equine clinical pathology

Question 1

What must we remember about anaemia in horses

Answer 1

Reticulocytes are not released into circulation in significant numbers so it is hard to tell whether an anaemia is regenerative or not (cannot use polychromasia)

Question 2

What are markers of regeneartive anaemia in horses

Answer 2

Macrocytosis
Increased red cell distribution width; anisocytosis
Do not see hypochromasia as in other species
Serial rise in PCV without increase in protein

[definitive diagnosis needs bone marrow biopsy that shows >5% polychromatophils]

Question 3

Categories of causes of haemolysis

Answer 3

IMHA
Oxidative damage e.g onions, maple leaves
Equine infectious anaemia
Babesia/theileria
–> These infections would only be seen in imported horses or those that received imported blood

Question 4

What things can cause secondary IMHA

Answer 4

Infectious agents: clostridia, rhodococcus, strep equi
Neoplasia
Drugs e.g TMPS, penicillin

Question 5

Categories of causes of non-regnerative anaemia

Answer 5

Primary bone marrow disorder
Anaemia of chornic inflammatory/neoplasitc disease
Anaemia of chronic liver disease
Chronic kidney disease

Question 6

What primary bone marrow disorders can cause non-regnerative anaemia (inc toxicoses)

Answer 6

Toxins: phenylbutazone, chloramphenicol
Leukaemia
Myelofibrosis

Question 7

How much of the red cell mass can the spleen store

Answer 7

50%

Question 8

What equine blood groups have the most transfusion reactions

Answer 8

EAA and EAQ
(more common in TBs)

Question 9

Why does endotoxaemia cause a neutropenia

Answer 9

By causing margination of neutrophils

Question 10

Out of neutrophilia and monocytosis what is a more specific marker of inflammation

Answer 10

Monocytosis; because NOT associated with stress/steroids

Question 11

What are the two acute phase proteins in horses

Answer 11

Serum amyloid A; specific; rises within 24 hrs
Fibrinogen; less specific, rises in 24-72hrs of inflammation

Question 12

Markers of hepatocellular damage in horses and how do their locations within the cell influence what they tell us

Answer 12

SDH; found in cytoplasmm so released quickly after damage - peaks after 2 days then normalised
–> But rarely measured bceause too labile

AST = cytoplasmic and mitochondria; LESS SPECIFIC because also in muscles and RBCs

GLDH/GDH = mitochondrial location so increases wiht SEVERE cell injury

Question 13

Markers of biliary cell injury/cholestasis and which is more sensitive

Answer 13

GGT; more sensitive
ALP

Question 14

Markers of hepatic function in the horse and which is more specific

Answer 14

Bile acids; more specific
Bilirubin

Question 15

What is uncongugated vs conjugated bilirubin

Answer 15

Unconjugated (indirect) = breakdown product of haemoglobin transported with albumin; going towards liver

Conjugated = product made soluble by liver and excreted in bile

Question 16

When do we most commonly see hyperbilirubinaemia in horses and why

Answer 16

SEcondary to fasting/inappetence
Because get fatty acid mobilisation which interferes with uptake of bilirubin into hepatocytes

Question 17

How does bilirubin specifically change that tells us it is probably due to fasting

Answer 17

Get a disproportionate increase in unconjugated bilirubin

Question 18

When might we see increased bilirubin other than fasting

Answer 18

CHolestasis, hepatocellular dsysfucntion, haemolysis

Question 19

What proportion increase in direct vs indirect bilirubin do we see with cholestasis

Answer 19

Greater increase in direct (conjugated_ bilrubin

Question 20

What kind of urea: creatitine ratio do we expect to see with CKD vs AKI

Answer 20

AKI: <10
CKD > 10

Question 21

What electrolyte abnormalities do we expect to see with AKI vs CKD in horses

Answer 21

AKI: low CL- and Na+
CKD: high K+, high Ca2+, low phosphat

Question 22

What things can lead to hyponatraemia in horses

Answer 22

Sequestratino of fluids in GI tract; ileus or obstruction
Gastric reflux
Sweating (then drink plain water to make up)
Uroperitoneum
Third space loss

Question 23

How can colic lead to hypocalcaemia

Answer 23

Due to endotoxaemia and inflammatino and impairment of parathyroid functino

Question 24

Difference between hyperlipidaemia and hyperlipaemia

Answer 24

Hyperlipidaemia: TGs<5.7mmol/l, don’t see gross lipaemia or clinical signs

Hyperlipaemia; have triglycerides >5.7mmol/l, visible lipaemia of blood, fatty infiltrate of liver etc

Question 25

What type of hyperlipidaemia cause is more common in horses

Answer 25

Secondary to another disease e.g colic, pregnancy lactation Where hyporexic + negative energy balance Get increase in glucagon, catecholamines, cortisol etc which all stimulate HSL and mobilisation of fat

Question 26

What animals can get primary hyperlipidaemia nd what are the risk factors

Answer 26

Pnoies esp shetlands Donkeys Stress and obesity and risk factors

Question 27

NOrmal volumes of fluid in pleura/peritoneum in a horse

Answer 27

Pleura; <8ml Peritoneum 10-100ml

Question 28

What makes effusion a transudate vs exudate

Answer 28

Transudate = <10x10^9/L cells Exudate = >10/10^9/L cells (normal fluid has <12)

Question 29

Difference between protein rich and poor transudate

Answer 29

Protien rich: >20g/L protein Protein ppor <20g/L protein

Question 30

When might we find a protein poor transudate

Answer 30

Acute uroabdomen Marked hypoalbuminaemia causing ascites Decreased lymph drainage e.g in torsion

Question 31

When might we find a protein rich transudate

Answer 31

Right sided CHF Portal hypertension (due to liver cirrhosis, R CHF) Neoplasia

Question 32

How can we use glucose of exudate to tell us if it is septic or not

Answer 32

In. a septic exudate, we expect the glucose to be >2.8mmol/l LOWER than serum glucose due to bacteria using it up

Question 33

What can cause sterile peritonitis

Answer 33

Pancreatitis Bile leakage

Question 34

What are cell counts usually like with chemical synovitis

Answer 34

Usually <10 x10^9/L but can be up to 30

Question 35

In terms of neutrophils/40X field what do we expect with septic arthritis

Answer 35

>10

Question 36

What do we expect to see in RAO vs IAD BAL

Answer 36

RAO: neutrophilic BAL and more mucus IAD: still increased neutrophils but generaly <20%, also lymphocytes, eosinophils, mast cells

Question 37

What does increases MCHC in horses mean

Answer 37

Always an artefact e.g haemolysis, lipaemia, icterus

Question 38

When might spleen contract and release RBCs vs sequester them

Answer 38

Contract in response to adrenaline; can mask an underlying anaemia Sequester RBCs during anaestehsia so can look anaemic; must take care with interpreting PCV taken under GA

Question 39

Characteristics of normal body cavity fluids

Answer 39

Protein <35g/L Cells <12x10^9/L Clear/sligjtly yellw Mostly neutrophils; fewer macrophages/lymphovytes

Question 40

What are the fluid lactate levels normally like with ischaemic necrosis exudate

Answer 40

>1mmolL