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Equine > equine clinical pathology > Flashcards

equine clinical pathology Flashcards

1
Q

What must we remember about anaemia in horses

A

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)

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2
Q

What are markers of regeneartive anaemia in horses

A

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]

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3
Q

Categories of causes of haemolysis

A

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

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4
Q

What things can cause secondary IMHA

A

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

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5
Q

Categories of causes of non-regnerative anaemia

A

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

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6
Q

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

A

Toxins: phenylbutazone, chloramphenicol
Leukaemia
Myelofibrosis

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7
Q

How much of the red cell mass can the spleen store

A

50%

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8
Q

What equine blood groups have the most transfusion reactions

A

EAA and EAQ
(more common in TBs)

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9
Q

Why does endotoxaemia cause a neutropenia

A

By causing margination of neutrophils

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10
Q

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

A

Monocytosis; because NOT associated with stress/steroids

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11
Q

What are the two acute phase proteins in horses

A

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

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12
Q

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

A

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

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13
Q

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

A

GGT; more sensitive
ALP

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14
Q

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

A

Bile acids; more sensitive
Bilirubin

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15
Q

What is uncongugated vs conjugated bilirubin

A

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

Conjugated = product made soluble by liver and excreted in bile

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16
Q

When do we most commonly see hyperbilirubinaemia in horses and why

A

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

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17
Q

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

A

Get a disproportionate increase in unconjugated bilirubin

18
Q

When might we see increased total bilirubin (not disproportionately more unconjugated)

A

CHolestasis, hepatocellular dsysfucntion, haemolysis

19
Q

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

A

Greater increase in direct (conjugated_ bilrubin

20
Q

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

A

AKI: <10
CKD > 10

21
Q

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

A

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

22
Q

What things can lead to hyponatraemia in horses

A

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

23
Q

How can colic lead to hypocalcaemia

A

Due to endotoxaemia and inflammatino and impairment of parathyroid functino

24
Q

Difference between hyperlipidaemia and hyperlipaemia

A

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

25
Q

What type of hyperlipidaemia cause is more common in horses

A

SEcondary to another disease e.g colic, pregnancy lactation
Where hyporexic + negative energy balance

Get increase in glucagon, catehcolamines, cortisol etc which all stimualte HSL and modbilisation of fat

26
Q

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

A

Pnoies esp shetlands
Donkeys

Stress and obesity and risk factors

27
Q

NOrmal volumes of fluid in pleura/peritoneum in a horse

A

Pleura; <8ml
Peritoneum 10-100ml

28
Q

What makes effusion a transudate vs exudate

A

Transudate = <10x10^9/L cells

Exudate = >10/10^9/L cells

(normal fluid has <12)

29
Q

Difference between protein rich and poor transudate

A

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

30
Q

When might we find a protein poor transudate

A

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

31
Q

When might we find a protein rich transudate

A

Right sided CHF
POrtal hypertension
Neoplasia

32
Q

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

A

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

33
Q

What can cause sterile peritonitis

A

Pancreatitis
Bile leakage

34
Q

What are cell counts usually like with chemial synotivits

A

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

35
Q

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

A

> 10

36
Q

What do we expect to see in RAO vs IAD BAL

A

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

37
Q

What does increases MCHC in horses mean

A

Always an artefact
e.g haemolysis, lipaemia, icterus

38
Q

When might spleen contract and release RBCs vs sequester them

A

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

39
Q

Characteristics of normal body cavity fluids

A

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

40
Q

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

A

> 1mmolL

Equine (19 decks)

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