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Ettinger > Haematology and immune mediated disease > Flashcards

Haematology and immune mediated disease Flashcards

1
Q

What is the difference between petechiae and ecchymoses?

A

Petechiae - <3mm, capillary bleeding

Ecchymoses - larger, small arteriole bleeding

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2
Q

Causes of thrombocytopenia

A

Increased destruction, consumption, sequestration

Reduced production

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3
Q

Coagulation abnormalities in DIC

A

Initially hypercoagulable, progresses to consumptive coagulopathy

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4
Q

Causes of increased platelet consumption

A

DIC

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5
Q

Causes of platelet sequestration

A

Hepatomegaly, splenomegaly, hypotension, hypothermia, endotoxaemia

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6
Q

Name some inherited thrombopathias and the breed association

A

Glanzmann’s - Great Pyrenees/Otter Hounds
Thrombopathia of Bassett Hounds and Spitz
Delta storage pool deficiency - American Cocker Spaniel

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7
Q

Causes of acquired thrombopathias

A

Infectious - rickettsial
Hepatic disease/uraemia
Neoplasia
Drugs - aspirin/clopidogrel, carprofen, hydroxylethyl starch solutions, omega-3 FA (in vitro only)

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8
Q

Likely cause of surface bleeding in patient with normal platelet number and function

A

Vascular disorder

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9
Q

Vascular disorders

A

Primary immune-mediated

Secondary to medications, infections, neoplasia

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10
Q

Normal BMBT (dogs and cats)

A

<4 mins (dogs)

<2 mins (cats)

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11
Q

Clinical signs of primary haemostat disorder

A

Petechiation, ecchymoses, mucosal bleeding, ocular haemorrhage, haematoma formation

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12
Q

Calculation for manual platelet count

A

Platelets/hpf x 15-20

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13
Q

What haematology findings are suggestive of increased platelet production?

A

Increased MPV, PDW, reticulated platelets

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14
Q

What is the general pathogenesis of most immune-mediated haematological diseases (Th-1/Th-2)

A

Th-2 (antibody-mediated)

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15
Q

What are the mechanisms through which immunosuppressive medication act to reduce immune-mediated disease?

A

1 - reduced production of antibody by lymphocytes

2 - suppressing clearance of opsonised cells by macrophages or complement

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16
Q 
Which antibody class is most associated with IMHA?
What is it's half-life?
A

IgG

7 days

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17
Q

How can platelet function be assessed?

A

Impedance whole blood aggregometry
Plasma-based light transmission aggregometry
Platelet function analysed (PFA-100)

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18
Q

Which PFA cartridge has the highest sensitivity for canine platelets?

A

Collagen/ADP

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19
Q

What is assessed by platelet aggregation?

A

Platelet number
Platelet function
vWF

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20
Q

Which pathway and factors are assessed by PT?

A

Extrinsic

FVII, X, V, II, I

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21
Q

What does an elevated PT with a normal aPTT indicate?

A

FVII deficiency

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22
Q

What pathways and factors are assessed by aPTT?

A

Contact pathway, intrinsic pathway, common pathway

Prekallikrein, FXII, FXI, FVIII, FIX, FX, FV, FII, FI

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23
Q

Which factors do not affect aPTT?

A

FVII and FXIII

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24
Q

Are PT/aPTT affected by heparin?

A

PT - no

aPTT - yes

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25
Q

What is a common clinically irrelevant incidental finding on coagulation testing in cats

A

Factor XII deficiency (prolonged aPTT, normal PT)

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26
Q

What conditions are associated with an elevated aPTT but normal PT?

A

Haemophilia (A, B, C), heparin, FXII def

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27
Q

What conditions are associated with elevated PT and aPTT?

A

Rodenticide toxicity, liver disease, DIC, hypo-/dysfibrinogenaemia

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28
Q

What is tested by the ACT?

A

All factors but VII and XIII

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29
Q

What are FDPs?

