Clinical pathology random quiz — Veterinaria Madrid

Question 1/10

6-year-old male Miniature Schnauzer with episodes of tremors, stiffness, facial rubbing and one generalised seizure. Not on treatment and no toxin exposure.

Parameter	Result	Reference
Ionised calcium	0.68 mmol/L	1.20–1.40
Phosphorus	8.4 mg/dL	2.5–6.0
Creatinine	0.9 mg/dL	0.5–1.5
Albumin	3.2 g/dL	2.6–4.0
PTH	< 0.3 pmol/L	0.5–5.8

What is the diagnosis and the appropriate maintenance treatment?

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A. Renal secondary hyperparathyroidism: renal diet and phosphate binders

There would be azotaemia and a high PTH. Here creatinine is normal and PTH undetectable.

B. Nutritional secondary hyperparathyroidism: correct the diet

It occurs in young animals on calcium-poor diets (e.g. meat only), with high PTH and normal or slightly low calcium, not with severe hypocalcaemia and undetectable PTH.

C. Primary hypoparathyroidism: supplement with oral calcium alone

The diagnosis is right, but without PTH the gut barely absorbs calcium because vitamin D is not activated. Oral calcium alone is not enough: calcitriol is needed.

D. Primary hypoparathyroidism: calcitriol and oral calcium after stabilising with IV calcium gluconate

Correct. Ionised hypocalcaemia with hyperphosphataemia, normal renal function and inappropriately low PTH is diagnostic. Stabilise with slow IV calcium gluconate under ECG monitoring and maintain with calcitriol and oral calcium, aiming for calcium at the low end of the range.

lightbulb Key takeaway

Always interpret PTH alongside ionised calcium: with hypocalcaemia, a 'normal' or low PTH is inappropriate. On calcitriol, aim for low-normal calcium and monitor frequently at first to avoid hypercalcaemia.

Question 2/10

4-year-old spayed crossbreed bitch, otherwise healthy, with pollakiuria, stranguria and haematuria for 2 days. It is her first episode. The sediment shows pyuria and abundant rods.

According to ISCAID guidelines, what is the most appropriate management?

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A. Enrofloxacin for 14 days with no need for culture

Fluoroquinolones are not first-line for sporadic cystitis and should be reserved based on culture. Long courses also do not improve outcome and promote resistance.

B. Culture of a free-catch sample: any growth confirms infection

Free-catch urine is contaminated by urethral and genital flora and is only interpretable with very high counts. By cystocentesis, by contrast, even low growth is significant.

C. Urine culture by cystocentesis and, while awaiting results, amoxicillin or trimethoprim-sulfonamide for 3–5 days, adjusted to susceptibility

Correct. ISCAID recommends culture by cystocentesis and, if treating empirically, first-line antibiotics (amoxicillin or trimethoprim-sulfonamide) in short 3–5-day courses for sporadic cystitis. An NSAID may relieve signs.

D. Amoxicillin-clavulanate for 4–6 weeks to prevent recurrence

Courses lasting weeks are reserved for conditions such as bacterial prostatitis. In sporadic cystitis they do not prevent recurrence and increase adverse effects and resistance.

lightbulb Key takeaway

Sporadic cystitis (≤ 2 episodes a year, no complicating factors): culture by cystocentesis, a first-line drug and 3–5 days. If recurrent, culture is mandatory and the underlying cause must be sought (uroliths, vulvar conformation, endocrinopathies).

References: ISCAID guidelines for the diagnosis and management of bacterial urinary tract infections in dogs and cats (2019)

Question 3/10

11-year-old Golden Retriever with sudden weakness, pale mucous membranes and abdominal distension. Ultrasound shows a cavitated splenic mass and free fluid. Dark red fluid is obtained by abdominocentesis.

Parameter	Result	Reference
PCV (blood)	24 %	37–55
PCV (effusion)	21 %	—
Platelets on effusion smear	None seen	—
Fluid clotting in plain tube	Does not clot	—

Which statement about this fluid is correct?

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A. As its PCV is similar to blood, the spleen or a vessel was probably punctured

Acute haemoabdomen has a PCV similar to blood. What identifies accidental puncture is that the sample clots and contains platelets, not the PCV value.

