Blood Results

Question 1

Define in terms of daily water consumption, polydipsia in the cat

Answer 1

Normal water intake for cats is <45mls/kg/d

Question 2

What are the practical challenges when measuring water consumption in cats

Answer 2

Many cats are both inside and outside therefore difficult to know if sourcing water elsewhere – eg puddles/ponds.

Need to consider wet cat food

Question 3

An 18 year old male cat, Timmy, has a history of increased thirst and weight loss (0.3kg since a visit 6 months ago). The owner reports he is becoming increasingly lethargic but his appetite is OK.

On examination he has a body condition score of 2/5 and his kidneys feel a bit small and irregular. You can’t find any other abnormalities.

List your top 4 differentials

Answer 3

CKD

DM

Hepatic disease

GI problem causing malabsorption within SI

Question 4

An 18 year old male cat, Timmy, has a history of increased thirst and weight loss (0.3kg since a visit 6 months ago). The owner reports he is becoming increasingly lethargic but his appetite is OK.

You perform a biochemistry screen, PCV, a blood smear and a urine dipstick and sediment exam

USG: 1.016 (refractometer)

Urine protein:creatinine ratio: 0.8

Sediment exam: A few struvite crystals but otherwise NAD

Blood pressure (systolic) – 160mmHg

List the clinical pathology abnormalities and for each abnormality discuss the differential diagnoses that may cause these changes.

Answer 4

Increased creatinine – muscle breakdown, indicated in dehydration, CKD indicates IRIS stage III

Increased BUN –CKD, due to functional loss of nephrons

Hyperglycaemia – Diabetes Mellitus, stress,

Hyperphosphataemia – CKD

Hypokalaemia can be increased or decreased in CKD, might be due to decreased intake due to anorexia

Decreased PCV with normocytic normochromic anaemia – often mild non-regen anaemia in CKD, due to decreased EPO production

Proteinuria – CKD (marker for glomerular capillary hypertension)

Trace of blood –UTI secondary to CKD

Trace of glucosuria -DM

Refractometer USG: 1.016 – hyposthenuric, unable to concentrate urine, CKD

UPC ratio 0.8 – proteinuria, CKD

Few struvite crystals – UTI secondary to CKD

Blood pressure 160mmHg – CKD (moderate risk of target organ damage), hypertension?

pH 6.8 – if >7 might indicate cystitis, secondary to CKD?

Question 5

With CKD on the list we have done bloods and urinalysis what should we do next?

Answer 5

Urine culture – to identify any bacterial cause of UTI

SDMA? – although only useful for early CKD

Diagnostic imaging – unhelpful as kidneys both already small

Question 6

An 18 year old male cat, Timmy, has a history of increased thirst and weight loss (0.3kg since a visit 6 months ago). The owner reports he is becoming increasingly lethargic but his appetite is OK.

On examination he has a body condition score of 2/5 and his kidneys feel a bit small and irregular. You can’t find any other abnormalities.

= CKD!

How do we treat?

Answer 6

Fluid therapy – Hartmanns? restore deficit, provide maintenance, cover ongoing losses

Correct hyperkalaemia – low phosphate diet, +/- phosphate binders

Anti-emetics – maropitant

Gastroprotectant – sucralfate

Treat secondary underlying UTI – as a cat likely to not be infection?

Manage anaemia (might be responsible for lethargy CS)– darbepoietin and iron supplements

Question 7

Barney is an overweight (38kg, BCS 4/5) male neutered Labrador Retriever. His owner has presented him to you because he is urinating in the kitchen overnight. Prior to the appointment you ask his owner to collect a urine sample and measure how much he drinks in a 24hour period.

The owner thinks he drinks about 3 litres and has a mixture of dry and wet food

You elect to do blood biochemistry, PCV, and blood smear (Barney was starved before he was brought in this morning)

The urine results are:

List the clinical pathology abnormalities and for each abnormality discuss the differential diagnoses that may cause these changes.

Answer 7

USG 1.020 – ok?!

PU/PD – HAC, Addisons, pyelonephritis, kidney disease, hepatic disease, DM

Urea high – renal disease, hepatic disease, dehydration?