What does an elevation suggest?

A

Created when plasmin lyses fibrinogen, fibrin monomers, insoluble fibrin, cross-linked fibrin
Plasmin activity

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30
Q

What are D-dimers?
What does their elevation indicate?
What is their half life?

A

Form of FDP generated from cross-linked fibrin
Thrombin generation, fibrin formation, cross linking by FXIIIs and plasmin activity
Short half life (5h) - indicate recent fibrinolysis

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31
Q

How does altered PCV affect TEG analysis?

A

Higher hct - hypo coagulable tracing

Lower hct - hyper coagulable tracing

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32
Q

What is assessed by a calibrated automated thrombogram (CAT)?

A

The ability to generate thrombin in real time in-vitro in response to a specific stimulus
Used with platelet-poor or platelet-rich plasma

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33
Q

Virchow’s triad

A

Vascular stasis
Increased coagulability
Disruption or activation of vascular endothelium

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34
Q

By how much does a clotting factor need to be reduced to elevate PT/aPTT

A

30-50%

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35
Q

List acquired hyper coagulable states

A 
IMHA
Cardiac disease (HCM, endocarditis, dirofilaria)
PLE
PLN
Neoplasia
Endocrine dz (HAC, hypoT, DM)
Prednisolone
Inflammation/Sepsis
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36
Q

List acquired hypo coagulable states

A

Vit K deficiency - rodenticide
Hepatic failure
DIC
Factor VIII and IX inhibitory antibodies as consequence of multiple transfusions in haemophilia

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37
Q

Vit K dependent coagulation factors?

A

II, VII, IX, X

Protein C+S

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38
Q

How to anticoagulant rodenticides cause bleeding?

A

Inhibit vitK epoxide reductase - reduced vita essential for carboxylation of glutamic acid residues on coagulation factors

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39
Q

How soon after rodenticide ingestion is bleeding typically observed?

A

2-5 days

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40
Q

What can be measured to indicate rodenticide ingestion?

A

PIVKA - elevates within 12 hours of ingestion

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41
Q

What is the primary mediator of DIC?

A

Tissue factor

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42
Q

What are the risk factors for DIC development?

A

Prolonged hypotension
SIRS
Disturbed blood flow to major organ
Major tissue trauma

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43
Q

What has been associated with Increased mortality in dogs with DIC?

A

High D-dimer, low antithrombin, hypo coagulable TEG trace

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44
Q

Are the following indicated in DIC;

  • Heparin
  • Plasma
A

Heparin - no

Plasma - if active bleeding

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45
Q

Labile clotting factors?

A

V and VIII

46
Q 
Scott syndrome
Breed
Inheritance
Signs
Cause
Test
A

GSD
Autosomal recessive
Epistaxis, soft tissue haemorrhage, surgical haemorrhage
Defect in procoagulant activity on platelet surface
Prothrombin consumption assay

47
Q 
Haemophilia - factor deficiency?
Signs
Test
Grading
Prognosis
A 
A - VIII
B - IX
Prolonged bleeding, haematoma formation, mucosal bleeding, haemarthrosis
Prolonged aPTT/ACT, normal PT
Measurement of factor activity
Mild - 6-20%
Moderate - 2-5%
Severe - <2%
Variable
48
Q

Where does erythropoiesis occur in:

a) The foetus
b) Normal Adult
c) Anaemic adult

A

a) BM and liver
b) BM
c) BM, liver and spleen (EMH)

49
Q

How long does it take for red blood cells to mature and be released from the bone marrow?

A

5-7 days

50
Q

Describe cat’s reticulocytes

A

Aggregate reticulocytes develop into punctate reticulocytes, then remain in circulation for 2-3 weeks

51
Q

How is the corrected reticulocyte count calculated? When is it useful?

A

CRC = (reticulocyte count x hct)/normal hct

RC normally expressed as % of circulating RBCs, may falsely elevate in anaemia

52
Q

How long does it take for reticulocytosis to develop after haemorrhage/haemolysis?

