weakness (hypokalaemia, uraemia, anaemia)
  6. Constipation (dehyrdation from excess water loss)

Similar for AKI

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42
Q

List the 5 steps to approaching a patient with kidney disease

A
  1. Confirm its the kidneys
  2. Is it acute or chronic
  3. Is it chronic, but has an acute flare up?
  4. Staging
  5. Consider secondary consequences
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43
Q

What are 3 top ddx for PU/PD?

That is not CKD

A
  1. Diabetes mellitus
  2. Hypoadrenocorticism
  3. Hyperadrenocorticism
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44
Q

List 3 parameters you can measure to diagnose CKD

A
  1. Reduced concentration ability
  2. Azotaemia
  3. Elevated SDMA
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45
Q

How can you differentiate between acute and chronic kidney disease?

A
  1. Duration of clinical signs (4-5 weeks consider chronic)
  2. BCS (no muscle condition consider chronic)
  3. Tolerance of azotaemia (good tolerance consider chronic)
  4. Kidney size (irregular or stretched)
  5. Renal pain (painful consider chronic)
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46
Q

What does it mean to have an acute on chronic kidney injury?

A

A chronic patient can be stable for a long time, but when they have a flare up of clinical signs they are considered acute-on-chronic

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47
Q

For the consequence of CKD, why does it happen and list a treatment

Dehydration

A

Why: the animal can’t concentrate urine and conserve any water
Treatment: add water to diet, fluid therapy (at home or in hospital)

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48
Q

What is the dose and duration of at home SQ fluids for a cat?

A

75-125 mL SC for 1-3 days

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49
Q

For the consequence of CKD, why does it happen and list a treatment

Cachexia

A

Why: anorexia and inflammation
Treatment: dietary management (restrict protein, increase fat and B vitamins)

Can try a renal diet

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50
Q

For the consequence of CKD, why does it happen and list a treatment

Hyperphosphataemia

A

Why: Decreased GFR means not enough PO4 is excreted, this stimulates PTH, PTH stimulates Ca release from bone (secondary renal hyperparathyroidism)
Treatment: restrict phosphate in the diet or use phosphate binders (reduces PO4 absorption from GI tract)

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51
Q

When should you reassess phosphate levels after starting treatment (dietary or drugs) in a patient with hyperphosphataemia?

A

After 4 weeks

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52
Q

For the consequence of CKD, why does it happen and list a treatment

Proteinuria

A

Why: damage to glomeruli and tubules causes protein to leak through (viscious circle - the more protein they lose the worse it gets)
Treatment: ACE inhibitors (dilate efferent arteriole to decrease the pressure in the glomeruli) or angiotensin receptor blockers (treats whole body hypertension)

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53
Q

What is a risk of giving ACE inhibitors for proteinuria?

A

It can worse azotaemia (urea and creatinine are retained bc decreased GFR)

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54
Q

For the consequence of CKD, why does it happen and list a treatment

Hypertension

A

Why: Altered renal BF, activation of RAAS, sympathetic drive for hypertension
Treatment: ACE inhibitors/ARBs, amlodipine besylate (Ca channel blocker for cats)

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55
Q

For the consequence of CKD, why does it happen and list a treatment

Urinary tract infections

A

Why: Dilute urine, polyuria and immunodeficiency
Treatment: Abx or appropriate management

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56
Q

For the consequence of CKD, why does it happen and list a treatment

Hypokalaemia

A

Why: Polyuria, anorexia, and fluid therapy
Treatment: K+ supplementation

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57
Q

For the consequence of CKD, why does it happen and list a treatment

Anaemia

A

Why: decreased EPO, GI blood loss, and iron deficiency
Treatment: blood transfusion or erythrocyte stimulating agents (2-8 weeks to effect)

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58
Q

What is a risk of giving erythrocyte stimulating agents for anaemia?