B. The absence of platelets indicates a sampling error

It is the other way round: platelets are consumed quickly in the cavity, so their absence supports haemorrhage that has been in the abdomen for some time.

C. Fluid cytology will reliably diagnose haemangiosarcoma

Haemangiosarcoma cells exfoliate poorly into effusions and are confused with reactive mesothelial cells. Diagnosis requires histopathology of the mass.

D. Its failure to clot and lack of platelets confirm haemorrhage that preceded the puncture

Correct. Blood in the cavity is defibrinated and platelets are consumed within a short time, so it no longer clots. Erythrophagia or haemosiderophages indicate longer-standing haemorrhage.

lightbulb Key takeaway

In older dogs with non-traumatic haemoabdomen, splenic haemangiosarcoma is the most common cause, although haematomas and other benign lesions also occur. Perform thoracic radiographs and echocardiography (right atrium) before splenectomy and do not rely on cytology for diagnosis.

Question 4/10

10-year-old cat with diabetic ketoacidosis treated for 24 h with fluids supplemented with potassium chloride and a constant-rate infusion of regular insulin. It is now weaker and the microhaematocrit plasma is pink.

Parameter	Result	Reference
Phosphorus	0.9 mg/dL	3.0–6.5
Potassium	2.7 mEq/L	3.5–5.2
Haematocrit	22% (36% on admission)	30–45
Glucose	240 mg/dL	70–150

What is the most likely cause of the anaemia and what should you do?

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A. Haemolysis due to hypophosphataemia: supplement IV potassium phosphate

Correct. Insulin and correction of acidosis shift phosphorus and potassium into cells. With phosphorus < 1 mg/dL, red cells lose ATP and lyse. Replace part of the potassium chloride with potassium phosphate and monitor phosphorus, potassium and magnesium every few hours.

B. Immune-mediated haemolytic anaemia: start prednisolone

Primary IMHA is uncommon in cats, and here the haemolysis coincides with severe hypophosphataemia after starting insulin. Corticosteroids would worsen glycaemic control.

C. Haemodilution from fluid therapy: reduce the fluid rate

Fluid therapy lowers the haematocrit somewhat, but not this much and not with pink plasma. Haemolysed plasma indicates red cell destruction.

D. Increase potassium chloride and keep insulin unchanged

It corrects only potassium and ignores phosphorus, which is the cause of the haemolysis and also contributes to the muscle weakness.

lightbulb Key takeaway

In ketoacidosis, total body phosphorus and potassium are depleted even if the initial value is normal: insulin shifts them into cells. Measure potassium before starting insulin and monitor phosphorus, potassium and glucose every 4–8 h during treatment.

Question 5/10

13-year-old female cat with stable IRIS stage 2 CKD. At a routine check-up she has no dysuria, pollakiuria or haematuria, and creatinine is unchanged. Cystocentesis urine culture grows Escherichia coli (10⁴ CFU/mL) susceptible to amoxicillin.

What do the ISCAID guidelines recommend?

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A. Treat for 7 days because CKD increases the risk of pyelonephritis

CKD alone does not justify treatment. Treatment would only be indicated if pyelonephritis were suspected (worsening renal function, fever, renal pain) or another specific indication existed.

B. Do not treat with antibiotics and monitor for signs

Correct. Without lower urinary signs or evidence of pyelonephritis, this is subclinical bacteriuria. ISCAID generally advises against treating it, including in cats with CKD or diabetes, because it does not improve outcome and selects for resistance.

C. Treat because by cystocentesis any count ≥ 10³ CFU/mL is significant

The count shows the bacteria are genuinely in the bladder, not that they need treating. The decision depends on clinical signs, not on culture alone.

D. Treat and repeat culture until negative

Pursuing microbiological eradication in an asymptomatic animal leads to repeated courses of antibiotics and selects for multidrug-resistant bacteria.

lightbulb Key takeaway

Treat the patient, not the culture: bacteriuria without clinical signs is not a urinary tract infection. Reasonable exceptions: before urological surgery or if pyelonephritis is suspected. Do not perform surveillance cultures in animals without signs unless there is a specific indication.