A

2-5 days

53
Q

Ddx for erythrocyte destruction

A

Non-immune haemolytic anaemia (intoxication, infection, red cell fragmentation syndrome, hereditary, hypophosphataemia (C))
Haemophagocytic anaemia
IMHA (associative/non-associative)

54
Q

What is the mechanism of hypophosphataemia causing haemolysis?

A

Inhibition of ATP production

Leads to decreased membrane stability, increased osmotic fragility, susceptibility to oxidative stress and haemolysis

55
Q

Name 3 infections associated with haemolysis

A

Babesia
Haemoplasmosis
Feline cytauxzoonosis

56
Q

Name 3 red cell fragmentation syndromes

A

Microangiopathic haemolytic anaemia - HSA, other neoplasia, CHF, glomerulonephritis, myelofibrosis
Haemolytic uraemia syndrome - renal arterial/arteriolar endothelial lesions induce local thrombi
DIC

57
Q

What are the hereditary haemolytic anaemias? What are their mechanisms?

A

Pyruvate kinase deficiency and phosphofructokinase deficiency - impaired erythrocyte energy metabolism

Stomatocytosis - genetic membrane disorder

58
Q 
Pyruvate kinase deficiency
Species
Inheritance
Clinical presentation
Age at diagnosis
A

Dogs and cats
Autosomal recessive
Varying degree of regenerative anaemia. Progressive iron overload => haemosiderosis and liver fibrosis.
Dogs (not cats) develop progressive myelofibrosis and sclerosis
Dogs young, cats old

59
Q

Phosphofructokinase deficiency
Species
Inheritance
Clinical presentation

A

Dogs only
Autosomal recessive
Some have no clinical signs, most have persistent haemolytic anaemia exacerbated by sporadic haemolytic crises secondary to exercise-induced hyperventilation alkalaemia

60
Q

Haemophagocytic anaemia

Breed predispositions

A

Bernese Mountain Dog, Rottweiler, Golden Retriever, Flat Coat

61
Q

Haemophagocytic anaemia

Pathogenesis

A

Sub-group of histiocytic sarcoma derived from macrophages. Demonstrate infiltrative growth in liver, spleen, lung and BM

62
Q

Haemophagocytic anaemia

Clinical signs

A

Vague
Most have hepatosplenomegaly
Moderate-severe anaemia with abundant reticulocytosis

63
Q

Haemophagocytic anaemia

Diagnosis

A

Demonstration of histiocytes containing RBCs or haemosiderin deposits
Immunophenotyping CD11/CD18

64
Q

Haemophagocytic anaemia

Prognosis

A

MST 4 weeks

65
Q

When does feline alloimmune haemolysis occur?

A

When type A/AB cat receives type B colostrum

66
Q

What genetic mutation has been associated with polycythaemia vera in humans and dogs?

A

JAK2

67
Q

What other haematological abnormality is described in cats with primary polycythaemia?

A

Thrombocytosis

68
Q

What are the pathways for erythrocytosis?

A

Renal hypoxia => hypoxia inducible factor => erythropoietin (cortical fibroblasts)
Thyroid hormone => increased proliferation of erythroid progenitor cells
=> increased hypoxia induced EPO production
Glucocorticoids - synergise with HIF - form burst forming units - erythroid cells capable of self renewal
Growth factor - directly stimulates erythropoiesis

69
Q

Which 2 endocrine conditions are associated with erythrocytosis?

A

Hyperthyroidism

Hyperadrenocorticism

70
Q

What are the ddx for erythrocytosis

A

Physiological
Primary
Secondary - physiologically appropriate
(R=>L shunt, PDA, TOF, pulmonary disease)
- physiologically inappropriate (renal hypoxia/aberrant EPO production)

71
Q

What are the clinical signs of erythrocytosis?

