Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What things can cause secondary IMHA

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

Toxins: phenylbutazone, chloramphenicol
Leukaemia
Myelofibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How much of the red cell mass can the spleen store

A

50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What equine blood groups have the most transfusion reactions

A

EAA and EAQ
(more common in TBs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why does endotoxaemia cause a neutropenia

A

By causing margination of neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

Monocytosis; because NOT associated with stress/steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

GGT; more sensitive
ALP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

Bile acids; more sensitive
Bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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 (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions