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ACVIM: SAIM Specialty boards study 2023 > General hematology > Flashcards

General hematology Flashcards

1
Q

What factors are associated with the development of hospital-acquired anemia?

A

Cumulative phlebotomy >3% total blood volume
Surgery (OR 10)

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2
Q

Deficiencies in what ATP generation pathway lead to hemolytic anemia in dogs and cat? Why?

A

Anaerobic glycolysis - RBCs lack a mitochondria and rely on anaerobic glycolysis to produce ATP

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3
Q

What is the role of pyruvate kinase in anaerobic glycolysis?

A

Catalyzes the conversion of phosphoenolpyruvate to pyruvate, thus generating one ATP molecule

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4
Q

How is pyruvate kinase deficiency inherited?

A

Autosomal recessive - heterozygous dogs show no clinical signs, homozygous affected

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5
Q

Describe the clinical presentation in dogs with pyruvate kinase deficiency

A
  • Chronic, low grade hemolysis rather an an acute presentation
  • Icterus is rare, but will present with signs of anemia
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6
Q

Describe the anemia present in dogs with pyruvate kinase deficiency

A
  • Moderate to severe anemia (median HCT 21%)
  • Regenerative (high retic counts - average 500,000 to 1,500,000)
  • Macrocytic, hypochromic
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7
Q

Why do dogs with pyruvate kinase deficiency have normal to increased PK activity on testing?

A

The erythrocytes of affected dogs lack the normal, adult R isozyme of PK but have persistence of the M2 isoform normally found in fetal tissue and precursor cells - causes the total RBC PK activity to seem normal

M2 form NOT found in cats - PK activity will be decreased

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8
Q

Erythrocytes in dogs with pyruvate kinase deficiency have increased concentrations of what molecule?

A

2,3-diphosphoglycerate (2,3-DPG)

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9
Q

What is the function of 2,3-DPG?

A

Binds to deoxygemoglobin and facilitates oxygen release from hemoglobin

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10
Q

What is the consequence of increased 2,3-DPG in dogs with pyruvate kinase deficiency?

A

Lower blood oxygen affinity compared to normal dogs - promotes oxygen delivery to the tissues and helps compensate for anemia (decreases clinical signs)

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11
Q

What other organs are affected by pyruvate kinase deficiency?

A

Liver - hemosiderosis and fibrosis develop due to progressive iron overload

Bone - myelofirbosis and osteosclerosis also likely due to damage from iron overload or chronic EPO stimulation

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12
Q

What is the expected lifespan of dogs with pyruvate kinase deficiency?

A

1-5 years, typically die of bone marrow or liver failure

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13
Q

What is the role of phosphofructokinase in glycolysis?

A

Converts fructose-6-phosphate to fructose 1,6-diphosphate

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14
Q

The PFK isoform found in RBCs is found in what other tissue?

A

Skeletal muscle (M type PFK)

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15
Q

How is PFK deficiency inherited and what breeds are affected?

A

Autosomal recessive
Usually spaniels (English Springer, Cocker Spaniels, German Spaniels)

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16
Q

What is the 2,3-DPG concentration in dogs with PFK deficiency?

A

Low - 2,3-DPG is formed after the PFK reaction

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17
Q

What is the consequence of decreased 2,3-DPG in dogs with PFK deficiency?

A

Increased oxygen affinity for hemoglobin leads to tissue hypoxia => erythropoiesis and reticulocytosis, even if anemia isn’t present

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18
Q

How do dogs with PFK deficiency present?

A
  • Persistent, low grade, compensated anemia with sporadic episodes of intravascular hemolysis and hemoglobinuria, especially with exercise
  • Hyperbilirubinemia (always in males, sometimes in females)
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19
Q

What are the clinical signs of an acute hemolytic crisis from PFK deficiency?

A

Lethargy, weakness, pale or icteric MM, fever

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20
Q

What other clinicopathologic abnormalities may be seen in dogs with PFK deficiency?

A

Elevated bilirubin, iron, ferritin, ALP, and CK (twice healthy dogs)

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21
Q

Why does a hemolytic crisis occur in dogs with PFK deficiency?

A

Secondary to hyperventilation-induced alkalemia - due to a lack of 2,3-DPG (the major anion in RBCs), the RBCs are very alkaline-fragile

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22
Q

What is the prognosis of dogs with PFK deficiency?

A

Can have normal lifespans - avoid strenuous exercise, excitement or high temps that cause hyperventilation and crisis

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23
Q

What genetic mutation can cause methemoglobinemia in cats and dogs?

A

Cytochrome B5 reductase

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24
Q

What causes methemoglobinemia?

A

Hemoglobin with a ferric iron (Fe3+) instead of ferrous iron (Fe2+) - ferric iron cannot carry oxygen

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25
Q

Cyanosis is noted when the methemoglobin fraction of the blood is greater than what percent? What percent is fatal?

