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Internal Medicine > Haematology > Flashcards

Haematology Flashcards

1
Q

Why would a regenerative anaemia appear non-regenerative?

A

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

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2
Q 
Reticulocyte counts for anaemia in the Cat
Negligible 26-46
Mild 20-25
Moderate 12-19
Substantial <11
A

<50
50-100
100-200
>200

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3
Q 
Dog reticulocyte counts
Negligible 35-55
Mild 25-34
Mod 15-24
Substantial <14
A

<60
100-150
200-300
400-500

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4
Q

Causes of hypophosphataemia

A

Diabetes Mellitus
Phosphate binding antacids
Hepatic lipidosis
Re-feeding syndrome

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5
Q

Causes of haemolytic anaemia

A

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

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6
Q

Non-regenerative anaemia DDx

A

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)

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7
Q

When may a Coombs test be positive?

A 
IMHA
Hyperglobulinaemia
Pancreatitis
Myelodysplastic syndromes 
Babesiosis
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8
Q

Pure red cell aplasia

A

Immune- mediated
Can be secondary to FeLV (if so it is invariably fatal)
Sometimes positive Coombs test

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9
Q

Aplastic anaemia

Causes

A 
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
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10
Q

Myelodysplastic syndrome(includes dysmyelopoeisis)
What type of anaemia is seen
Causes
Treatment

A

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

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11
Q

Myeloproliferative diseases

What is it and how is it categorised

A

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

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12
Q

Myelophthisis

What is it

A

Space occupying bone marrow lesion which displaces normal haematopoietic cells: neoplasia, leukaemia, myelofibrosis (myelofibrosis can be idiopathic or secondary to chronic bone marrow disease)

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13
Q

Blood film exam: wbc count, reticulocyte count and platelet count

A

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)

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14
Q

Thrombocytosis causes

A

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

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15
Q

Causes of platelet dysfunction

Decreased function

A 
Uraemia
Liver dz 
NSAIDs
Antibiotics: beta lactams 
Calcium channel
Blockers 
Infectious agents (e.canis, FeLV, yersinia pestis)
Toxins (snake venom)
Neoplasia
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16
Q

Causes of enhanced platelet function

A 
Diabetes mellitus
Nephrotic syndrome
Erythropoietin tx
Neoplasia
FIP
Heart worm
Allergy respiratory dz
17
Q

What is a prolonged buccal mucosal bleeding time?

Why might it be prolonged?

A

> 4 minutes

Thrombocytopenia
Platelet aggregation defects
VWD
Anaemia
Hyperproteinaemia

Rarely performed as non-specific and lack or predictive value for surgical bleeding

18
Q

Haemophilia A

Haemophilia B

What would you see on a coagulation profile and what clotting factors are affected

A

VIII

IX

Would see prolonged aPPT, normal PT and TCT

Usually males affected

19
Q

Findings associated with leukaemia

And diagnosis

A

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

20
Q 
Acute leukaemia
Acute lymphoblastic leukaemia (ALL)
Acute myeloid leukaemia (AML) 
Clinical features
Diagnosis
Treatment
Prognosis
A

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

21
Q

How to differentiate ALL from stage V lymphoma

A

Milder lymphadenopathy and more severe bone marrow infiltration resulting in more severe myelosuppression

Cd34 is expressed by cells in ALL but not lymphoma

22
Q

Clinical features of chronic leukaemia

A

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

23
Q

Chemotherapy for chronic leukaemia and myeloma

A

CLL - chlorambucil and prednisolone

CML - hydroxyurea and busulfan

Multiple myeloma - melphalan, prednisolone plus bisphosphonates if skeletal lesions present

Primary polycythaemia - hydroxyl real

24
Q 
Multiple myeloma (plasma cell proliferation)
Clinical features
A 
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

25
Q

Specific conditions associated with neutropaenia

A

Cyclic haemaotpoiesis (grey collies, border collies)

B12 malabsorption

Immune-mediated neutropaenia

Border collie neutropaenia

26
Q

Causes of CD8+ lymphocyte expansion

A

Malignancy

E. Canis

27
Q

Increases in urea:creatinine ratio

A

BABESIA
Dehydration
Haemolytic disease (ish)
GI bleeding

28
Q

Breed specific enzyme defects causing haemolysis

A

Phosphofructokinase deficiency in springer spaniels (dna test available)

Pyruvate kinase deficiency (eg beagle, basenji, Abyssinian and Somali cats)

29
Q

Treatment of IMHA

A

Immunosuppression
May require transfusions
Anticoagulant therapy

30
Q

Risk factors for thrombus formation

A 
Steroids
Sepsis
PLN
PLE
IMHA
pancreatitis
Nonovert DIC
Neoplasia

Internal Medicine (11 decks)

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