Kidney

Question 1

Where is renin released from? Why would it be released?

Answer 1

Released from the kidney (juxtamedullary apparatus) when baroreceptors at the glomerulus detect a fall in bp. It is released to start the RAAS mechanism to increase bp.

Question 2

How does angiotensin II increase bp?

Answer 2

1. Stimulates aldosterone release from the adrenal gland
2. Causes vasoconstriction

Question 3

How does aldosterone increased bp?

Answer 3

It increases sodium reabsorption in the kidney, water follows and more water is re absorbed from filtrate. This increased stroke volume and bp. Less water enters final filtrate and urine is more concentrated (reducing UOP).

Question 4

How does the pituitary respond to a fall in bp or increased solutes in the blood?

Answer 4

Releases ADH which increases water reabsorption from urine filtrate, increasing stroke volume and bp. Increases thirst drive to increase water intake. ADH acts directly on vessels to cause vasoconstriction (slower onset but more prolonged activity compared to other vasopressors).

Question 5

Why might a patient with chronic hypertension be prescribed ACE inhibitors?

Answer 5

Angiotensin converting enzyme converts the angiotensin I into angiotensin II. Inhibiting this enzymes reduces up regulation of this pathway (RAAS) and may contribute to reducing BP.

Question 6

Where is angiotensinogen produced from? What role does it play in the RAAS mechanism?

Answer 6

Liver produces this peptide. When renin is released by the kidney due to a fall in bp, it converts angiotensinogen into angiotensin I and begins the cascade of reactions to increase BP.

Question 7

What is a natriuretic peptide?

Answer 7

It is any substance that prevents the re-absorption of sodium from urine. They would encourage sodium to be excreted.

Question 8

Where in the body would you find stores of pro-BNP and pro-ANP? When would they be triggered for release?

Answer 8

Mainly in the atria, stored in granules. Stretch of the atria triggers release (due to after load pressure?)

Question 9

Why is blood urea nitrogen (BUN) in the urine filtrate only an estimate of glomerular filtration rate?

Answer 9

BUN is freely excreted at the glomerulus however some is passively reabsorbed in renal tubules.

Question 10

What is the difference between azotaemia and uraemia ?

Answer 10

Azotaemia refers to any increase in blood urea nitrogen (BUN) and/or creatinine. Uraemia is the clinical manifestation of significant accumulative uremic toxins.

Question 11

What percentage of nephron function must be impaired for an azotaemia to develop

Answer 11

75%

Question 12

A patient presents with lethargy, inappetence and vomiting. The clinician requests blood sampling to evaluate BUN and creatinine. Why is it important to also evaluate PCV and/or USG?

Answer 12

If an azotaemia is present, it is important to add data to concurrently assess for dehydration. Dehydration can be a pre-renal cause for azotaemia.

Question 13

A patient has a panhypoproteinaemia with protein losing enteropathy. How is protein loss different with renal disease?

Answer 13

Usually hypoalbuminaemic, due to damage to glomerulus)

Question 14

What class of drug are used to manage urethral sphincter mechanism incompetence ?

Answer 14

Alpha-adrenergic agonists (eg phenylpropanolamine) and oestrogen

Question 15

Describe the pathophysiology of struvite stone development

Answer 15

Formed of magnesium ammonium phosphate and smaller amounts of calcium phosphate.
In dogs these crystals form as a consequence of UTIs.
Urease producing bacteria can convert urea into ammonia and bicarbonate. Ammonia precipitates with magnesium or phosphate.
Struvite stones are more likely to form In alkali urine; the bicarb production as part of urea use increases likelihood of stones forming.

Question 16

Which bacteria predispose to urinary struvite crystal formation, by utilising urea as an energy substrate?

Answer 16

Staphylococcus, klebsiella, pseudomonas, proteus

Question 17

Should you be able to identity uroliths from struvite or calcium oxalate origin on radiography ?

Answer 17

Yes

Question 18

Which type of urolith is more likely to be found in the feline kidney or ureter?

Answer 18

Calcium oxalate

Question 19

Male and female dogs differ in which urolith they are more likely to have. Which sex is more likely to have which stone?

Answer 19

Struvite more likely in females, calcium oxalate more likely in males

Question 20

Which species are more likely to have sterile struvite urolithiasis?

Answer 20

Cats. UTIs associated with canine struvite urolithiasis

Question 21

Which two breeds are over represented in patients diagnosed with urate urolithiasis?

Answer 21

Dalmatian’s and English bull dogs

Question 22

What are the risk factors that are found to contribute to the production of urate uroliths? (6marks)

Answer 22

Salt is ammonium urate, Portosystemic shunts or severe liver disease is a greater risk factor, young to middle aged, more often in males than females. Not typically associated with concurrent infections, however the presence of urease producing bacteria increase incidents of salt formation. Dalmatian’s and EBD over represented,

Question 23

At which concentration of glucose in the blood will result in glucosuria?

Answer 23

Dogs 180 mg/dL, cats 300 mg/ dL (18 g/dL = 1 mmol)
Dogs 10 mmol/L, cats 16.6mmol/L