A

Cyanosis: >15%
Fatal: >70%

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26
Q

What is the methemoglobin spot test?

A

Dark blood is exposed to air - with methemoglobin, it does not turn red (where it will with other causes of cyanosis)

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27
Q

In the cat, what causes oxygen release from hemoglobin?

A

Chloride - not 2,3-DPG like in the dog

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28
Q

What are the most common presenting signs in cats with primary erythrocytosis?

A

Seizures, mentation changes

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29
Q

In cats with lymphocytosis, expansion of B cell and heterogenous phenotypes were more consistent with what diagnosis and presentation?

A
  • Non-neoplastic disease
  • Polyclonal antigen receptors
  • Younger age
  • Lower lymphocyte counts
  • Prolonged survival
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30
Q

In cats with lymphocytosis, what were the most common neoplastic lymphocytes on flow cytometry?

A

CD4+

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31
Q

In cats with lymphocytosis of neoplastic origin, what was the survival of cats with CD4+ vs CD8+ vs double negative lymphocytosis?

A

CD4+ = prolonged survival 750 days
Double negative = 271 days
CD8+ = 27 days

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32
Q

What is the typical presentation of dogs with sterile, steroid responsive lymphadenopathy?

A

Young (3 years), female over-represented
Pyrexia, lethargy, and anorexia

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33
Q

How rapidly did dogs with sterile, steroid responsive lymphadenopathy improve with prednisone?

A

Rapidly - 12 to 48 hours in 96%

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34
Q

What breed is predisposed to idiopathic pyogranulomatous lymphadenitis?

A

English Springer Spaniel

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35
Q

Aspiration of splenic nodules revealed clinically important results (neoplasia or suppurative inflammation) in what percent of cases?

A

20%

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36
Q

What ultrasonographic findings were associated with clinically important cytologic findings on splenic ultrasound?

A

Splenic nodules 1-2cm in diameter, peritoneal fluid, >1 targetoid nodule

NOT associated: echogenicity, margins

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37
Q

What dog breed is more likely to be diagnosed with neoplasia when splenomegaly is observed (vs benign splenic changes)?

A

Wheatens

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38
Q

Is hemoperitoneum a predictor of splenic malignancy in small breed dogs?

A

No

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39
Q

Name 3 reasons to perform bone marrow sampling

A
  1. Unexplained hemic abnormalities on CBC (cytopenias, elevations in cell numbers, atypical morphology)
  2. Searching for occult disease/neoplasia (fever of unknown origin, hyperproteinemia, hypercalcemia)
  3. Cancer staging
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40
Q

What percent of dogs/cats develop complications from bone marrow sampling and what are the most common complications?

A

14% = pain most common, hematomas can rarely occur

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41
Q

When evaluating bone marrow, how many megakaryocytes should be present in a spicule?

A

2-7

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42
Q

When evaluating bone marrow, what percent of lymphocytes is normal?

A

<10% of nucleated cells

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43
Q

What is a normal M:E ratio in dog and cat bone marrow?

A

Dog: 0.9-1.8 : 1
Cats: 1.2-2.1 : 1

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44
Q

Name 2 causes of a decreased M:E ratio

A
  • Increased erythroid production without concurrent inflammation: hemolytic anemia
  • Decreased myeloid production: peripheral consumption of myeloid cells => depletion of maturation and storage pool
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45
Q

Name 2 causes of an increased M:E ratio

A
  • Decreased erythroid production with normal or increased myeloid production: anemia of chronic disease, CKD
  • Increased myeloid production with normal erythroid numbers: inflammation
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46
Q

80% of the nucleated erythroid cells in the bone marrow should be what stages of development?

A

Rubricytes or metarubricytes

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47
Q

80% of the nucleated myeloid cells in the bone marrow should be what stages of development?

A

Metamyelocytes, bands, or segmented neutrophils

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48
Q

What is ineffective hematopoiesis?

A
  • Death or destruction of hematopoietic cells within the marrow - mature cells are not released into circulation
  • Hypercellular marrow with concurrent peripheral cytopenia
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49
Q

What stain is used to assess iron stores in bone marrow?

A

Prussian Blue - better to directly stain slides, as destaining and then restraining with Prussian Blue underestimates iron stores

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50
Q

What flow cytometry maker identifies monocytes?

A

CD14, CD172a

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51
Q

What flow cytometry maker identifies B cells?

A

CD19, CD20, CD79a = all B lymphocytes
CD21 = mature B lymphocytes

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52
Q

What flow cytometry maker identifies hematopoietic stem cells?

A

CD34

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53
Q

What bone marrow changes may be seen with acute bone marrow injury?

A

Neutrophilic inflammation, myelonecrosis, hypo-aplasia, or dysmyelopoiesis

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54
Q

Name 2 drugs that cause dose-dependent myelotoxicity

A

Chemotherapeutics
Cephalosporins
Estrogen

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55
Q

Name 3 drugs that cause idiosyncratic myelotoxicity

A

Sulfonamides, chloramphenicol, griseofulvin, antiparasitics

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56
Q

What hormone is secreted by Sertoli cell tumors?

