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Michaelmas 5th year > Small animal nephrology / urology > Flashcards

Small animal nephrology / urology Flashcards

1
Q

What is polydipsia; with figures for dogs and cats

A

= excessive drinking
Water intake >90ml/kg/day in dogs and >50ml/kg/day in cats

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2
Q

What leads to the release of ADH and how does this stimulate water retention

A

Increase Na+ conc in the blood (increase osmolality) is detected by the hypothalamic osmoreceptors which stimulates ADH release from the posterior pituitary
ADH causes insertion of aquaporins into the collecting duct of the nephrons, making them permeable so water moves out into the hypertonic medulla from the urine

+ ADH stimulates thirst

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3
Q

Differentials for primary polydipsia with secondary polyuria

A

Hyperthermia
Pain, stress, exercise
Psychogenic polydipsia

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4
Q

Most common causes of PU/PD in the dog

A

Diabetes mellitus
Hyperadrenocorticism
Chronic kidney disease

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5
Q

Most common causes of PU/PD in the cat

A

Diabetes mellitus
Hyperthyroidism
Chronic kidney disease

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6
Q

What is the basic mechanism behind nephrogenic diabetes insipidus

A

There are normal levels of ADH but this is not working properly at the collecting duct
- Could be primary i.e congenital lack of ADH receptors but this is very rare
- More commonly is secondary where there is a lack of response to ADH

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7
Q

What are some things that could cause nephrogenic diabetes insipidus

A

Hyperadrenocorticism
Hyperthyroidism
Liver disease; means increased glucocorticoid concentrations which interfere with ADH
Renal inflammation, CKD
Hypercalcaemia decreases ability of tubule to respond to ADH
Acromegaly
Hyperaldosteronism
Etc

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8
Q

What is osmotic diuresis

A

When the plasma solute concentration exceeds the capacity for prox tubule reabsorption so water held in the tubule

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9
Q

What things could cause osmotic diuresis

A

Glucosuria e.g in diabetes mellitus
Renal disease so not enough functional nephrons to reabsorb solutes
Post-obstructive diuresis
Osmotic diuretics
High salt diets

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10
Q

What is central diabetes insipidus

A

Complete or partial ADH deficiency
May be idiopathic, trauma, neoplasia, post-hypophysectomy

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11
Q

What is renal medullary washout

A

Where there is high tubular flow rate so not enough time for countercurrent multiplier reabsorption to occur and get low renal medullary tonicity and decreased water reabsorption

e.g from PU/PD, IV fluids, hyperthyroidism

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12
Q

Things that can lead to low renal medullary tonicity

A

Renal medullary washout: PU/PD, IV fluids, increased symp tone in hyperthyroidsim

CKD
Hypoadrenocorticism; because have low Na+
Low protein diet or liver disease; because means low urea

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13
Q

What is primary polydipsia

A

Pschyogenic polydipsia

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14
Q

What USG values make us think the animal doesn’t actually have PU/PD in dogs and cats

A

Dogs: >1.03
In cats: >1.035

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15
Q

WHat do we need to be aware of when doing the USG measurement in an animal with diabetes

A

Glucosuria can affect the USG

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16
Q

What drugs can naturally cause PU/PD

A

Steroids, phenobarbitone, progestogens, diuretics

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17
Q

Characteristics of incontinence

A

Lack of awareness of leakage
Soiled hair coat
Puddles of urine whre they are lying
Normal water consumption and urine volume (vs with PU/PD)

NB: animals with severe PU/PD can develop incontinence due to high volumes of water

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18
Q

Which breed is prone to hyperparathyroidism

A

Keeshonds

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19
Q

Which breeds are prone to hyperadrenocorticism

A

Terriers, miniature poodles

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20
Q

What might an entire male be more likely to have as a cause of PU/PD

A

prostatic disease with E coli infection

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21
Q

What might an entire female be more likely to have as a cause of PU/PD

A

Pyometra
Diabetes mellitus flare up during dioestrus phase

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22
Q

Why might neoplasia cause PU/PD and what are some examples

A

Via paraneoplatic hypercalcaemia (calcium interferes with ability of tubules to respond to ADH
e.g anal sac adenocarcinoma, lymphoma

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23
Q

What might cause increased protein in urine

A

Hyperadrenocorticism
Pyelonephritis
Pyometra
Glomerulonephritis

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24
Q

What radiographic findings might we get in a dog with hypercalcaemia

A

Evidence of neoplasia e.g lymphoma, lytic bone lesions suggestive of multiple myeloma
Calcium oxalate uroliths

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25
Q

What might cause glucosuria

A

Diabetes mellitus
Fanconi
Primary glucosuria

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26
Q

When does a water deprivation test end

A

When the urine has been concentrated i.e >1.015 or 5% of body weight has been lost

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27
Q

Why do we avoid doing water deprivation test if possible

A

Can put early kidney disease animals into renal failure
UTI patients may become septic

+ expensive, risk of false diagnosis

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28
Q

What differentials are left when we do a water deprivation test

A

Central diabetes insipidus
Primary nephrogenic diabetes insipidus
Psychogenic polydipsia

