Haematology Flashcards
Why would a regenerative anaemia appear non-regenerative?
Chronic blood loss - iron deficiency (kitten with fleas)
Concurrent disease can impair regen response (FeLV, Cat flu etc)
FeLV can cause macrocyclic anaemia although it is non-regen. So can myelodysplastic syndrome
Reticulocyte counts for anaemia in the Cat Negligible 26-46 Mild 20-25 Moderate 12-19 Substantial <11
<50
50-100
100-200
>200
Dog reticulocyte counts Negligible 35-55 Mild 25-34 Mod 15-24 Substantial <14
<60
100-150
200-300
400-500
Causes of hypophosphataemia
Diabetes Mellitus
Phosphate binding antacids
Hepatic lipidosis
Re-feeding syndrome
Causes of haemolytic anaemia
Primary IMHA
Secondary imha (FeLV, mycoplasma, babesia, ehrlichia, Anaplasma, zinc, neoplasia eg lymphoma, drugs eg TMPS, blood transfusion reactions and neonatal isoerythrolysis
Infections: FeLV, mycoplasma, babesia, cytauxzoonosis
Oxidant injury: onions, garlic, paracetamol, zinc, propylene glycol
Hypophosphataemia (<0.35mmol/l)
Microangiopathic haemolytic anaemia (schistocytes)
Inherited RBC defects: osmotic fragility syndrome and pyruvate kinase deficiency in Abyssinian and Somali cats
Animal venom
Histiocytic disease
Non-regenerative anaemia DDx
Drug induced
Toxins eg Lead
Secondary to chronic disease (Addison’s, hypothyroidism, liver, renal, neoplasia)
Infectious disease (FeLV, FIV, FIP, mycoplasma, leishmania, babesia)
Pure red cell Aplasia
Aplastic anaemia
Dysmyelopoiesis
Myelonecrosis
Myleophthisis (neoplasia - lymphoma, leukaemia, multiple myeloma, malignant histiocytosis)
Inflammatory bone marrow disorders (FIP, immune-mediated, Sepsis)
When may a Coombs test be positive?
IMHA Hyperglobulinaemia Pancreatitis Myelodysplastic syndromes Babesiosis
Pure red cell aplasia
Immune- mediated
Can be secondary to FeLV (if so it is invariably fatal)
Sometimes positive Coombs test
Aplastic anaemia
Causes
Bi/pancytopaenia Bone marrow 95% adipose tissue Causes: FeLV, FIV, late stage CKD, FIP, parvo, ehrlichiosis, Toxoplasmosis, starvation. Drugs: methimazole, griseofulvin, oestrogen and some chemotherapy agents Sometimes idiopathic Grave prognosis if no underlying cause
Myelodysplastic syndrome(includes dysmyelopoeisis)
What type of anaemia is seen
Causes
Treatment
Maturation defects in one or more cell lines
See macrocytosis in the blood
Can be associated with FeLV
Many of these go on to develop leukaemia
Treatment: cytosine arabinoside (differentiating agent), anabolic steroids or haematopoeitic growth factors
Prognosis: poor - a matter of weeks if FeLV positive
Dysmyelooeisis is the same but secondary to something else eg IMHA, pyometra, cytotoxic drugs, myeloma, drugs etc
Myeloproliferative diseases
What is it and how is it categorised
Abnormal production of any marrow precursors typically due to neoplasia
Acute: >30% blast cells
Chronic <30% blast cells
Tx: chemo, blood transfusion if severe anaemia, antibiotics if neutropaenic
Prognosis: poor for acute better for chronic
Myelophthisis
What is it
Space occupying bone marrow lesion which displaces normal haematopoietic cells: neoplasia, leukaemia, myelofibrosis (myelofibrosis can be idiopathic or secondary to chronic bone marrow disease)
Blood film exam: wbc count, reticulocyte count and platelet count
1) no. Of WBCs p 40x field x2000
2) no. Platelets per 100x oil field x 20,000
(<2 = very low, 2-5 = low, 5-25 adequate, 25-50 increased >50 marked increase
3) % reticulocytes In 500-1000 rbcs on smear x rbc count (x10^12/L) (use aggregate reticulocytes in cats)
Thrombocytosis causes
Physiologic: mobilisation of splenic and pulmonary platelet pools
Catecholamine
Exercise
Post-splenectomy (resolves 6 weeks)
Drugs: steroids, vincristine, cyclosporine, Miconazole, epinephrine
Reactive/secondary: inflammatory/infectious, neoplasia, GI dz, endocrine, iron deficiency anaemia
Essential: myeloproliferative disorder - diagnosis of exclusion and support
Causes of platelet dysfunction
Decreased function
Uraemia Liver dz NSAIDs Antibiotics: beta lactams Calcium channel Blockers Infectious agents (e.canis, FeLV, yersinia pestis) Toxins (snake venom) Neoplasia
Causes of enhanced platelet function
Diabetes mellitus Nephrotic syndrome Erythropoietin tx Neoplasia FIP Heart worm Allergy respiratory dz
What is a prolonged buccal mucosal bleeding time?