A

Estrogen (70% are functional)

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57
Q

Bone marrow is considered one of the most sensitive tissues to sample for the diagnosis of what infectious agent?

A

Leishmania

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58
Q

What histopathologic changes can be seen with chronic bone marrow injury?

A

Chronic inflammation, myelofibrosis, osteosclerosis, and/or gelatinous transformation

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59
Q

What is the most common cell type noted in the bone marrow of cats with chronic inflammation? In dogs?

A

Cats: Benign lymphocytosis - usually aggregates of B cells
Dogs: Plasmacytosis

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60
Q

Bone marrow plasmacytosis has been noted with what two infectious diseases in dogs?

A

Ehrlich canis, Leishmania

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61
Q

What is the definition of myelofibrosis?

A

Proliferation of fibroblasts, collagen, or reticulin fibers in the hematopoietic space

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62
Q

What causes primary myelofibrosis?

A

Clonal myeloproliferative neoplasms - in humans, often secondary to mutations in JAK2, CALR, or MPL

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63
Q

What causes secondary myelofibrosis?

A

Likely a reactive change secondary to bone marrow injury and cytokine stimulation of fibroblasts

Associated with myelonecrosis, neoplasia, drugs, IMHA, irradiation, PK deficiency (dogs), FIP, CKD (cats)

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64
Q

What causes gelatinous transformation (aka serous atrophy of fat)?

A

Prolonged starvation or anorexia

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65
Q

What is myelodysplasia or dysmyelopoiesis?

A

Heterogenous group of bone marrow disorders characterized by abnormalities in precursor cell maturation => dysplastic changes and ineffective hematopoiesis

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66
Q

What is found on bone marrow histopathology on cases of myelodysplasia?

A
  • Peripheral cytopenia with hyper cellular marrow
  • Evidence of dysplastic changes to one or more cell lines
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67
Q

What causes primary myelodysplastic syndrome?

A

Clonal expansion of a defective pluripotent hematopoietic stem cell

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68
Q

What causes secondary myelodysplastic syndrome?

A

Still a clonal disorder but caused by exposure to gamma radiation, FeLV infection, or drug exposure

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69
Q

What causes cyclic hematopoiesis?

A

Impaired intracellular trafficking and misdirection of proteins to the membrane rather than granules => cyclic neutropenia with granulocytic hypoplasia in the bone marrow

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70
Q

What causes secondary dysmyelopoiesis?

A
  • NOT clonal (unlikely myelodysplasia)
  • Drug associated (vincristine, chloramphenicol, phenobarbital, estrogen, lead)
  • Disease associated (lymphoma, myeloma, IMHA, ITP, etc)
  • Iron or cobalamin associated
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71
Q

Where is the majority of the total body iron located?

A

Hemoglobin and myoglobin

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72
Q

Where can iron be stored in the body?

A

Within hepatocytes, within macrophages of the spleen, liver and bone marrow

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73
Q

What is hemosiderin?

A

Partially degraded ferritin (less soluble)

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74
Q

What transporter is located on the apical surface of enterocytes and allows iron absorption from the gut?

A

DMT1

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75
Q

What regulates proteosomal-degredation of DMT1 and ferroportin?

A

Hepcidin - so when hepcidin concentrations are high, DMT1 and ferroportin are degraded and less iron is absorbed

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76
Q

What transporter is located on the basolateral membrane of enterocytes and allow iron to be absorbed from the enterocyte into the blood?

A

Ferroportin

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77
Q

What other cells express ferroportin? What is the effect of hepcidin on these cells?

A
  • Hepatocytes and macrophages - allows storage of iron
  • Hepcidin also causes decreased ferroportin on these cells => sequestration of iron
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78
Q

What factors cause increased hepcidin transcription (leading to decreased iron absorption and increased sequestration)?

A

High iron stores/plasma iron
Inflammation

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79
Q

What factors cause decreased hepcidin transcription (leading to increased iron absorption and decreased sequestration)?

A

Anemia, hypoxia, iron deficiency

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80
Q

Ferritin is usually considered an indicator of total body iron. However, what can increase ferritin levels?

A

Inflammation - acute phase protein
So iron deficient animals with significant inflammation may have “normal” ferritin

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81
Q

Do cats store iron in their bone marrow?

A

No - lack of hemosiderin staining is normal

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82
Q

What blood product could be used instead of fresh frozen plasma to treat vitamin K deficient/rodenticide?

A

Cryopoor plasma

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83
Q

What causes hemophilia A?

A

Factor VIII deficiency

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84
Q

Hemophilia A will result in prolongation of what clotting test?

A

aPTT
NOT PT

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85
Q

In dogs with heatstroke, what coagulation parameters were associated with outcome?