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29
Q

If an animal can concentrate urine after a water deprivation test what diagnosis will this give us

A

Psychogenic polydipsia

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30
Q

IF an animal can’t concentrate urine after a water deprivation test what are the two things is could be and how to we distinguish between them

A

Either nephrogenic or central diabetes insipidus
- Then measure the response to desmopressin (i.e ADH); if the urine becomes concentrated, then it is central diabetes insipidus
If urine stays dilute then it is nephrogenic diabetes insipidus; i.e kidney can’t respond to ADH

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31
Q

What is the risk if desmopressin is given as a therapeutic trial in psychogenic polydipsia

A

Get reduction in urine output but not water input
So can lead to water intoxication and severe hyponatraemia

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32
Q

What is dysuria

A

difficult and/or painful urination

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33
Q

What is pollakiuria

A

Abnormal frequency of passnig urine

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34
Q

WHat is stranguria

A

Slow and painful urination

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35
Q

Signalment of prostatic cancer

A

Male neutered dogs mostly

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36
Q

What dysuria causes are young cats more prone to

A

Idiopathic cystitis
Urethral obstruction

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37
Q

What to do if a urinary obstruction is present

A

Catheterise
If this isn’t possible may have to empty via cysto (note risk of bladder rupture)

38
Q

What does azotaemia, hyperkalaemia and hyperphosphataemia on biochemistry suggest in relation to urinary disease

A

Urinary obstruction is present

39
Q

What extra-urinary diseases can cause haematuria

A

Coagulopathy e.g disseminated intravascular coagluopathis, vit K rodenticide ingestion, thrombocytopaenia/pathia

Heatstroke

40
Q

What do we need to be aware of with urine samples where the issue is coming from the genital tract

A

A cysto sample is likely to be completely normal
vs free catch sample will be full of bacteria

e.g in prostatitis since bacteria more caudal than the bladder

41
Q

How to tell the difference between haematuria and haemoglobinuria/myoglobinuria

A

Spin down urine
- If it is haematuria, will get a pellet of RBCs at the bottom

In myoglobinuria will probably see evidence of muscle damage on bloods

42
Q

What might a suction biopsy on the bladder be used to diagnose

A

Transitional cell carcinoma

43
Q

At what degree of kidney damage do we get PU/PD and when do we get azotaemia

A

AT 66-75% non-functioning nephrons get PU/PD since have lost the concetrating ability

At >75% nephrons non-functional get azotaemia due to accumulation of nitrogenous waste

44
Q

What is azotaemia

A

elevated blood concentration of non-protein nitrogenous waste

45
Q

Which is a more accurate marker of GFR out of urea and creatinine

A

Creatinine because it is not reabsorbed or secreted at the renal tubules so there is less of an effect of dehydration

46
Q

Characteristics of creatinine handling

A

Produced constantly (from creatine breakdown from skeletal muscle) and influenced by skeletal muscle mass

Non-protein bound and freely filtered; not reabsorbed or secreted

47
Q

Characteristics of urea handling

A

= major nitrogenous waste product via ammonia detoxification; freely filtered then some is reabsorbed at the tubules and CDs which is enhanced during dehydration (urea follows water)

48
Q

What would it suggest is happening if we see very high serum urea and only mildly elevated or normal serum creatinine

A

Hypovolaemia i.e dehydration

This is a pre-renal cause of azotaemia

49
Q

What is pre-renal cause of azotaemia

A

Dehydration i.e hypovolaemia

50
Q

In what cases is creatinine a much less accurate marker of GFR

A

Where there is abnormal muscle mass
In thyroid disease

51
Q

What might cause an increase in serum urea

A

Reduced renal excretion; from hypovolaemia (pre-renal) or from renal disease

High dietary protein
GI bleeding (blood digested which contains lots of protein)
High rate of endogenous protein catabolism i.e in starvation, hyperthyroidism, fever

52
Q

What might lead to a reduction in serum urea concentration

A

Very reduced hepatic function; so don’t get detoxification of ammonia to urea
Portosystmic shunt so ammonia bypasses the liver
Low protein diet

Anything that keeps water in the tubules (urea follows water) i.e glucosuria, diabetes insipidus

53
Q

What is SDMA

A

a molecule produced in nuclei of all cells at a constant rate which is freely filtered at glomerulus and not reabsorbed so should give better correlation with GFR as not affected by muscle mass changes so much

BUT found to have similar correlation with GFR as creatinine does
May be useful in cats with reduced muscle mass

54
Q

If an animal has which concurrent disease do we need to be careful about interpreting urea/creatinine as GFR measures

A

Thyroid disease; complex effects

55
Q

Pre-renal causes of azotaemia

A

Dehydration
Blood loss
Heart failure (reduced GFR)

Increased production of nitrogenous waste

56
Q

Renal causes of azotaemia

A

Acute kidney injury
Chronic kidney disease

57
Q

Post-renal causes of azotaemia

A

Urinary tract obstruction
Urinary tract rupture and uroperitoneum

58
Q

Distinguishing pre-renal and renal azotaemia

A

Urine specific gravity; will be normal if pre-renal and isothenuric/minimally concentrated in renal azotaemia

