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BSAVA ECC > Haematology and Haemostasis Module > Flashcards

Haematology and Haemostasis Module Flashcards

1
Q

What is anaemia

A

A decrease in Hb in the concentration of whole blood

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2
Q

What are the three compensatory mechanisms for aneamia?

A
  1. Vasoconstriction - Muscle, skin, GIT blood is diverted to major organs
  2. Increased CO through tachycardia + bounding pulses
  3. Quick to normal CRT but male mm
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3
Q

Stabilising anaemia - What are the factors to influence/improve

A

PaO2 - supplemental O2 concentration, can affect PaO2 diffusion gradients - minimal impact
Q (flow)- degree of hypovolaemia in anaemic patients (bleeding, panting, lack of eating/drinking) - correct hypovolaemic and maximise CO
Hb - pRBCs, WB, synthetic colloid (oxyglobin)

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4
Q

What are the suggested criteria for transfusion?

A

Hyperlactaemia
PCV less that 20% or dropping fast
If going for surgery/anaesthesia
Clinical signs: tachycardia, weak, inappettent etc.

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5
Q

What are the three broad causes of anaemia

A

Blood loss, haemorrhage and lack of RBCs
Split into the regenerative v. non-regenerative
Regenerative - primary v. secondary (infectious, drygs, deficiency, neoplasia)
Non-regen - haem v. haemolysis (intra v. extravascular)

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6
Q

How to differentiate between regenerative and non-regenerative anaemia

A

Absolute reticulocyte count greater than 80,000 cells/uL (d), 50,000 cells/uL
If very acute (less than three days) the body may not have had time to mount a response

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7
Q

On a smear what would be present with regenerative anaemia?

A

Reticulocytes
Elevated MCV - marcocytosis
Decreased MCHC - hypochromasia
Increased RDW - anisocytosis
Basophilic RBCs - polychromasia
Nucleated RBCS - anisocytosis

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8
Q

Investigating anaemia/bleeding

A

Comprehensive Haematology: size of RBCs (iron deficiency/liver disease), thormbocytosis (GI bleeding) v. Thrombopenia (cause of problem), schistocytes (intravascular haem), spherocytes (intravascula haem), hereditary red cell defects, changes to red cells associated with infection

Biochemistry - liver testing, protein

Urinalysis

Coags

BP measurement

A-vasorum testing

Meleana/haematachezia

Haemataemesis/coffee grounds

  • multiple sites of
    bleeding = systemic
    disease

AFAST - bleeding

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9
Q

Non-traumatic bleeding causes

A
  1. Neoplasia - haemangiosarcoma
  2. Primary Coagulopathies - haemophillia A
  3. Toxin induced coagulopathies : rodenticide
  4. Immune mediated - IMTP
  5. Urinary/GIT
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10
Q

Causes of non-regenerative anaemia

A
  1. Chronic disease - typically mild and self limiting : inflammatory cytokines limiting/reducing erythropoiesis
  2. Endocrine diseases: addisons, hypot4, hyperestrogenism
  3. CKD
  4. Infectious diseases: FeLV, FIV, Leishmania, Ehrlich
  5. Drugs: oestrogens, pheno, cytotoxic
  6. Deficiencies - B12, cobalt, iron
  7. Neoplasia - leukaemia, lymphoma
  8. Primary BM diseases - myelodysplastic syndromes, myelofibrosis
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11
Q

Prognostic indicators of immune mediated haemolytic anaemia

A

IgM - intravascular
Bilirubin - extravascular
Urea
Lower platelets

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12
Q

What are 5 causes of congenital haemolytic anaemia

A
  1. Hereditary stomacytosis - abnormal and fragile erythrocytes (malmutes, poms, schnau)
  2. Elliptocytosis (xbreeds) or spherocytes
  3. PK deficiency (PCR available)
  4. Phosphofructokinase deficiency - episodic haemolytic anaemia as RBCs have alkaline gradility leading to haemolysis (panting)
  5. Osmotic fragility - membrane defect that leads to increased RBC turnover and occasional IMHA - somali/abyssian cats
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13
Q

What are 4 causes of infectious haemolytic anaemia?

A
  1. Babesia spp
  2. Haemotrophic mycoplasma - haemobartonella - intravascular haemolysis
  3. Cytazuxzoonosis : intravascular haem in cats - florida
  4. Lepto - no reported in dogs and cats
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14
Q

How to diagnosis IMHA?