A

Prolonged PT, aPTT, total protein C activity, and low fibrinogen at 12-24 hours

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86
Q

In a clinical trial comparing lyophilized platelets vs cryopreserved platelets, which treatment had improved bleeding scores 1 hour after administration? At 24 hour?

A

Lyophilized platelets - improved DOGiBAT score at 1 hour
Both groups similar at 24 hours

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87
Q

What effect did twice daily Yunnan Baiyao have on TEG parameters in healthy dogs after one week?

A

Increased the strength of the clot - increased G, A30 and A60. Decreased LY30 and LY60

88
Q

On a TEG, what is the R values and what does it correspond to?

A

Initiation phase of a clot - reflects activity of factors 12, 11, 9, and 8

89
Q

On a TEG, what is the K value and what does it correspond to?

A

Amplification phase of a clot, clot formation time - influenced by factors II, VIII, platelet number, thrombin formation, fibrin concentrations

90
Q

On a TEG, what is the MA and what does it correspond to? What is the G value?

A

MA: Final clot strength - influenced by fibrin, fibrinogen concentrations, platelet numbers/function, thrombin, factor XIII

G: log derivative of MA

91
Q

In a clinical trial evaluating the use of Yunnan Baiyao on healthy cats, what effect did the drug have on TEG parameters?

A

None

92
Q

What were the side effects of Yunnan Baiyao in cats?

A

18% of cats - vomiting
Significant reduction in HCT and RBC count

93
Q

Compared to dogs receiving clopidogrel alone, dogs receiving clopidogrel and prednisone had what response?

A

Increased platelet dysfunction - over controlled based on AUC in aggregometry
- 11 times more likely to have an excessive response

94
Q

In a study comparing clopidogrel vs aspiring for dogs with PLN, what differences were noted on aggregometry?

A

Clopidogrel: aggregometry differed at all time points after ADP stimulation of platelets but not arachidonic acid stimulation (may be able to overcome ADP inhibition and activate platelets by other mechanisms)

Aspirin: no difference at any time point

95
Q

Low dose aspirin inhibits cyclosporine-induced synthesis of what platelet factor?

A

Thromboxane

96
Q

Does the use of cyclosporine alter the anti-platelet effects of aspirin?

A

No

97
Q

When given to cats, when is the peak effect of rivaroxaban?

A

3 hours post-administration

98
Q

In cats, plasma rivaroxaban concentration correlated with what coagulation parameters?

A

Prothrombin time and aXa

99
Q

In cats, how long did it take coagulation parameters to return to normal after stopping rivaroxaban therapy?

A

24 hours

100
Q

In dogs treated with rivaroxaban, what coagulation test correlated well with anti-Xa activity?

A

PT (r = 0.915 in one study, 0.82 in another) - may be a second line monitoring option if anti-Xa is not available

aPTT was ok (r = 0.77)

101
Q

In dogs treated with rivaroxaban, what coagulation test did not correlated well with anti-Xa activity?

A

Rapid TEG performed with strong activators in one study, but in another study R value did correlate

102
Q

In 4 patients with thrombosis (2 PTE and 2 systemic) treated with rivaroxaban, what happened to clot size?

A

Decreased thrombus size

103
Q

Did administering rivaroxaban with food, sucralfate, or omeprazole inhibit drug absorption?

A

Technically, rivaroxaban alone resulted in higher anti-Xa activity 36 hours after administration. But clinically, no difference

104
Q

What prolongation in PT is required to achieve therapeutic anti-Xa concentrations of rivaroxaban in healthy dogs?

A

1.5-1.9x delay in PT

105
Q

When diagnosing overt DIC in dogs, what DIC score yields a 73% sensitivity and 80% specificity for mortality and was accurate in 78% of cases?

A

A score of 3/6: increase PT, aPTT, or D dimers; decreased antithrombin, fibrinogen, and platelet count

106
Q

In cats, >90% of aortic thromboembolism are secondary to what?

A

Cardiac disease

107
Q

In dogs, what are the most common causes of aortic thromboembolism?

A

A wide variety of disease can cause it
- PLN most consistently diagnosed: 10-35%
- Cardiac disease 0-38%
- Neoplasia 0-33%

108
Q

What are the advantages of low molecular weight heparin over unfractionated heparin?

A
  • More reliable activity
  • Increased anti-Xa activity
  • Decreased binding to thrombin
109
Q

What is the mechanism of action of warfarin?

A

Inhibition of vitamin K epoxide reductase

110
Q

At low shear rates (as in venous flow), what is platelet adhesion to the vessel wall dependent on? At high shear rates (as in arterial flow)?

A

Low shear: dependent on fibrinogen
High shear: dependent on vWF

111
Q

Compare arterial and venous thrombi

A

Arterial: platelet rich
Venous: small numbers of platelets, large numbers of RBCs, WBC, and fibrin

112
Q

What are the clinical signs of dogs presenting for aortic thrombus?