A

Hypervolaemia - ocular - engorged retinal vessels, uveitis, retinal detachment, glaucoma
- engorged mucous membranes
Hyperviscosity - CNS - weakness, ataxia, seizures
Haemorrhage
PUPD
V/D

72
Q

What ABG findings are consistent with a physiologically appropriate secondary erythrocytosis?

A

Arterial O2 sat <92%

73
Q

What medical treatments have been described for primary erythrocytosis?

A

Hydroxyurea
Chlorambucil (humans only)
Radiophosphorus

74
Q

What are the possible complications with phlebotomy?

A

Iron deficiency

Hypoproteinaemia => oedema

75
Q

What are the three components of primary haemostats?

A

Platelets
VWF
Vessel wall

76
Q

Describe platelet development

A

Megakaryocyte precursor cells form platelet-specific organelles and surface proteins
Develop large pseudopodia, stretch to form pro-platelet processes
Platelet organelles move to end of pro platelet
Branch and constrict - beaded appearance
Proplatelets break away from megakaryocyte and fragment into platelets

77
Q

What is the lifespan of a platelet in the circulation?

A

6-10 days

78
Q

Describe platelet activation

A

Triggered by injury to vessel

Platelets transform into adhesive spiny spheres - recognise and bind sub endothelial matrix

79
Q

What are coated platelets?

A

Subset of collagen and thrombin-activated platelets
Scramble phosphatidylserine from inner membrane to outer - release PS micro-particles - act as scaffold for tens assembly

80
Q

What substances antagonise platelet receptors and dampen platelet reactivity?

A

Prostacyclin, PGE2, PGD2

81
Q

What is the most abundant platelet integrin receptor? What is it’s function

A

Alpha-IIb-beta-3 complex (GPIIb/IIIa)

Activation-dependent receptor for fibrinogen, fibronetin, vWF

82
Q

What autoantibody target has been identified in fogs with ITP?

A

GPIIb/IIIa

83
Q

Which drugs have been implicated in development of ITP?

A

Sulphonamides, cephalosporins

84
Q

What infectious agents have been implicated in 2ndry ITP?

A

Anaplasma phagocytophilum, Babesia sp, Ehrlichia Canis, Leptospira sp, Leishmania infantum

85
Q

What conditions have been associated with platelet-bound antibodies in dogs?

A

Lymphoma, HSA, histolytic sarcoma

Chronic hepatitis, pancreatitis, SIRS

86
Q

What are the mechanisms by which neoplasia causes thrombocytopenia?

A

Consumption (bleeding/DIC), sequestration, myelopthisis, platelet bound antibodies

87
Q

How can a diagnosis of ITP be further supported? What are the limitations of the test?

A

Flow cytometric assay for platelet-bound antibody
Sensitive but not specific
Increase in stored samples

88
Q

For which agent is there evidence as a sole agent in ITP?

A

MMF

89
Q

What are the recognised types of vWD?

What are their characteristics?

A

Type I - low VWF concentration, full array of multimers, mild-moderate bleeding
Type II - variable reduction in VWF concentration, absence of high molecular weight multimers, moderate-severe bleeding
Type III - complete absence of VWF - severe bleeding

90
Q

Which breeds are associated with type I VWD?

A

BMD, Corgi ,Coton de Tulear, Doberman, Dutch Partridge dog, German Pinscher, Goldendoodle, Irish Setter, Kerry Blue Terrier, Manchester Terrier, Papillon, Poodle, Stabyhound, WHWT

91
Q

Which breeds are associated with type II VWD?

A

GSHP, GWHP

92
Q

Which breeds are associated with type III VWD?

A

Dutch Kooiker, Scottish Terrier, Shetland Sheepdog

93
Q

What laboratory assessments of VWF are available?

A

VWF:Ag (ELISA)
DNA testing
Qualitative assay - WWF:collagen-blinding assay

94
Q

How is VWF:Ag interpreted?

What factors can alter it?