ALP/ALT high hepatic disease, HAC

Cholesterol high – DM, HAC, nephrotic syndrome, acute pancreatitis, hypothyroidism

Bile acids – high end of normal HAC

Increased number of neutrophils on blood smear – inflammatory response, stress response? - HAC

Question 8

Barney is an overweight (38kg, BCS 4/5) male neutered Labrador Retriever. His owner has presented him to you because he is urinating in the kitchen overnight. Prior to the appointment you ask his owner to collect a urine sample and measure how much he drinks in a 24hour period.

Is this polydipsic?

Answer 8

40-60ml/kg/d is normal

Barney is 38kg so 2.28 litres would be normal, 3 litres = polydipsic

Question 9

Barney is an overweight (38kg, BCS 4/5) male neutered Labrador Retriever. His owner has presented him to you because he is urinating in the kitchen overnight. Prior to the appointment you ask his owner to collect a urine sample and measure how much he drinks in a 24hour period

An ACTH stim is done. How is this done?

Answer 9

Fast animal for 12h

Collect 5ml heparinised/clotted blood

Inject synacthen (synthetic ACTH) 0.25mg

Collect 5ml blood 1h later

Separate serum/plasma

Perform cortisol assay on both samples

Question 10

Interpret these ACTH stim results

Pre-stimulation cortisol: 194 nmol/l (range 28-250)

Post-stimulation cortisol: 835 nmol/l (range 200-600)

Answer 10

As post stimulation cortisol high, indicates HAC

• cannot determine whether ADH or PDH, and if under chronic stress may develop adrenal hyperplasia that can lead to abnormal ACTH response until Tx of underlying disease

Question 11

What is the effect of dehydration on BUN?

Answer 11

This is increased in animals which are dehydrated. This is because the perfusion of the kidneys is lower = less BUN gets filtered out and so remains in the blood

Question 12

What is the effect of dehydration on creatinine?

Answer 12

Waste product which originates from muscles. This is increased in dehydrated patients because, like BUN, the perfusion of kidneys is lower in dehydration, so less is filtered and excreted out of blood.

Question 13

What is the effect of dehydration and sodium?

Answer 13

May or may not be increased in dehydrated patients.

Question 14

Why is total protein increased with dehydration?

Answer 14

Increase due to relative increase in albumin levels.

Question 15

What is the effect of dehydration on calcium?

Answer 15

Increase due to increased albumin associated with dehydration (calcium is usually bound to albumin.

Question 16

What is the effect of abnormal renal function on BUN?

Answer 16

Increase in BUN occurs when there is 75% + non-functional kidney. This is because there are less functional nephrons = decreased GFR. BUN is primarily excreted by filtration.

Less filtration = less BUN excreted = uraemia.

Question 17

What is the effect of abnormal renal function on creatinine?

Answer 17

Increase in kidney disease. Same reason as BUN.

BUN -

Increase in BUN occurs when there is 75% + non-functional kidney. This is because there are less functional nephrons = decreased GFR. BUN is primarily excreted by filtration.

Less filtration = less BUN excreted = uraemia.

Question 18

What is the effect of abnormal renal function on Albumin?

Answer 18

Decrease in cases of protein losing nephropathy.

Question 19

What is the effect of abnormal renal function on Sodium?

Answer 19

May or may not be decreased in animals with renal disease due to loss of kidney function.

Question 20

What is the effect of abnormal renal function on potassium?

Answer 20

Active absorption occurs at the proximal tubule (70%) and ascending loop of Henle (10-20%) à leaving ~10% in distal tubule. The final amount excreted out of the collecting duct is determined by the net resorption/secretion which occurs in the collecting duct which is controlled by aldosterone.
So changes in potassium excretion can be dependent on the type of renal dysfunction –

It can be increased in cases of severe renal failure (especially in terminal cases). This is due to the decline in function nephrons and so decreased excretion into urine.
K+ can also be decreased in cases of chronic renal dysfunction – due to decreased resorption?

Question 21

What is the effect of abnormal renal function on calcium?

Answer 21

Decreased in cases of renal failure (as Calcium is not absorbed by the kidneys as well, and Vit D isn’t activated, get secondary renal hyperparathyroidism)

Question 22

What is the effect of abnormal renal function on phosphate?

Answer 22

Increases in cases of renal failure (secondary to renal hyperparathyroidism, and less secretion by the kidney)

NB; secondary hyperparathyroidism is due to excessive secretion of PTH due to low calcium as a lack of absorption and decreased filtration of phosphate in renal failure because of decreased GFR.