A

Hind limb weakness most common (exercise intolerance to complete paraplegia)
Hind limb pain, decreased femoral pulses, decreased CP

Unlike cats, cold extremities and cyanosis uncommon
Often chronic signs rather than acute

113
Q

What is the mechanism of action of tissue plasminogen activator (TPA)?

A

Converts plasminogen to plasmin => fibrin degradation
More specific for fibrin-bound plasminogen and less likely to lead to systemic lytic states

114
Q

What does a shortened PT or aPTT correlate with?

A

Increased D dimer concentration, more thrombus formation, increased suspicion of PTE compared to dogs with normal PT and aPTT

May be indicative of a hypercoagulable state

115
Q

81% of dogs undergoing splenectomy developed thrombocytosis post-operatively. When did this occur?

A

Platelet count peaked at day 7 post-operatively (715K) and had decreased slightly by day 14 (580K)

116
Q

In dogs post-op for splenectomy, higher platelet counts correlated with what other coagulation test?

A

Thromboelastography - 89% of dogs were hypercoagulable on TEG at day 7

117
Q

In dogs with aortic thrombosis, what physical exam finding correlated with survival to discharge?

A

Ambulation status - non-ambulatory dogs less likely to survive

118
Q

What is the prognosis of dogs with aortic thrombus in Lynch’s JVIM study?

A

57% survived to discharge, but only 16% were alive at 180 days :(

119
Q

Studies evaluating dogs with acute pancreatitis have identified these dogs as hypercoagulable. What changes in coagulation have been noted?

A
  • Decreased thrombomodulin expression
  • Decreased antithrombin activity
  • Decreased fibrinolysis
120
Q

What form of pancreatitis may be more associated with thrombosis?

A

Acute necrotizing pancreatitis - consider anti-thrombotic for this population

121
Q

What effect does prednisone have on hemostasis in healthy dogs?

A
  • Increased coagulation factors and fibrinogen
  • Increased platelet aggregation
  • Increased clot strength
  • Increased thrombin generation
  • Reduced antithrombin
122
Q

What form of cancer is more associated with hypercoagulability in several studies?

A

Carcinoma

123
Q

In the CURATIVE guidelines, what diseases are considered high risk for thrombosis and should be treated with anti-thrombotics?

A
  • Dogs with IMHA, PLN
  • Cats with cardiomyopathy and left atrial dilation, spontaneous echo contrast, or reduced LA appendage flow rate
  • Dogs or cats with >1 disease/risk factor for thrombosis, including: pancreatitis, sepsis, hyperadrenocorticism, cancer, glucocorticoid administration
124
Q

In the CURATIVE guidelines, what conditions are considered low/moderate risk for thrombosis?

A
  • Dogs/cats with a single risk factor or disease
  • Dogs/cats with a known risk factor condition that, with treatment, is likely to resolve in days to weeks
125
Q

In cats with ATE, is treatment with aspirin or clopidogrel superior?

A

Clopidogrel - significantly prolonged survival time and time to a subsequent thrombotic event (75% recurrence of ATE with aspirin vs 36% with clopidogrel)

126
Q

What new anti-platelet agent blocks alphaIIb-beta3 integrin?

A

Abciximab, lotrafiban

127
Q

What is the mechanism of action of clopidogrel?

A

Irreversibly binds to the platelet ADP receptor, P2Y12 - reduces activation of the platelets by ADP, inhibits full activation of the GPIIb/IIIa complex

128
Q

The CURATIVE guidelines suggest that aspirin may be effective in what disease state? It is not recommended for what disease state?

A
  • May be effective in canine ATE
  • No evidence for or against canine venous thrombi
  • NOT recommended as a sole agent for feline ATE
129
Q

In patients receiving unfractionated heparin, what should the anti-Xa target be? For low molecular weight heparin?

A

Unfractionated: 0.35-0.7 U/mL
LMW: 0.5-1.0 U/mL 2-4 hours post dose

130
Q

Do unfractionated heparin, low molecular weight heparin, or oral anti-Xa agents need to be tapered prior to discontinuation? Why?

A

Unfractionated and oral anti-Xa - yes
LMW - no

Abrupt discontinuation can lead to “rebound hypercoagulability” caused by increased thrombin production

131
Q

What are eicosanoids?

A

Signaling molecules derived from oxidation of fatty acids

132
Q

What fatty acid is esterified in membrane phospholipids? This fatty acid is released from the membrane under inflammatory stimuli via what enzyme?

A

Arachiadonic acid
Released by phospholipase A2

133
Q

Arachidonic acid is then turned into what substances by COX1 and COX2 enzymes?

A

Prostanoids - prostaglandins, prostacyclins, and thromboxane

134
Q

Arachidonic acid is then turned into what substances by LOX enzymes?

A

Leukotrienes and lipoxins

135
Q

What drug blocks the actions of phospholipase A2, thus inhibiting the release of arachidonic acid from membranes in inflammation?

A

Corticosteroids

136
Q

How long does clopidogrel take to inhibit platelet activation? How long does inhibition last after stopping the drug?

