equine clinical pathology Flashcards
What must we remember about anaemia in horses
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)
What are markers of regeneartive anaemia in horses
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]
Categories of causes of haemolysis
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
What things can cause secondary IMHA
Infectious agents: clostridia, rhodococcus, strep equi
Neoplasia
Drugs e.g TMPS, penicillin
Categories of causes of non-regnerative anaemia
Primary bone marrow disorder
Anaemia of chornic inflammatory/neoplasitc disease
Anaemia of chronic liver disease
Chronic kidney disease
What primary bone marrow disorders can cause non-regnerative anaemia (inc toxicoses)
Toxins: phenylbutazone, chloramphenicol
Leukaemia
Myelofibrosis
How much of the red cell mass can the spleen store
50%
What equine blood groups have the most transfusion reactions
EAA and EAQ
(more common in TBs)
Why does endotoxaemia cause a neutropenia
By causing margination of neutrophils
Out of neutrophilia and monocytosis what is a more specific marker of inflammation
Monocytosis; because NOT associated with stress/steroids
What are the two acute phase proteins in horses
Serum amyloid A; specific; rises within 24 hrs
Fibrinogen; less specific, rises in 24-72hrs of inflammation
Markers of hepatocellular damage in horses and how do their locations within the cell influence what they tell us
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
Markers of biliary cell injury/cholestasis and which is more sensitive
GGT; more sensitive
ALP
Markers of hepatic function in the horse and which is more sensitive
Bile acids; more sensitive
Bilirubin
What is uncongugated vs conjugated bilirubin
Unconjugated (indirect) = breakdown product of haemoglobin transported with albumin; going towards liver
Conjugated = product made soluble by liver and excreted in bile
When do we most commonly see hyperbilirubinaemia in horses and why
SEcondary to fasting/inappetence
Because get fatty acid mobilisation which interferes with uptake of bilirubin into hepatocytes
How does bilirubin specifically change that tells us it is probably due to fasting
Get a disproportionate increase in unconjugated bilirubin
When might we see increased bilirubin other than fasting
CHolestasis, hepatocellular dsysfucntion, haemolysis
What proportion increase in direct vs indirect bilirubin do we see with cholestasis
Greater increase in direct (conjugated_ bilrubin
What kind of urea: creatitine ratio do we expect to see with CKD vs AKI
AKI: <10
CKD > 10
What electrolyte abnormalities do we expect to see with AKI vs CKD in horses
AKI: low CL- and Na+
CKD: high K+, high Ca2+, low phosphat
What things can lead to hyponatraemia in horses
Sequestratino of fluids in GI tract; ileus or obstruction
Gastric reflux
Sweating (then drink plain water to make up)
Uroperitoneum
Third space loss
How can colic lead to hypocalcaemia
Due to endotoxaemia and inflammatino and impairment of parathyroid functino
Difference between hyperlipidaemia and hyperlipaemia
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
What type of hyperlipidaemia cause is more common in horses
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
What animals can get primary hyperlipidaemia nd what are the risk factors
Pnoies esp shetlands
Donkeys
Stress and obesity and risk factors
NOrmal volumes of fluid in pleura/peritoneum in a horse
Pleura; <8ml
Peritoneum 10-100ml
What makes effusion a transudate vs exudate
Transudate = <10x10^9/L cells
Exudate = >10/10^9/L cells
(normal fluid has <12)
Difference between protein rich and poor transudate
Protien rich: >20g/L protein
Protein ppor <20g/L protein
When might we find a protein poor transudate
Acute uroabdomen
Marked hypoalbuminaemia causing ascites
Decreased lymph drainage e.g in torsion
When might we find a protein rich transudate
Right sided CHF
Portal hypertension (due to liver cirrhosis, R CHF)
Neoplasia
How can we use glucose of exudate to tell us if it is septic or not
In. a septic exudate, we expect the glucose to be >2.8mmol/l LOWER than serum glucose due to bacteria using it up
What can cause sterile peritonitis
Pancreatitis
Bile leakage
What are cell counts usually like with chemical synovitis
Usually <10 x10^9/L but can be up to 30
In terms of neutrophils/40X field what do we expect with septic arthritis
> 10
What do we expect to see in RAO vs IAD BAL
RAO: neutrophilic BAL and more mucus
IAD: still increased neutrophils but generaly <20%, also lymphocytes, eosinophils, mast cells
What does increases MCHC in horses mean
Always an artefact
e.g haemolysis, lipaemia, icterus
When might spleen contract and release RBCs vs sequester them
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
Characteristics of normal body cavity fluids
Protein <35g/L
Cells <12x10^9/L
Clear/sligjtly yellw
Mostly neutrophils; fewer macrophages/lymphovytes
What are the fluid lactate levels normally like with ischaemic necrosis exudate
> 1mmolL