Question 23

What are the 3 hormones in secondary hyperparathyroidism and the effect?

Answer 23

Parathyroid hormone serves to increase blood concentrations of calcium. Mechanistically, parathyroid hormone preserves blood calcium by several major effects:

• Stimulates production of the biologically-active form of vitamin D within the kidney.
• Facilitates mobilization of calcium and phosphate from bone. To prevent detrimental increases in phosphate, parathyroid hormone also has a potent effect on the kidney to eliminate phosphate (phosphaturic effect).
• Maximizes tubular reabsorption of calcium within the kidney. This activity results in minimal losses of calcium in urine.

Vitamin D acts also to increase blood concentrations of calcium. It is generated through the activity of parathyroid hormone within the kidney. Far and away the most important effect of vitamin D is to facilitate absorption of calcium from the small intestine. In concert with parathyroid hormone, vitamin D also enhances fluxes of calcium out of bone.

Calcitonin is a hormone that functions to reduce blood calcium levels. It is secreted in response to hypercalcemia and has at least two effects:

• Suppression of renal tubular reabsorption of calcium. In other words, calcitonin enhances excretion of calcium into urine.
• Inhibition

Question 24

What is the effect of renal and metabolic states on blood gas levels?

Answer 24

Acid/base control: The normal kidney needs to excrete 50-100meq of acid each day. This is achieved by secreted H+ in the proximal tubule and collecting duct – this is essential in maintaining acid base ratios. The H+ cannot be secreted as free ions so they bind to buffers in the tubular lumen (HCO3-, phosphate and ammonia). Some buffers such as HCO3- are then resorbed into the peritubular capillaries, but some, such as phosphate and ammonia are not. This means that the H+ which are bound to these buffers are secreted into the urine.
In pathological conditions such as circulating volume, aldosterone levels and plasma potassium levels can all effect the amount of acid (H+) excreted.

In metabolic acidosis, there is loss of HCO3- and increase in non-volatile acids, OR there is impaired renal excretion of H+ (ie. increased retention of H+).
The decreased H+ secretion occurs in kidney diseases such as glomerulonephritis (immune/infection) or can occur when there is increased NVA (non-volatile acid) production and kidney disease causes insufficient HCO3- reabsorption (to buffer the NVA) and insufficient H+ excretion.
Increased loss of HCO3- usually occurs due to diarrhoea.

NVA can be produced by prolonged heavy exercise, circulatory shock (lactic acid production due to decreased oxygen delivery), ketosis and diabetes mellitus (increased metabolism of triglycerides à increased beta-hydroxybuteric and acetoacetic acids).

Question 25

What haematology abnormalities may be seen in urinary tract disease?

Answer 25

Renal failure can cause a depression of erythropoietin production. This will result in a non-regenerative, macrocytic, hypochromic anaemia. = low PCV is usually seen.

Urinary infections will show increased WBC count?

Question 26

What are the primary causes of PD? (6)

Answer 26

Psychogenic, hepatic insufficiency/portosystemic shunt, central lesion effecting thirst centre in hypothalamus, pain, fever, compensatory change to water loss when animal is hot and dietary change (wet to dry).

Question 27

What are the primary cuases of PU (13)?

Answer 27

Hepatic disease, Hyperthyroidism, Hyperadrenocorticism, Hypoadrenocorticism, Hypokalemia, Hypercalcaemia, Diabetes mellitus (DM), Diabetes insipidus (DI), Pyometra, Pyelonephritis, Post-obstructive, Renal disease, Iatrogenic.

Or

• Renal
• Hepatic
• Endocrine – diabetes mellitus, diabetes insipidus, hyperthyroidism, hyperadrenocorticism, hypoadrenocorticism
• Infectious – pyelonephritis, pyometra
• Electrolytes – hypokalemia, hypercalcaemia
• Iatrogenic – diuretics, steroids etc

Question 28

What tests can we do to determine causes of PUPD?

Answer 28

Take through history!! Ask owner to try to measure the amount of water consumed.
URINALYSIS – urine specific gravity (>1.035 is concentrated)

Urine dipstick.
Cytology and bacteriology for infection?

Full clinical exam – check body condition score, hydration status

Haematology – BUN, Creatinine, Phosphate, TP.

Appropriate tests for any of the conditions listed above (eg hyperadrenocorticism).