A
  • Inhibition within 24 hours, consistent inhibition after 3 days
  • Persists for 5-10 days (irreversibly binds, so must generate new platelets that can be activated)
137
Q

What is the function of tissue factor pathway inhibitor?

A

Forms a complex with factors VIIa and Xa to inhibit these factors; expressed by the endothelium

138
Q

At rest, platelet membranes express neutral phospholipids on the outer surface (phosphatidylcholine). What enzyme maintains this?

A

Floppase (ATP dependent)

139
Q

At rest, procoagulant phospholipids are maintained on the inner surface of platelets (phosphatidylserine). What enzyme maintains this?

A

Flippase (ATP dependent)

140
Q

During coagulation and platelet activation, what enzyme results in expression of pro-coagulant phospholipids (phosphatidylserine) on the OUTER surface of the membrane?

A

Scramblase

141
Q

Name 3 pro-thrombotic effects of thrombin?

A
  • Strong activator of platelets
  • Catalyzes the conversion of fibrinogen to fibrin
  • Activates factor XIII, which is needed for cross linking fibrin in clots
142
Q

What are the 3 stages of coagulation in the cell based model?

A

Initiation, amplification, propagation

143
Q

What occurs in the initiation stage of coagulation?

A

Tissue factor bearing cells initiate thrombin production (similar to the extrinsic pathway)

144
Q

What occurs in the amplification stage of coagulation?

A

Platelet activation - membrane flipping, shape change, release of granules

145
Q

What occurs in the propagation stage of coagulation?

A

Similar to the intrinsic pathway - ongoing of production of thrombin and fibrin

146
Q

What is the most common presenting complaint of young male dogs with hemophilia A?

A
  • Lameness from hemarthrosis most common
  • Bleeding from vaccines, while teething, or at neuter also observed
147
Q

What clotting factor is deficient in hemophilia B?

A

Factor IX

148
Q

In both hemophilia A and B, what clotting tests will be prolonged?

A

aPTT and ACT - intrinsic pathway defect

149
Q

What blood products can be given to hemophilia patients to provide clotting factors?

A
  • Both - fresh frozen plasma
  • Known hemophilia A - can also use cryoprecipitate
  • Known hemophilia B - can also use frozen plasma or cry-poor plasma
150
Q

What disorders can be treated with fresh frozen plasma?

A
  • All hereditary or acquired coagulation factor deficiencies and vWF
  • Coagulopathy of trauma
151
Q

What disorders can be treated with cryoprecipitate?

A
  • Hemophilia A
  • vWD
  • Hypofibrinogenemia
152
Q

What disorders can be treated with cryo-poor precipitate?

A
  • Hemophilia B and deficiencies of II, VII, X, and XI
  • Vitamin K deficiency/antagonism
153
Q

What is a normal measurement of vWF:Ag? What is abnormal?

A

Normal: >70%
Abnormal: <49%
Grey zone in between

154
Q

What is Glanzmann thrombasthenia? What breeds does it occur in?

A
  • Absence or deficiency of the fibrinogen receptor GPIIb-IIIa
  • Otterhounds, Great Pyrenees
155
Q

What platelet disorder is present in up to 60% of Greater Swiss Mountain Dogs?

A

P2Y12 receptor disorder => impaired binding of ADP to the receptor

156
Q

What is Scott syndrome and what breed does it affect?

A

Impaired platelet membrane phosphatidylserine externalization and decreased prothrombinase activity
German Shepherds

157
Q

Do dogs have naturally occurring alloantibodies to blood types? Which blood types?

A

Yes
DEA 3 - 20%
DEA 5 - 10%
DEA 7 - 0-38%

158
Q

Are the naturally occurring alloantibodies to blood types in dogs clinically relevant?

A
  • Do not cause acute hemolytic transfusion reactions
  • May result in premature removal of transfused RBCs (delayed hemolytic reaction, 3-5 days post-transfusion)
159
Q

What 3 factors in a transfusion recipient influence the severity of an alloimmune hemolytic transfusion reaction?

A
  • Alloantibody titer (higher = more severe reaction)
  • Alloantibody type (hemolytic reactions mediated by IgM, where IgG tends to cause agglutination)
  • Alloantibody binding affinity
160
Q

What 2 factors in a transfusion donor influence the severity of an alloimmune hemolytic transfusion reaction?

A
  • Antigen expression on RBC surface (more expression = more severe reactions)
  • Transfusion volume (higher dose of antigen = more severe)
161
Q

2 Dal negative dogs were transfused with Dal positive blood in a 2017 study. When did anti-Dal antibodies develop post-transfusion? When was the highest agglutination titer reached?

A
  • IgG detected on day 4 in one dog and day 21 in the other
  • Highest titers at 4 weeks and 8 weeks
162
Q

In general, the canine population is 50/50 DEA positive vs negative. What breed is primarily DEA negative, however?