A 
Normal - 70-180%
Boderline - 50-69%
Abnormal - 0-49%
Decrease - haemolysis
Increase - ill - inflammatory/septic, pregnancy
95
Q

What are the modes of inheritance for VWD

A

Type I - autosomal dominant or recessive
Type II - autosomal recessive
Type III - autosomal recessive

96
Q

How are qualitative VWF assays (CBA) interpreted?

A 
Used to diagnose type II VWD
Assesses binding to collagen type I/III - dependent on high molecular weight multimers
Reported as ratio of VWF:CBA to VWF:Ag
1 = normal
2 = Type II VWD
97
Q

When should VWD be treated?

A

Type II and III - bleeding inevitable
Type I - phenotype variable
Aim to control spontaneous/trauma-related bleeding

98
Q

What are the treatment options for VWD?

A

Desmopressin - 30 mins before surgery or SID
Blood component - FWB, FFP, CRYO
Cryo ideal - 1 unit/10kg, ever 8-12 hours

99
Q

What is the half life of plasma VWF?

A

12 hours

100
Q

What is the evidence for DDAVP use in dogs with Type I VWD? Effect on VWF:Ag?

A

Raises plasma VWF concentration from 10 => 17%
Improved haemostat function (PFA-100)
Shortened BMBT

101
Q

What are the risks of DDAVP treatment of VWF, particularly at high doses?

A

Water retention and hyponatraemia
Tachyphylaxis
Failure to stimulate VWF release from Weibel-palade bodies with repeat administration

102
Q

What has been associated with acquired VWD in dogs?

A

MMVD and sub aortic stenosis (CKCS)
Following tetrastarch bolus
Angiostrongylus (case report)

103
Q

What type of VWD has been reported in cats?

A

Type III

104
Q

List some hereditary platelet dysfunctions

A

Glanzmann thrombasthenia
Calcium-diacylglycerol guanine exchange factor thombopathia (Basset thrombopathia)
Platelet procoagulant deficiency (Scott syndrome)

105
Q

What tests are available for the diagnosis of Scott syndrome?

A

Flow cytometry

DNA testing

106
Q

What acquired platelet dysfunctions have been recognised in dogs?

A

Uraemia, hepatobiliary disease, paraproteinaemia

107
Q

What anti-platelet medications are available and what are their mechanisms?

A

Aspirin - irreversible cyclooxygenase inhibitor

Clopidogrel - P2Y12 ADP receptor antagonist

108
Q

What congenital WBC disorders are described in dogs/cats?

A 
Chediak-Higashi Syndrome
Pelger-Huet Anomaly
LAD
Trapped neutrophil syndrome
Pyruvate kinase deficiency
X-linked SCI
Autosomal recessive SCI
Cyclic haematopoiesis of grey collies
Common variable immunodeficiency
Lysosomal storage disease
109
Q

What secondary WBC disorders are described?

A 
Immune-mediated neutropaenia
Primary MDS
Secondary MDS
Secondary dysmyelopoiesis
Myeloproliferative disease
Myelopthisis
Myelotoxicosis
Viral - parvo/distemper/FeLV/FIV/FIP
Rickettsial/fungal
110
Q

What are the causes of immune-mediated neutropaenia?

A

Primary
Secondary - tick-borne
- drugs (phb, cephalosporins)

111
Q

How is primary immune-mediated neutropenia diagnosed?

A

Exclude other causes - overwhelming demand, reduced production (haemic neoplasia), drug-induced, sequestration (splenomegaly)
Flow cytometry (anti-neutrophil ABs) described
Rapid response to immunosuppression

112
Q

What are the features of MDS?

A

Non-regen anaemia or multiple cytopaenias
Normal/hypercellular BM
BM - increased immature precursors, increased dysplastic cells, megaloblasts and erythroid precursors
Blast cells <30% nucleated cells
Lack of increased myeloid cells

Ettinger (13 decks)

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