References: ISCAID guidelines for the diagnosis and management of bacterial urinary tract infections in dogs and cats (2019)

Question 6/10

8-month-old Yorkshire Terrier, smaller than its littermates, with episodes of disorientation and head pressing one to two hours after meals. Urine contains ammonium biurate crystals.

Parameter	Result	Reference
MCV	56 fL	60–77
Urea	9 mg/dL	20–50
Albumin	2.4 g/dL	2.6–4.0
Cholesterol	105 mg/dL	130–300
Fasting bile acids	45 µmol/L	< 10
Postprandial bile acids	180 µmol/L	< 25

What is the most likely diagnosis?

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A. Portal vein hypoplasia without portal hypertension (microvascular dysplasia)

It also raises bile acids and is common in Yorkshire Terriers, but is usually found in asymptomatic dogs without encephalopathy, microcytosis or biurate crystals. It is diagnosed after ruling out a macroscopic shunt.

B. Congenital extrahepatic portosystemic shunt

Correct. Small breed, stunted growth, postprandial encephalopathy, microcytosis, low urea and cholesterol, biurate crystals and very high bile acids (especially postprandial) are the classic picture. Confirm with Doppler ultrasound or CT angiography.

C. Chronic hepatitis

Chronic hepatitis affects middle-aged adult dogs and usually causes raised ALT. In a puppy with lifelong signs, a congenital vascular anomaly is far more likely.

D. Juvenile hypoglycaemia of toy breeds

It causes neurological signs in toy puppies, but when fasted rather than after meals, and does not explain the microcytosis, biurates or raised bile acids.

lightbulb Key takeaway

Pre- and postprandial bile acids assess hepatobiliary function and portal circulation in non-icteric patients. Signs after meals, microcytosis, low urea and biurates in a young small-breed dog: think portosystemic shunt.

Question 7/10

4-year-old female Poodle with weeks of intermittent vomiting and lethargy that partly improve with fluids. Heart rate 70 bpm despite dehydration.

Parameter	Result	Reference
Sodium	128 mEq/L	140–155
Potassium	7.1 mEq/L	3.5–5.8
Na:K ratio	18	> 27
Lymphocytes	3,900/µL	1,000–4,800

Which test confirms the most likely diagnosis?

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A. Basal cortisol: a value < 2 µg/dL confirms the diagnosis

Basal cortisol is very sensitive but not specific: a value > 2 µg/dL practically rules out hypoadrenocorticism, but a low value does not confirm it (it also occurs in healthy dogs or dogs sick for other reasons).

B. Low-dose dexamethasone suppression test

This is a test for hyperadrenocorticism (Cushing’s), not hypoadrenocorticism.

C. Urine cortisol:creatinine ratio

It is used to screen for hyperadrenocorticism thanks to its high negative predictive value. It does not confirm Addison’s disease.

D. ACTH stimulation test

Correct. It is the gold standard: post-ACTH cortisol < 2 µg/dL confirms hypoadrenocorticism. Hyponatraemia, hyperkalaemia, relative bradycardia and no stress leukogram in a sick dog are highly suggestive.

lightbulb Key takeaway

A sick dog with normal or high lymphocytes (no stress leukogram) should make you think of Addison’s. A Na:K ratio < 27 is suggestive but not specific (whipworms, kidney disease, effusions). Atypical Addison’s presents with normal electrolytes.

Question 8/10

10-year-old female Dachshund with hyperadrenocorticism confirmed by low-dose dexamethasone suppression, with no suppression at 4 h. On ultrasound, the left adrenal is 7.5 mm thick and the right 6.8 mm, with no masses. The ACTH sample was collected in EDTA, chilled and centrifuged immediately.

Parameter	Result	Reference
Cortisol at 4 h (dexamethasone)	3.9 µg/dL	< 1.4
Cortisol at 8 h (dexamethasone)	4.2 µg/dL	< 1.4
Endogenous ACTH	88 pg/mL	10–45

What is the most appropriate interpretation?

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A. Adrenal origin, because there was no suppression at 4 h

Lack of suppression does not differentiate: it occurs in all adrenal tumours but also in roughly a third of pituitary cases. A functional adrenal tumour would suppress ACTH, not raise it.

B. Pituitary-dependent hyperadrenocorticism

Correct. A normal-high or high endogenous ACTH, properly handled, indicates a pituitary origin, and fits with symmetrical adrenals at the upper limit with no masses. With an adrenal tumour ACTH would be low or undetectable.

C. Iatrogenic hypercortisolism due to undisclosed corticosteroids

Exogenous corticosteroids suppress ACTH and cause adrenal atrophy, and endogenous cortisol would be low. This is the opposite of what is seen.

D. It cannot be differentiated without a high-dose dexamethasone suppression test

The high dose only helps if suppression occurs; many pituitary cases do not suppress with it either. Endogenous ACTH and ultrasound are the preferred tools today.

lightbulb Key takeaway

To determine the origin, combine endogenous ACTH and adrenal ultrasound: normal-high ACTH with symmetrical adrenals indicates a pituitary origin; low or undetectable ACTH with a mass and a small contralateral gland, an adrenal tumour. ACTH is very labile: EDTA, cold and prompt centrifugation.

Question 9/10

4-year-old crossbreed dog that ate the leftovers of a stew with plenty of onion 3 days ago. It has lethargy, pale mucous membranes and dark urine.

Parameter	Result	Reference
Haematocrit	26%	37–55
Reticulocytes	95,000/µL	< 60,000
Total bilirubin	1.2 mg/dL	0.1–0.5

Which blood smear finding would support the diagnosis?

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A. Spherocytes and autoagglutination

They are the hallmarks of immune-mediated haemolytic anaemia, in which macrophages remove antibody-coated membrane.

B. Numerous schistocytes

They indicate mechanical fragmentation (DIC, haemangiosarcoma, vasculitis, iron deficiency), not oxidative damage.

C. Acanthocytes

They are associated with altered membrane lipids, mainly in haemangiosarcoma and liver disease. They are not typical of onion toxicosis.

D. Eccentrocytes and Heinz bodies (visible with new methylene blue)

Correct. The sulphur compounds in Allium oxidise haemoglobin, which precipitates (Heinz bodies), and fuse the membrane, pushing haemoglobin to one side (eccentrocytes). Both indicate oxidative haemolysis.

lightbulb Key takeaway

Onion, garlic and leek are toxic raw, cooked or dried, and the effect is cumulative. Other causes of oxidative damage include zinc, paracetamol, propylene glycol and naphthalene. Heinz bodies can falsely raise haemoglobin and MCHC on analysers.

Question 10/10

9-year-old Miniature Schnauzer with a history of pancreatitis. He has had vomiting, marked jaundice and pale faeces for a week.

Parameter	Result	Reference
Haematocrit	44 %	37–55
Total bilirubin	8.2 mg/dL	0.0–0.4
Alkaline phosphatase (ALP)	2,150 U/L	20–150
GGT	68 U/L	0–10
ALT	420 U/L	10–100
Cholesterol	480 mg/dL	130–300

How do you classify the jaundice and what is the most useful next step?

chevron_right Show answer and explanation

A. Prehepatic; Coombs' test and blood smear for spherocytes

Prehepatic (haemolytic) jaundice is accompanied by anaemia, usually regenerative. With a normal haematocrit, haemolysis cannot explain a bilirubin of 8 mg/dL.

B. Hepatic; measure pre- and postprandial bile acids

Bile acids add no information in an icteric patient without haemolysis: they will be high because of the cholestasis itself, whether hepatic or posthepatic.

C. Hepatic; immediate liver biopsy

Before a biopsy, an obstructive cause must be ruled out by imaging and coagulation assessed. Extrahepatic obstruction requires surgery, not biopsy.

D. Probably posthepatic; abdominal ultrasound to look for biliary obstruction

Correct. With no anaemia, very high ALP and GGT, hypercholesterolaemia, acholic faeces and a history of pancreatitis, extrahepatic biliary obstruction is most likely. Ultrasound shows common bile duct dilation and the cause (pancreatitis, mucocele, choleliths, neoplasia).

lightbulb Key takeaway

With jaundice, look at the haematocrit first: if there is anaemia, think haemolysis; if not, distinguish hepatic from posthepatic causes with ultrasound. Do not request bile acids in an icteric patient without haemolysis.