59
Q

Why can animals with CKD develop a pre-renal azotaemia

A

Because they aren’t drinking enough to match urine output

60
Q

What USG value indicates normal renal concentrating ability in a dog and cat

A

Dog: >1.03
Cat: >1.035

61
Q

What is the isosthenuric range of USG

A

1.007 - 1.013

62
Q

What does hyposthenuria mean and what USG value it is

A

< 1.007
When the urine is being actively diluted
Kidneys must be functional because they are active, usually associated with loss of ADH activity e.g central/nephrogenic diabetes indipidus

63
Q

What do we need to be aware of when interpreting USG

A

Correlatie with clinical signs
Normal dog could have whole range of USG as normal physiological response to changes in water consumption

64
Q

Is USG relevant in post-renal azotaemia

A

No; variable dependent on hydration and any concurrent renal disease

65
Q

Diagnosing post-renal azotaemia

A

Use history i.e straining, not urinating, large hard bladder
And biochem; raised serum K+ is main one

66
Q

What things other than post-renal azotaemia can cause hyperkalaemia

A

Acute kidney injury (= renal azotaemia)
Artefact e.g EDTA contamination, delayed serum deparation

67
Q

When do we see hypokalaemia in azotaemic animals

A

Chronic kidney disease

68
Q

Which part of the dipstick test strip do we ignore

A

USG and leucocytes

69
Q

What is normal pH of urine in a carnivore

A

slightly acidic; 6-7.5

70
Q

What can cause aciduria

A

Metabolic acidosis
Renal tubular acidosis
Hypokalaemia

71
Q

What can cause alkalinuria

A

Main one = UTI due to urease containing bacteria

Old sample
Metabolic alkalosis

72
Q

What must we interpret dipstick protein in conjunction with

A

USG; concnetration of urine affects how significant the protein reading is

73
Q

WHat is normal urine protein: creatinine in dogs vs cats and why is this measure advantageous to dipstick protein measures

A

Dogs: <0.5
Cats: <0.2

Don’t need to interpret protein amount in relation to urine concentration, not affected by method of collection, fasted/fed state etc

74
Q

What is the most common cause of proteinuria

A

Post-renal
i.e from inflammation or infection of the urinary tract

75
Q

Does iatrogenic blood contamination of. a sample cause artefactual proteinuria

A

No
A sample would need to be grossly haematuric to cause this

76
Q

What is a marked UPC >2 assocaited with

A

Renal glomerular proteinuria i.e reduced selectivity of the glomerular barrier e.g in glomerulonephritis, amyloidosis

77
Q

What is renal tubular proteinuria

A

Where the small amount of protein that is normally filteres is not reabsorbed
Get a lower magnifutre proteinuria with UPC <1
E.g with renal tubular disease such as CKD and other disease hypertension/hyperthyroidism/hyperadrenocorticism/steroids/inflammation

78
Q

What is pre-renal proteinuria

A

Relatively uncommon occurrence where there is an increase in the serum conctration of small proteins such that is overhwelms the reabsorptive capacity of the prox tubules

May see with intravascular haemolysis, myopathy

79
Q

What is the renal threshold for blood glucose in dogs and cats

A

Cats = 16mmol/L
Dogs = 10-12mmol/L

80
Q

What things can cause false +ves and false -ves on urine glucose

A

False +ve: chlorine bleach, cephalosporins, enrofloxacin
False -ve: cold samples

81
Q

Which ketone is primarilty produced and excreted and made earlier in the line of ketosis

A

Beta-hydroxybutyrate; BUT the dipstick bad is less good at detecting this c/d acetoacetate and acetone

82
Q

Why do we spin urine sediment out at low speed

A

To avoid smashing up any crystals present

83
Q

What do we do with the condenser when examining urine

A

Lower it to increase light refraction to make crystals more visible

84
Q

What is the most common crystal to find in urine and when do we see it

A

Struvite (coffin lid)
- Can be seen in normal urine
- Forms in alkaline urine or urine with bacteria e.g UTI

Not a reliable indicator of struvite stones

85
Q

What are pyramid looking crystals in urine

A

Calcium oxalate dihydrate
Associated with hypercalcaemia

86
Q

What crystals may be seen in ethylene glycol poisoing

A

Calcium oxalate dihydrate
Calcium oxalate monohydrate

87
Q

When do we see calcium oxalate monohydrate crystals in urine

A

Very rarely normal; tends to be pathological

88
Q

Which small mammal might have calcium carbonate crystals in normal urine

A

Rabbits

89
Q

What crystals in urine have a thorn apple appearance and when do they form + which breeds might normally have them

A

Ammonium biurate/uric acid
Form in neutral to acidic urine

Associated with ammonia not being metbaolised in liver i.e hepatic disease, portosstemic shunt

+ in dalmations due to metabolic defect, english bulldog

90
Q

What is a normal number of red and white blood cells to see in urine

A

<5 of each per 40X field

91
Q

Can azotaemia cause an increase in lipase

A

Yes

92
Q
A

Michaelmas 5th year (41 decks)

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