A

They are a synthetic form of EPO, so you can risk the animal developing an immune response to them and shutting down their own EPO production

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59
Q

Define IRIS stage I kidney disease

Creatinine & SDMA

A

No clinical signs
Creatinine normal
SDMA > 14

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60
Q

Define IRIS stage II kidney disease

Creatinine & SDMA

A

Mild clinical signs
Creatinine below 250
SDMA 18-35 dogs (18-25 cats)

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61
Q

Define IRIS stage III kidney disease

Creatinine & SDMA

A

Clinical signs present
Creatinine 251-440
SDMA 36-54 dogs (26-38 cats)

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62
Q

Define IRIS stage IV kidney disease

Creatinine & SDMA

A

Severe clinical signs
Creatinine greater than 440
SDMA greater than 54 dogs (>38 cats)

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63
Q

A BP greater than __ is considered severely hypertensive

A

180

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64
Q

UP:C less than __ is considered non-proteinuric

A

0.2

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65
Q

In which stage of AKI does irreversible damage occur?

A

Maintenance - the kidney learns to adapt

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66
Q

How much of the cardiac output do the kidneys receive?

A

25%

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67
Q

List 2 reasons why the kidneys are very susceptible to injury

A
  1. They receive 25% of the blood supply
  2. They have a large metabolic and oxygen demand
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68
Q

List 3 possible causes of AKI

A
  1. Hypotension
  2. Anaesthesia
  3. Post-renal obstruction
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69
Q

List 3 things you can look for on a clinical exam that could indicate AKI

A
  1. Paraspinal pain
  2. Small bladder size
  3. Hallitosis
70
Q

What is a top infectious ddx for AKI?

A

Leptospirosis

71
Q

List 5 diagnositc tests (and what you’re looking for) that you would want to do when presented with a patient with kidney problems

A
  1. Haematology (anaemia or sepsis)
  2. Biochemistry (azotaemia, K+, Ca+, phosphate, cortisol)
  3. Urinalysis (SG, crystals)
  4. Lepto testing
  5. Radiography
72
Q

How can you differentiate between an AKI and hypoadrenocorticism on a biochem?

A

In hypoadrenocorticism:
-azotaemia is not as marked
-phosphate is high normal
-potassium is high
-sodium is low

73
Q

What is a top hormonal ddx for kidney injury?

A

Hypoadrenocorticism

74
Q

What would you use as emergency treatment while treating hyperkalaemia and hypocalcaemia? Why?

A

Calcium gluconate
This protects the heart while you correct electrolyte imbalances

75
Q

What is your first line treatment for kidney injury, why, and what do you need to be careful of?

A

Fluid therapy (maintenance, but account for loses)
You want to get the kidneys to produce urine
You need to be careful of fluid overload

76
Q

List 3 supportive treatments for a patient with kidney injury

A
  1. Nutritional support
  2. Vitamin B12 supplement
  3. Analgesia
77
Q

Define renal dysplasia

A

Abnormal development of renal tissue with fetal glomeruli present

78
Q

How would you treat renal dysplasia in a puppy/kitten?

A

Treat as CKD, but consider dietary management in a growing animal

Its grossly indistinguishable from CKD

79
Q

Define renal agenesis/hypoplasia

What is the prognosis?

A

The absence of one kidney from birth (really small or not there)

Usually good unless insufficiency develops

80
Q

What is the primary biochemical sign associated with acute kidney injury?

81
Q

What is the primary clinical symptom associated with glomerular disease?

A

Proteinuria

82
Q

How does polycystic kidney disease affect kidney function?

A

As cysts on the kidney enlarge, the volume of functional nephrons reduces, causes renal insufficiency then failure

83
Q

List 3 natural defence mechanisms of the kidney against pyelonephritis

A
  1. They produce concentrated urine
  2. There is peristaltic unidirectional flow of urine
  3. There is frequent voiding of urine to flush bacteria
84
Q

Where does pyelonephritis usually arise from?

A

The lower urinary tract (it is an ascending infection)

85
Q

List 3 diagnositc tests for pyelonephritis, and what changes you’d expect to see

A
  1. Haematology (lots of leukocytes and anaemia in chronic disease)
  2. Biochemistry (azotaemia and electrolyte imbalances)
  3. Urine culutre (bacteria)
86
Q

List 3 ultrasound findings you will see in a kidney with pyelonephritis

A
  1. Hyperechoic kidney
  2. Pelvic dilation
  3. Bladder sediment
87
Q

Describe your treatment options for pyelonephritis, including considerations for Abx and surgery

A

General: analgesia, fluids, anti-nausea/emetics

Abx: very important if presenting as clinically ill, make sure you sample urine 1 week into tx to see if there is a response, and culutre 1 week after stopping course

Surgery: last resort, need to make sure other kidney can cope on its own, and the tx as CKD thereafter

88
Q

Explain the progression of glomerular disease to CKD

A

In GD, there is a loss of basement membrane selectivity and protein leaks through into the urine. Animals are not azotaemic initially, but they are proteinuric. The protein damages the tubules over time, progressing to CKD

89
Q

A UP:C greater than __ suggests disease is glomerular in origin

90
Q

What is the eitology of glomerulonephritis?