Why might it be prolonged?
> 4 minutes
Thrombocytopenia Platelet aggregation defects VWD Anaemia Hyperproteinaemia
Rarely performed as non-specific and lack or predictive value for surgical bleeding
Haemophilia A
Haemophilia B
What would you see on a coagulation profile and what clotting factors are affected
VIII
IX
Would see prolonged aPPT, normal PT and TCT
Usually males affected
Findings associated with leukaemia
And diagnosis
Anaemia, neutropaenia, thrombocytopenia, leukocytosis, cells with abnormal morphology
Hypercalcaemia Hyperglogulinaemia Renal failure Liver failure Low USG and UTIs DIC
Bone marrow to confirm diagnosis and immunophenotyping to classify leukaemia
Acute leukaemia Acute lymphoblastic leukaemia (ALL) Acute myeloid leukaemia (AML) Clinical features Diagnosis Treatment Prognosis
2/3 cats with ALL are FeLV +ve
AML more aggressive than ALL
In ALL blast cells infiltrate organs - liver and spleen
Sepsis and uncontrolled haemorrhage due to DIC are common with AML
Do >30% blast cells in the bone marrow and similar in the blood
Can differentiate the two with immunophenotyping (and cytochemical stains like myeloperoxidase)
Tx: ALL standard lymphoma protocols
AML cytosine arabinoside and anthracyclines
Poor prognosis mean survival if going into remission is around 2 months
How to differentiate ALL from stage V lymphoma
Milder lymphadenopathy and more severe bone marrow infiltration resulting in more severe myelosuppression
Cd34 is expressed by cells in ALL but not lymphoma
Clinical features of chronic leukaemia
50% are asymptomatic
Males more commonly affected
Change from mature cell to blast cell (blast cell crisis) can occur with CML but not CLL giving it a poorer prognosis
Lethargy, anorexia, PUPD, pyrexia, weight loss, vomiting
Myelosuppression - milder than acute leukaemia
Secondary infections
Monoclonal gammopathy In 25% of cases with CLL
Mild lymphadenopathy
Infiltration of organs
Hyperviscosity syndrome
Dx CLL > 30% small lymphocytes in the bone marrow and blood
CML is characterised by marked neutrophilia often with a severe left shift. Hepatosplenomegaly. Need to exclude all causes of infection/inflammation, demonstrate granulopoeisis in the spleen/liver and essence of dysplastic maturation. Toxic changes in neutrophils suggest a leukaemoid reaction. Cytochemical staining and glow cytomeyry not useful in differentiating leukaemia from leukaemoid reactions
Chemotherapy for chronic leukaemia and myeloma
CLL - chlorambucil and prednisolone
CML - hydroxyurea and busulfan
Multiple myeloma - melphalan, prednisolone plus bisphosphonates if skeletal lesions present
Primary polycythaemia - hydroxyl real
Multiple myeloma (plasma cell proliferation) Clinical features
Bence Jones proteinuria Monoclonal gammopathy Cytopaenia Pyrexia Skeletal lesions Hypercalcaemia 15-20% cases Renal dz Hyperviscosity Immunicompromise (immune cripples) Bleeding Sepsis Vasculopathy
Prognosis guarded - survivals of 12-18 months could be achieved if responding to tx
Specific conditions associated with neutropaenia
Cyclic haemaotpoiesis (grey collies, border collies)
B12 malabsorption
Immune-mediated neutropaenia
Border collie neutropaenia
Causes of CD8+ lymphocyte expansion
Malignancy
E. Canis
Increases in urea:creatinine ratio
BABESIA
Dehydration
Haemolytic disease (ish)
GI bleeding
Breed specific enzyme defects causing haemolysis
Phosphofructokinase deficiency in springer spaniels (dna test available)
Pyruvate kinase deficiency (eg beagle, basenji, Abyssinian and Somali cats)
Treatment of IMHA
Immunosuppression
May require transfusions
Anticoagulant therapy
Risk factors for thrombus formation
Steroids Sepsis PLN PLE IMHA pancreatitis Nonovert DIC Neoplasia
