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CVSOH1 Clinical Pathology and Clinical Biochemistry > Equine Haematological Disorders > Flashcards

Equine Haematological Disorders Flashcards

1
Q
  1. What tests and measurements can be run to assess quantity of erythrocytes in circulation?
  2. Note for age with these measurements?
A
  1. RBC count, Haemoglobin, PCV.
  2. First weeks of life, these measurements decrease rapidly.
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2
Q
  1. Haemoglobin conc. in normal horse?
    – When would there be an increase?
  2. What measurements can be taken from RBCs?
  3. What is anisocytosis?
  4. What are acanthocytes?
  5. What is Rouleaux formation?
  6. What is agglutination?
A
  1. 1/3 PCV.
    – Intravascular haemolysis.
  2. Mean Cell Volume, Mean cell haemoglobin conc., characterise anaemia, automated, calculate from RBC count and Hb and PCV.
  3. More variation in the size of the RBCs than normal.
  4. RBCs with spikes of varying sizes on the cell surface. They are associated with disease.
  5. Where RBCs stack/group together. Normal.
  6. The clumping together of RBCs associated with disease (antibody-antigen reaction).
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3
Q
  1. When would bone marrow aspirate for evaluation be indicated in the horse?
  2. What could be done with the aspirate?
  3. Method of taking bone marrow aspirate.
A
  1. If suspect disorder of haematopoietic system but cannot diagnose it from routine lab tests. Rare.
  2. Use to characterise anaemia.
    Evaluate iron stores.
    Explain quantitative or qualitative abnormalities of blood cells.
  3. At the sternum, clip and scrub, use LA, make a skin incision, and use Jamshedi needle with pressure and routine to enter the bone. Smear the aspirate and fix with formalin.
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4
Q
  1. Why is iron deficiency rare?
  2. What explains low iron levels in most cases?
A
  1. Well managed horses eat green leafy vegetable all day and should obtain enough iron via this.
  2. Disturbances of iron metabolism so anaemia of chronic disease.
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5
Q
  1. What is erythrocytosis?
  2. Effect on the blood?
  3. Consequence of this for animal?
A
  1. Increased RBCs.
  2. Increased viscosity.
  3. Tissue hypoxia, thrombosis, haemorrhage, weakness, lethargy, exercise intolerance.
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6
Q

In what cases would you get relative erythrocytosis?

A

Splenic contraction:
- due to excitement / stress.
- recover after a few hours.
Loss of plasma volume w/o change in RBC numbers:
- dehydration, endotoxic shock.

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7
Q

In what cases would you get absolute erythrocytosis?

A

Primary:
- Rare myeloproliferative disorder (cancer).
Secondary, appropriate:
- Response to tissue hypoxia e.g. cardiac anomalies.
Secondary, inappropriate:
- Increased erythropoietin release w/o hypoxia.
- Usually neoplasia.

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8
Q
  1. Measurements to indicate anaemia.
  2. Range of clinical signs.
A
  1. Decreased PCV, RBC count.
    And decrease in Hb, unless intravascular haemolysis.
  2. None/mild to severe hypoxia.
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9
Q
  1. Haematological causes of anaemia (basic).
  2. How could you tell if the anaemia was regenerative or non-regenerative?
A
    • Increased loss of RBCs.
      - Increased destruction of RBCs.
      - Decreased production of RBCs.
  2. Based on bone marrow response.
    MCV.
    MCHC.
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10
Q
  1. Where there is internal haemorrhage, what can be done to restore losses?
  2. Clinical signs of haemorrhage?
A
  1. Autotransfusion.
  2. Vary dept. on duration and severity of blood loss.
    Can lose up to 1/3 (10-12L) blood volume.
    Severe clinical signs at PCV 12-20%.
    In acute blood loss, PCV drop hidden initially, and protein drops too.
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11
Q
  1. Clinical signs of hypovolaemic shock.
  2. Recovery from haemorrhage.
A
  1. Tachycardia.
    Pale MMs.
    Weakness.
    Oliguria.
  2. PCV can increase by <1% per day but this is greater if blood loss is internal.
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12
Q

Treatment of haemorrhage.

A

Identify and stop source of bleeding.
Can us Tranexamic/aminocaproic acid.
Isotonic fluids (could increase BP and increase haemorrhage but equally need to replace losses so treat as case-by-case.
Colloids (same goes as isotonic fluids).
Oxyglobin is expensive!
NOT hypertonic saline!

