Haematology and Haemostasis Module Flashcards
What is anaemia
A decrease in Hb in the concentration of whole blood
What are the three compensatory mechanisms for aneamia?
- Vasoconstriction - Muscle, skin, GIT blood is diverted to major organs
- Increased CO through tachycardia + bounding pulses
- Quick to normal CRT but male mm
Stabilising anaemia - What are the factors to influence/improve
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)
What are the suggested criteria for transfusion?
Hyperlactaemia
PCV less that 20% or dropping fast
If going for surgery/anaesthesia
Clinical signs: tachycardia, weak, inappettent etc.
What are the three broad causes of anaemia
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)
How to differentiate between regenerative and non-regenerative anaemia
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
On a smear what would be present with regenerative anaemia?
Reticulocytes
Elevated MCV - marcocytosis
Decreased MCHC - hypochromasia
Increased RDW - anisocytosis
Basophilic RBCs - polychromasia
Nucleated RBCS - anisocytosis
Investigating anaemia/bleeding
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
Non-traumatic bleeding causes
- Neoplasia - haemangiosarcoma
- Primary Coagulopathies - haemophillia A
- Toxin induced coagulopathies : rodenticide
- Immune mediated - IMTP
- Urinary/GIT
Causes of non-regenerative anaemia
- Chronic disease - typically mild and self limiting : inflammatory cytokines limiting/reducing erythropoiesis
- Endocrine diseases: addisons, hypot4, hyperestrogenism
- CKD
- Infectious diseases: FeLV, FIV, Leishmania, Ehrlich
- Drugs: oestrogens, pheno, cytotoxic
- Deficiencies - B12, cobalt, iron
- Neoplasia - leukaemia, lymphoma
- Primary BM diseases - myelodysplastic syndromes, myelofibrosis
Prognostic indicators of immune mediated haemolytic anaemia
IgM - intravascular
Bilirubin - extravascular
Urea
Lower platelets
What are 5 causes of congenital haemolytic anaemia
- Hereditary stomacytosis - abnormal and fragile erythrocytes (malmutes, poms, schnau)
- Elliptocytosis (xbreeds) or spherocytes
- PK deficiency (PCR available)
- Phosphofructokinase deficiency - episodic haemolytic anaemia as RBCs have alkaline gradility leading to haemolysis (panting)
- Osmotic fragility - membrane defect that leads to increased RBC turnover and occasional IMHA - somali/abyssian cats
What are 4 causes of infectious haemolytic anaemia?
- Babesia spp
- Haemotrophic mycoplasma - haemobartonella - intravascular haemolysis
- Cytazuxzoonosis : intravascular haem in cats - florida
- Lepto - no reported in dogs and cats
How to diagnosis IMHA?
Need confirmation of immune targetting: spherocytes and autoagglutination
- Saline agg - 1:4
- Coombs test
- True agglutination - RBC washing
What are some possible causes of secondary IMHA?
Recent drugs/vaccs - zinc ingestion
infection - mycoplasma
neoplasia - splenic
foci of inflamm
Hypophosphataemia
Other therapies to speed up onset of remission
- Immunoglobulin therapy - distracts the microphages but also increases the rate of liver getting rid of antigens
- Splenectomy
- Plasmapheresis
Causes of IMHA deaths
- Takes 5 days for preds to kick in
- Thormboembolism - hyper-coagulable state (aspirin, clop, rovaroxaban)
- costs
What are 4 causes of neutropenia
- Consumption - most common, increased demand in peripheral tissues
- Neoplasia - consumption, myelopthisis (replacement of normal BM), inhibition of neutrophil production
- Drugs - any drug may trigger immune-mediated destruction
When to sample BM
- Staging neoplasia
- High degree of suspicion of BM pathology
- Unexplained syndromes
- Diagnosis of infection
Where to sample BM
- Humerus
- Wing of ileum
- Costo-chondral
- Head of femur
What are the patients that benefit from coagulation bloods - tests are sensitive not specific
- Bleeding from multiple sites - most likely systemic causes
- Bleeding without trauma
- Unexpected and excessive bleeding during minor surgery or routine spay
- Patients on drugs that affect clotting
- Breed variation
What is primary haemostasis?
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
What is secondary haemostasis?
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
How does the clotting cascade conclude?
Concludes with a series of reactions leading to the conversion of fibrinogen (soluble) to fibrin (insoluble) to the common pathway