A

Greyhounds - also tend to be DEA 3+ and 5+

163
Q

What breeds are more commonly Dal negative?

A

Dalmatians, Dobermans, Shih Tzu, Beagle

164
Q

What breeds were found to be 100% Dal positive?

A

Greyhounds, Labs, Goldens

165
Q

What situation could cause neonatal isoerythrolysis in cats?

A

Type B queen (strong alloantibodies against type A) mated with a Type A tom => giving birth to a type A or AB kitten

166
Q

What cat breeds are more commonly type B?

A

Turkish Angora, Devon Rex, British shorthair, Cornish Rex, Exotic shorthair, Birman, Somali, Sphinx

167
Q

Apart from type A or B, what alloantigens are recognized in cats?

A
  • Mik antigen
  • 5 new feline erythrocyte antigens (FEA) - although one is likely Mik

Why crossmatching is needed

168
Q

Cats developed alloantigens against blood antigens (other than AB) how many days post-transfusion?

A
  • 2 days in the 2017 JFMS study
  • 25% of cats developed alloantibodies against antigens outside the AB system
169
Q

In the 2017 JFMS study, were positive cross matches identified in transfusion naive cats?

A

No - likely do not need to cross match the first transfusion

170
Q

Point of care blood typing is available for what antigens in dogs?

A

DEA 1, 4, 5 and Dal

171
Q

Name 3 point of care assays that can be used for blood typing

A
  1. Card agglutination (if agglutination occurs, animal is positive for that blood type)
  2. Immunochromatographic cartridge (useful for patients with autoagglutination)
  3. Gel tube test
172
Q

What does the major cross match test for?

A

Alloantibodies in the recipient’s plasma against donor cells

173
Q

What does the minor cross match test for?

A
  • Alloantibodies in the donor’s plasma against the recipient cells
  • Rarely used
174
Q

What is considered the “gold standard” method for veterinary cross matching, although Mus hates it?

A

Laboratory tube agglutination assay - not standardized, subjective

175
Q

What cross matching method is used in human medicine and how is it interpreted?

A

Gel tube agglutination - agglutinated RBCs form a line at the top of the gel (incompatible) whereas non-agglutinated RBCs pass to the bottom (compatible)

176
Q

Cross matching predicts what type of transfusion reaction?

A

Acute, hemolytic reactions - does not necessarily predict delayed hemolysis or other types of reactions

177
Q

What is the most common adverse event associated with transfusion in dogs/cats?

A

Fever

178
Q

What defines febrile, non-hemolytic transfusion reaction?

A

Temperature >102.5F AND increase in temperature >1.8F during or within 4 hours of the transfusion (without other cause)

179
Q

What causes febrile, non-hemolytic transfusion reactions?

A

Donor WBC or platelet antigen-antibody reactions or transfer of proinflammatory mediators in stored blood products

180
Q

What is transfusion associated circulatory overload?

A
  • Acute, non-immunologic reaction secondary to an increase in blood volume from transfusion
  • Characterized by acute respiratory distress and hydrostatic pulmonary edema
  • Occurs during or within 6 hours of transfusion
181
Q

What is transfusion related acute lung injury (TRALI)?

A
  • Acute, immunologic reaction secondary to antigen-antibody interactions in the lungs
  • Acute hypoxemia with evidence of non-cardiogenic pulmonary edema
  • Occurs during or within 6 hours of transfusion
182
Q

In humans, what blood products carry the highest risk of TRALI and allergic transfusion reaction?

A

Plasma and platelet products

183
Q

What defines and allergic transfusion reaction?

A
  • Acute, immunologic reaction - type 1 hypersensitivity to an antigen in the blood product
  • Dogs: Erythema, urticaria, pruritus, facial/extremity angiodema, V/D, hemoabdomen
  • Cats: upper respiratory tract edema, bronchoconstriction, GI signs
  • Occurs during or within 4 hours of transfusion
184
Q

Blood type incompatibilities cause what type of transfusion reaction?

A

Acute, immunologic, hemolytic reaction - caused by type II hypersensitivity

185
Q

How are acute hemolytic transfusion reactions diagnosed?

A
  • New onset evidence of hemolysis within 24 hours of transfusion (hyperbilirubinemia, hemoglobinemia/uria, spherocytes, ghosts)
  • AND inadequate increase in PCV post-transfusion
186
Q

What causes delayed hemolytic transfusion reactions and when to they occur?

A
  • Caused by a secondary immune response to the donor RBCs (the recipient possesses low levels of antibodies not detected on crossmatching - new antibody production is stimulated by transfusion)
  • Occur 24 hours to 28 days after transfusion
187
Q

Transfusion of type A blood into a type B cat results in what type of reaction?

A

Acute hemolytic reaction - B cats have HIGH type A antibodies that rapidly destroy the transfused blood

188
Q

Transfusion of type B blood into a type A cat results in what type of reaction?