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13
Q
  1. Types of haemolysis and measurements that show this and consequences of one.
A
  1. Intravascular
    - Haemoglobinaemia (increased MCHC).
    - Haemoglobinuria.
    - Consequences: nephrotoxic and can lead to renal failure.
    Extravascular.
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14
Q
  1. What does IMHA stand for?
  2. How common is IMHA in horses?
  3. What does IMHA do?
  4. Where is IMHA more common in horses?
    – cause?
  5. Most IMHA intravascular or extravascular?
A
  1. Immune Mediated Haemolytic Anaemia.
  2. Uncommon.
  3. Production of antibodies that attach to surface of RBCs and destroy them.
  4. When it is secondary.
    – caused by alterations to RBC membrane by viral/bacterial/neoplastic disease. Can also be drug-induced (often antigen-antibody complex deposition). –> penicillin, TMPS.
  5. Extravascular.
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15
Q
  1. IMHA clinical signs.
  2. Diagnosis of IMHA.
A
  1. Insidious, fever, lethargy, weight loss.
  2. Decreased RBC count.
    Spherocytes.
    Increased MCV.
    Anisocytosis.
    Increased total and indirect bilirubin.
    Haemoglobinaemia.
    Autoagglutination.
    Coomb’s test.
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16
Q

Treatment of IMHA in horses.

A
  • Identify underlying cause?
  • Discontinue previously administered drug.
    – Treat underlying disease.
  • If severe, blood transfusion.
  • If haemoglobinuria, IV fluids as risk of nephropathy.
  • Corticosteroids.
    prognosis depends on cause
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17
Q
  1. What does EIAV stand for?
  2. Where is it endemic?
  3. Where is found?
  4. What is the basic mechanism of anaemia with EIAV?
A
  1. Equine Infectious Anaemia Virus.
  2. Parts of Europe and USA.
  3. Sporadic cases in UK.
  4. Haemolysis.
18
Q

What are the clinical syndromes of EIAV?

A
  • Acute infection.
  • Chronic infection.
  • Inapparent carrier.
19
Q
  1. Clinical signs of Acute EIAV?
  2. Why is acute EIAV difficult to diagnose?
  3. What tests can be run for diagnosis of acute EIAV?
A
  1. Fever, lethargy, anorexia, thrombocytopenia.
  2. Can take 40 days to seroconvert.
  3. AGID (Agar Gel Immnodiffusion Assay) / Coggins / C-ELISA.
20
Q
  1. Clinical signs of chronic EIAV infection.
  2. How is chronic EIAV infection easier to diagnose?
  3. How can an inapparent carrier be identified?
A
  1. Recurrent fever, weight loss, ventral oedema, anaemia.
  2. Seropositive.
  3. They will be seropositive.
21
Q
  1. How is EIAV transmitted?
  2. Why is slaughter often required for animals that are infected? – compensation?
A
  1. Blood-sucking insects.
    Mare to foal across placenta, via colostrum and milk.
    Aerosol?
    Iatrogenic – blood product transfusions or blood-contaminated instruments.
  2. Notifiable disease – £1 compensation.
22
Q
  1. How are horses infected with babesia?
  2. Why would babesia be relevant to us?
A
  1. Ticks.
  2. If horse has travelled.
23
Q
  1. What is non-regenerative anaemia basically caused by?
  2. What can cause this?
A
  1. Suppression of bone marrow erythropoiesis.
  2. Chronic disease w/ disturbance of iron metabolism.
    Iron deficiency usually due to chronic blood loss.
    Endocrine disease.
    Neoplastic disease.
24
Q

Most common cause of anaemia in the horse?

A

Chronic disease and using thoroughbred reference range.

25
Q
  1. What is haematopoietic neoplasia?
  2. When is this classified as leukaemia? – common?
  3. Types of haematopoietic neoplasia?
A
  1. Uncontrolled proliferation of 1 or more marrow-derived blood cell lines.
  2. When neoplastic cells are seen in peripheral circulation. – rare.
  3. Myeloid and lymphoid.
26
Q

Clinical signs of myeloid neoplasia.

A

Depression.
Weight loss.
Fever.
Oedema.
Petechial haemorrhage.
Anaemia.

27
Q
  1. Diagnosis of myeloid neoplasia in horses.
  2. Treatment?
  3. Prognosis?
A
  1. Peripheral blood smear.
    Bone marrow aspirate.
  2. No treatment found.
  3. Survive a few weeks.
28
Q
  1. Locations of lymphoid neoplasia in horses?
  2. Age affected?
  3. Clinical and lab changes from loss of organ function caused by?
A
  1. Generalised, intestinal, mediastinal, cutaneous.
  2. 5-10yrs.
  3. Infiltration of lymphocytes.
    Physical obstruction by tumour masses.
    Tumour cell cytokines.
29
Q

Clinical signs of lymphoid neoplasia in horses?