A

Immune-complex deposition in the glomerulus causes secondary inflammation, damaging the BM barrier

91
Q

What stain would you use to identify amyloidosis in the kidneys?

92
Q

What is the eitology of amyloidosis?

A

Excessive deposition of amyloid protein, in association which chronic inflammation or familial disease

93
Q

A UP:C greater than __ is characterisitc of protein losing nephropathy and/or nephrotic syndrome

A

1.0

Significant proteinuria

94
Q

What is the difference between glomerulonephritis and nephrotic syndrome?

A

Glomerulonephritis is a specific kidney disease, and nephrotic syndrome is the set of related symptoms associated with kidney disease

95
Q

List 3 symptoms of protein losing nephropathy/ nephrotic syndrome

A
  1. Proteinuria
  2. Hypoalbuminaemia
  3. Peripheral oedema
96
Q

List 3 tx options for protein losing nephropathy

A
  1. ACE inhibitors
  2. Asprin
  3. Spironolactone
97
Q

What is your tx goal for protein losing nephropathy?

A

Reduced GFR pressure, so decrease the pressure in the efferent arteriole

98
Q

What is Fanconi’s syndrome?

A

A tubular disease infecting the proximl tubule
Can be inherited or acquired (toxin and infection)

99
Q

What happens to the proximal tubule in Fanconi’s syndrome?

A

It is unable to reabsorb basically anything (glucose, bicarb, electrolytes, amino acids, etc.)

100
Q

List 5 diagnostic indicators of Fanconi’s syndrome

A
  1. Glucosuria w normal blood glucose
  2. Alkaline urine (pH > 7)
  3. Proteinuria
  4. Isothenuria
  5. Hypo-K/hypo-PO4
101
Q

What happens to the proximal tubule in primary renal glucosuria?

A

The proximal tubule is unable to reabsorb glucose

May progress to Fanconi’s

102
Q

Where does type II renal tubular acidosis affect?

A

The proximal tubule

103
Q

Where does type I renal tubular acidosis affect?

A

The distal tubule

104
Q

Outline the differences between type I and type II renal tubular acidosis

A

Type I (distal): tubule can’t excrete acid, there is severe acidosis, urine pH is > 6, and hypokalaemia is more severe
Type II (proximal): tubule can’t reabsorb bicarb, there is not severe acidosis, urine is < 6, and hypokalaemia is less severe

105
Q

What is the difference between central diabetes insipidus and nephrogenic diabetes insipidus?

A

In central, there is failure of ADH synthesis/release from the pituitary
In nephrogenic, the kidney fails to respond to ADH

Both cause the loss of ability to concentrate urine

106
Q

What hormone influences the concentrating abilities of tubules?

107
Q

In diabetes insipidus, the animal will produce large volumes of __ urine

A

Hyposthenuric (USG < 1.007)

108
Q

What test can you do differentiate psychogenic polydipsia from pathogenic polydipsia? Why is this dangerous?

A

Water deprivation test
If PD is from a pathology, you could be worsening/causing severe dehydration

109
Q

List 3 broad causes of dysuria

I.e., painful urination

A
  1. Inflammation
  2. Obstruction
  3. Neurological
110
Q

Which type of cystitis is more common in dogs?

A

Bacterial cystitis

Ascending infection

111
Q

Which type of cystitis is more common in cats?

A

Sterile cystitis

112
Q

List 3 predisposing factors for bacterial cystitis

A
  1. The animal is incontinent
  2. The animal is holding urine
  3. Catheter placement
113
Q

What are the two most common bacteria responsible for lower urinary tract infections?

Why?

A

E. coli and enterococcus faecalis

They are fecal pathogens, so they can easily get into u-tract

114
Q

What antibiotic would you use to treat a gram negative bacterial UTI?

A

TMPS or amxocicillin-clavulanate

115
Q

What antibiotic would you use to treat a gram positive bacterial UTI?

A

Ampicillin or amoxicillin

116
Q

How long should you treat a simple lower UTI for?

117
Q

In which demographic do you primarily see feline idiopathic cystitis?

A

Young, male cats

Also often neutered

118
Q

List 3 predisposing factors for FIC

A
  1. Multi-cat household
  2. Black and white colouring
  3. Stressful/anxious home environment
119
Q

How would you generally go about diagnosing a lower UTI?

A

Urinalysis: urine that is concentrated, bloody, has crystals and is there bacterial
Imagining: ultrasound, radiography and contrast urethrogram

You want to be as hands off as much as you can

120
Q

What are your tx options for a cat with a lower UTI?

A
  1. Analgesia
  2. Spasmolytics (relax smooth and skeletal muscle)
  3. Increase water intake

Consider Sx if cat keeps reblocking

121
Q

Describe the pathology of polypoid cystitis

A

Benign polyps deposit in the cranial bladder wall, usually secondary to chronic inflammation

122
Q

How do you approach diagnosing a dog presenting with incontinence?

A
  1. Make sure its actually incontinent (not behavioural)
  2. Evaluate PUPD
  3. Perform a neurological exam
123
Q

You perform a neuro exam on an incontinent dog and find its normal, what are your general ddx for the pathology?

A

There is abnormal anatomy or function

124
Q

You perform a neuro exam on an incontinent dog and find its abnormal, what are your general ddx for the pathology?

A

There is upper or lower motor neuron disease

125
Q

List 3 things you are looking for on a neurological exam for incontinence

A
  1. Anal tone & sensation
  2. Bulbocavernosus and perineal reflexes
  3. Urethral sphincter tone
126
Q

If you have upper motor neuron dysfunction, it will make the bladder __ to express

127
Q

If you have lower motor neuron dysfunction, it will make the bladder __ to express

128
Q

Describe the effect of the hypogastric nerve on the following muscle

Detrusor

A

Relaxation

129
Q

Describe the effect of the hypogastric nerve on the following muscle

Internal sphincter muscle

A

Contraction

130
Q

Describe the effect of the pelvic nerve on the following muscle

Detrusor

A

Contraction

131
Q

Describe the effect of the pudendal nerve on the following muscle

External sphincter muscle

A

Contraction

132
Q

What is the only urinary muscle you have control of, and what nerve innervates it?

A

External sphincter muscle, innervated by the pudendal nerve

133
Q

Explain how UMN dysfunction makes the bladder difficult to express

A

There is no longer communication between the brain and the bundles of nerves supplying the urinary tract, so there is no signals coming from the urinary tract telling the brain to stop sending contraction signals

134
Q

Explain how LMN dysfunction makes the bladder easy to express

A

The hypogastric nerve no longer receives any signals from the urinary tract, so the detrusor muscle constricts and the internal sphincter muscle relaxes (and all the nerves downstream of that don’t get any signals either)

135
Q

Describe a tx option for urinary spincter mechanism incompetence, and how it works

A

Phenylpropanolamine
It is an alpha receptor that acts along the urethra causing it to constrict a bit more

136
Q

You are presented with a young labrador that is constantly dribbling urine, what are you suspicious of?

A

Ectopic ureter

137
Q

Explain the difference between intramural and extramural ectopic ureter

A

Intramural: the ureter tunnels through the muscle and exits too far caudal
Extrinsic: the ureter connects to the bladder in the wrong place

138
Q

How would you treat intramural ectopic ureter?

A

Laser ablation

139
Q

How would you treat extramural ectopic ureter?

A

Transection and re-implantation

140
Q

What is the primary diagnosis for prostatic hyperplasia?

A

Rectal exam

141
Q

You are presented with a male dog with a UTI, what is your primary ddx?

A

Prostatic disease

142
Q

List 3 clinical signs of acute prostatitis

A
  1. Caudal abdominal pain
  2. Stilted gait
  3. Systemically unwell (pyrexia and sepsis)
143
Q

Which Abs would you use for acute prostatitis and not chronic, and why?