A

Need confirmation of immune targetting: spherocytes and autoagglutination
- Saline agg - 1:4
- Coombs test
- True agglutination - RBC washing

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15
Q

What are some possible causes of secondary IMHA?

A

Recent drugs/vaccs - zinc ingestion
infection - mycoplasma
neoplasia - splenic
foci of inflamm
Hypophosphataemia

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16
Q

Other therapies to speed up onset of remission

A
  • Immunoglobulin therapy - distracts the microphages but also increases the rate of liver getting rid of antigens
  • Splenectomy
  • Plasmapheresis
17
Q

Causes of IMHA deaths

A
  • Takes 5 days for preds to kick in
  • Thormboembolism - hyper-coagulable state (aspirin, clop, rovaroxaban)
  • costs
18
Q

What are 4 causes of neutropenia

A
  1. Consumption - most common, increased demand in peripheral tissues
  2. Neoplasia - consumption, myelopthisis (replacement of normal BM), inhibition of neutrophil production
  3. Drugs - any drug may trigger immune-mediated destruction
19
Q

When to sample BM

A
  1. Staging neoplasia
  2. High degree of suspicion of BM pathology
  3. Unexplained syndromes
  4. Diagnosis of infection
20
Q

Where to sample BM

A
  1. Humerus
  2. Wing of ileum
  3. Costo-chondral
  4. Head of femur
21
Q

What are the patients that benefit from coagulation bloods - tests are sensitive not specific

A
  1. Bleeding from multiple sites - most likely systemic causes
  2. Bleeding without trauma
  3. Unexpected and excessive bleeding during minor surgery or routine spay
  4. Patients on drugs that affect clotting
  5. Breed variation
22
Q

What is primary haemostasis?

A

Formation of a weak platelet plug and first step in haemostasis
- It is stimulated by endothelial damage and exposure of the blood to sub endothelial collagen - results in vasoconstriction, decrease in local blood flow and activated platelets which bind to the collagen and to each other
- Process of platelet activation and aggregation involves many complex signalling pathways - this is the target of anti-thrombotic therapies
- Most important substance - Von Willebrands factor - stick platelets together and to the subendothelium

23
Q

What is secondary haemostasis?

A

Formation of a stable fibrin clot
- Entraps cellular components of the blood to form a clot
- Clotting cascade forms clot and is triggered by tissue factor
- If tissue factor is exposed by endothelial damage and exposure of blood to subendothelial tissues –> Extrinsic pathways
- Alternatively cascade can be started by exposure of plasma proteins to a negatively charged surface –> Intrinsic pathways

24
Q

How does the clotting cascade conclude?

A

Concludes with a series of reactions leading to the conversion of fibrinogen (soluble) to fibrin (insoluble) to the common pathway

25
Q

What importance does fibrinoloysis have to the clotting pathways?

A

It is the resolution of the clot following tissue repair - degrades fibrin
Prevents the clot from extending beyond injury - re-estabolishes latency of vessel once vascular repair has occured
Fibrin is broken down by plasma

26
Q

What are clinical signs of disorders of primary haemostasis?

A
  • Petechiation and ecchymoses
  • Bleeding at mucosal surfaces - epitaxis, melena, haematemesis, haematuria, pulmonary and ocular haem
  • Multisite bleeding
  • Prolonged and repeated bleeding from wounds
27
Q

What are clinical signs of disorders of secondary haemostasis?

A
  • Haematoma formation
  • Bleeding into cavities - peritoneum, thorax, pericardium, joints
  • localised bleeding
  • delayed onset of bleeding
28
Q

Tests that can be used to test for Primary haemostatic coagulopathy

A
  • Platelet count - if below 30-50x10^3 (2-3 per hpf) as opposed to 8-15 per hpf)
  • BMBT
  • Von Willebrands factor measurement
  • Platelet function testing
29
Q

Tests that can be used to test for secondary haemostatic coagulopathy

A

PT - extrinsic and common pathway
- senstive for early Vit. K deficiency - due to factor 7 short half life
- not affected by primary haemostatic disorders
aPTT - intrinsic and common pathways
- prolonged in animals with hereditary facotor deficiency or hepatic synthetic dysfunction or DIC
- not affected by primary coagulopathies
ACT - intrinsic and common pathways
- can be affected by primary haemostasis or extrinsic pathways
Thrombin Time - assesses fibrin formation in response to excessive amounts of thrombin
- quality and quantity of fibrinogen
- fibrin and fibrinogen formed in the liver

BSAVA ECC (31 decks)

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