A

Vary w/ location.
Often chronic disease w/ sudden onset of more severe signs.
Weight loss.
Fever.
Ventral oedema.
Paraneoplastic syndromes.

30
Q

Diagnosis of lymphoid neoplasia in horses.

A

Demonstration of neoplastic lymphocytes in affected tissue.
Biopsy mass.
- If intestinal:
– rectal biopsy.
– Abdominoparacentesis.
– Laparoscopy.
– Laparotomy.

31
Q

Treatment of lymphoid neoplasia in horses.

A

Usually present in advanced stage of disease.
Could resect tumour, give chemotherapy, give radiotherapy.
– v expensive.
– Can achieve remission for 12-18mths.
Usually euthanise.

32
Q
  1. Clinical signs of thrombocytopenia?
  2. Mechanisms of thrombocytopenia.
A
  1. Abnormal primary haemostasis.
    Epistaxis.
    Petechial haemorrhage.
    • Decreased platelet production via bone marrow suppression.
      - Increased platelet destruction via IMTP or Equine Infectious Anaemia.
      - Abnormal platelet function.
33
Q
  1. What happens in primary haemostasis?
  2. What happens in secondary haemostasis?
  3. Clinical signs of disorders of haemostasis.
A
  1. Platelets plug vascular defect.
  2. Interaction of coagulation factors to form a fibrin mesh.
    Extrinsic, intrinsic, common pathways.
    • Abnormalities of primary haemostasis.
      - Abnormalities of secondary haemostasis w/ spontaneous or excessive haemorrhage in response to surgery or trauma.
34
Q

Diagnosis of disorders of haemostasis.

A
  • Whole blood clotting time.
  • Platelet count on smear.
  • Buccal mucosal bleeding.
  • Activated clotting time.
    – Time to clot formation on activation of whole blood.
    – Evaluates deficiencies of Factor VIII and IX, prothrombin, fibrinogen.
    – Not altered by abnormalities of Factor VII and platelets.
  • APTT (activated partial thromboplastin time)
    – Measure activity of factors V, VIII, IX, X, XI, XII.
    – APTT more reliable than PTT in horses.
  • PT – Extrinsic and common coagulation pathways.
  • FDPs, D-Dimer, TEG clotting (good – hospital based).
  • Specialised assays for components of cascade.
35
Q
  1. Hereditary disorders of haemostasis.
  2. Acquired disorders of haemostasis.
A
  1. Von Willebrand’s disease.
    Factors VIII deficiency.
    • Vasculitis from infectious diseases or immunologic diseases.
      - Disseminated Intravascular Coagulation.
36
Q
  1. What is thrombophlebitis?
  2. When is the risk of this increased?
  3. Important precaution?
  4. Treatment of thrombophlebitis?
  5. Risks associated with thrombophlebitis?
A
  1. (Infected) thrombus at a site of endothelial damage – usually catheter site.
  2. Sepsis, endotoxaemia, DIC.
  3. Aseptic technique for catheter placement and monitor catheter, replacing when necessary.
  4. Hot pack.
    Topical treatment.
    Systemic antibiotics if necessary.
    Aspirin.
  5. Bilateral thrombophlebitis.
    Endocarditis.
37
Q
  1. When is blood transfusion necessary?
  2. Signs of tissue hypoxia.
A
  1. If anaemia severe enough to impair tissue oxygenation.
    • Tachycardia.
      - Tachypnoea.
      - Lethargy.
      - Weakness.
      - Cool extremities.
      - Pale MMs.
38
Q
  1. When may blood transfusion be indicated?
  2. How are signs less obvious with chronic anaemia?
  3. How does blood donation work?
A
    • At PCV of10%-18% depending on rapidity of erythrocyte loss.
      - Severe haemorrhage with DIC to renew supplies of coagulation factors and platelets.
  2. It allows for physiological adaptation.
  3. Blood has to be collected for a patient, not able to store it, unless patient then does not need it, then can be stored in a fridge.
    Some hospitals have blood donors.
    Ideally perform major and minor cross match.
    Can do this before a planned major surgery.
39
Q

Blood transfusion for the critical patient.

A

No time to cross match.
Usually fine even to have multiple transfusion for the first 3-4 days.
Chances of an adverse reaction increase when either donors or recipients are mares that have been bred previously.

40
Q

Method of blood transfusion.

A

Usually safe to remove 5-10L from donor.
Sterile.
Catheter pointing up.
Commercial collection bags.
Transfuse slowly – monitor HR, RR, TEMP.
stop if reaction, supportive care.
Volume required can be calculate w/ equation.

41
Q
  1. What is the major sign of how a horse is coping w/ blood loss.
A
  1. HR.

CVSOH1 Clinical Pathology and Clinical Biochemistry (8 decks)

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