A

Cephalosporins and potentiated amoxycillin
These aren’t able to cross the blood-prostate barrier, and you need ones that can for chronic disease

144
Q

List 3 clinical signs of chronic prostatitis

A
  1. Cystitis
  2. Penile discharge/haemorrhage
  3. Dyschezia (hard time pooping)
145
Q

List the 4 stages of urolithiasis

A
  1. Nidus (bacteria + foreign material)
  2. Nucleus (aggregation of crystals)
  3. Stone (more crystals form a lattice)
  4. Outer surface crystals form (can be continuation of stone or different type of crystals)
146
Q

What is the triad of conditions that arise for a urinary stone to form?

A
  1. Urine is saturated with crystals
  2. A nidus forms
  3. There is a lack of inhibitory substances that stop crystals from sticking together
147
Q

List 3 clinical signs you will see with nephroliths

A
  1. Haematuria
  2. Renal pain (paraspinal)
  3. Clinical signs of obstruction (vomiting, azotaemia and pyrexia)

However, is often incidental

148
Q

List 3 tx options for nephroliths

A
  1. Shock wave therapy (only dogs)
  2. Endoscopic nephrolithotomy
  3. Surgery
149
Q

What is a distinguishing clinical sign of ureteroliths?

A

Big kidney little kidney

150
Q

List 3 tx options for ureteroliths

A
  1. Medical management (analgesia)
  2. Subcutaneous ureteral bypass
  3. Ureteric stenting
151
Q

List 3 tx options for urethroliths

A
  1. Catheter
  2. Retrograde hydropulsion (try to flush them out)
  3. Urethrotomy
152
Q

List 4 clinical signs of cystoliths

A
  1. Dysuria
  2. Abdominal pain
  3. Haematuria
  4. Exercise intolerance
153
Q

Which are the 2 most common types of uroliths?

A
  1. Struvite (40-50%)
  2. Calcium oxalate (40-45%)
154
Q

What are struvite crystals composed of?

What do they look like?

A

Magnesium, ammonia and phosphate (MAP)

They look like coffin lids

155
Q

Distinguish between dihydrate and monohydrate calcium oxalate crystals

A

Dihydrate: scotland flag shaped
Monohydrate: dumbell shape (would be dead before you know its stones)

156
Q

Which uroliths can you not see on radiographs?

A

Urate and cystine

157
Q

Which demographic are most prone to struvite crystals?

A

Young to middle aged female dogs

158
Q

Why are struvite crystals commonly associated with urease producing UTI’s in dogs?

A

Urease splits urea into H20, CO2 and ammonia
Ammonia is a component of struvite crystals

159
Q

List 3 tx for struvite crystals

A
  1. Treat the UTI
  2. Medical dissolution by decreasing pH, saturation of urine and components of crystals in diet (Mg, NH3, PO4)
  3. Sx if no improvement after 1 month
160
Q

Which demographic are most prone to calcium oxalate crystals?

A

Middle aged to older male dogs

161
Q

Which crystal is the most common nephrolith?

A

Calcium oxalate crystals

162
Q

What is the most appropriate tx option for a calcium oxalate urolith?

A

Surgery (cannot be medically dissoluted)

Also treat hypercalcaemia if present

163
Q

Struvite crystals form more commonly in __ urine

A

Neutral to alkaline

164
Q

Calcium oxalate crystals form more commonly in __ urine

A

Neutral to acidic

165
Q

Why would you want to reduce urinary excretion of Ca as a tx for calcium oxalate, even when these crystals form because of hypercalcaemia

A

You want to calcium to be in the body, not the urine, so you dont want the kidney to add this to the urine

But also make sure you’re treating the hypercalcaemia

166
Q

Urate crystals form more commonly in __ urine

A

Neutral to acidic

167
Q

What is the primary tx for xanthine crystals?

A

Withdraw allopurinol

168
Q

Cystine crystals form more commonly in __ urine

169
Q

Silicate crystals form more commonly in __ urine

A

Neutral to acidic

170
Q

List 3 possible tx options for cystine crystals

A
  1. Low protein alkalinising diet
  2. 2 MPG (makes cysteine more soluble)
  3. Castration

Cat & Dog (7 decks)

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