A

Delayed hemolytic reaction - type A cats have LOW antibody titers against B blood - results in delayed reactions in ~2 days

189
Q

What blood product has the highest level of citrate and is most at risk of causing citrate toxicity?

A

Fresh frozen plasma

190
Q

What are the clinical signs of citrate toxicity in dogs?

A
  • Nausea, vomiting
  • Tachycardia, QT prolongation, T wave inversion
  • Reddening of the pinnae, facial swelling, salivation
191
Q

What blood collection systems can be used in feline donors?

A

Any - closed, semi-closed, or open

Human closed systems may be impractical for cats due to small size. Studies show no change in bacterial contamination with the methods used

192
Q

Why might leukoreduction before blood storage be beneficial?

A

Stored WBC can produce inflammatory cytokines - in human medicine, leukoreduction reduces the risk of febrile transfusion reactions. Not enough evidence in vet med though

193
Q

What factor increased in vivo hemolysis of RBC transfusions?

A

Age of the RBC - increased in vivo hemolysis with stored vs fresh RBCs in dogs

194
Q

Fresher RBC transfusion products should be considered in dogs with what conditions?

A

Hemolytic anemia, sepsis

195
Q

In patients at risk of hyperammonemia (liver dysfunction, etc), transfused blood should be how old to reduce ammonia formation in storage?

A

Whole blood <24 hours
pRBC <7 days

196
Q

RBC units should be checked for hemolysis prior to administration. Units with what percent hemolysis should not be used? Why?

A

> 1%
- Increased risk of transfusion reactions
- Free hemoglobin can cause proximal renal tubular damage and redox injury of the endothelium

197
Q

Any dog that has been transfused more than ___ days prior should be crossmatched

A

> 4 days

198
Q

Type AB cats should receive what type of transfusion if AB blood is not available?

A

Type A blood

199
Q

Should transfusion naive cats be crossmatched? When should crossmatching be performed after transfusion?

A

Yes - type naive cats and then if they were transfused >2 days prior

200
Q

Should type specific plasma be given? Should crossmatching be performed prior to plasma administration?

A

Dogs: not recommended
Cats: yes, give typed plasma but no need to crossmatch

201
Q

What substance can be added to gel column and tube crossmatching techniques to improve accuracy?

A

Antiglobulin

202
Q

If canine blood is administered to a cat, what is the lifespan of the canine RBCs?

A

3 days (delayed hemolytic reactions common)

203
Q

If a second canine xenotransfusion is given to cats >6 days after the initial one, what can occur?

A

Significant risk of severe anaphylaxis and death

204
Q

What types of infusion pumps should be avoided when giving a transfusion?

A

Peristaltic or rotary pumps - can increase hemolysis

205
Q

Name 4 vector borne diseases that should be tested for (PCR and serology) in all canine blood donors?

A
  • Anaplasma phagocytophilum and platys
  • Babesia canis and gibsoni (especially Greyhounds, Pitbulls)
  • Bartonella
  • Ehrlichia canis
  • Mycoplasma hemocanis
206
Q

Name 4 vector borne diseases that should be tested for (PCR and serology) in canine blood donors in endemic areas?

A
  • Ehrlichia chaffeensis and ewingii
  • Hepatozoon canis/americanum
  • Leishmania
  • Trypanosoma cruzi
  • Brucella canis is intact or exposed dogs
207
Q

Name 4 diseases that should be tested for (PCR and serology) in all feline blood donors?

A
  • Anaplasma phagocytophilum
  • Bartonella
  • Mycoplasma haemofelis
  • FeLV/FIV
208
Q

In endemic areas, finding a PCR negative, seronegative donor may be difficult for some diseases. When is using a seropositive donor ok?

A
  • Anaplasma in dogs and cats
  • Bartonella in cats
  • DO NOT use Ehrlichia seropositive dogs - significant pathogen
209
Q

Can dogs infected with Dirofilaria pass the organism to another dog during transfusion?

A

No - microfilaria from an infected donor cannot lead to heartworm disease in the recipient. BUT donors should be screened for it - transfused blood could cause the recipient to test positive or infect mosquitos. Collection of large amounts of blood from the donor may not be safe

210
Q

In a group of 149 transfusion naive dogs, what percent were incompatible with at least one potential donor on cross match?

A

17%

211
Q

In a group of 149 transfusion naive dogs, did the results of cross matching affect the change in HCT after transfusion?

A

Yes - dogs that had crossmatching performed and were given compatible blood had a median change of 12.5% hematocrit vs 9.0% in dogs not crossmatched

212
Q

Are dogs most commonly positive or negative for Kai 1 and 2 blood types?

A

94% are Kai 1+ / Kai 2 -
No dogs were positive for both

213
Q

Concentrations of what proinflammatory eicosanoids increased in pRBC units during storage and transfusion?

A

PGF2alpha, 6-keto-PGF1alpha, and leukotriene B2

214
Q

What inflammatory substance is implicated in the development of TRALI in humans?

A

Neutrophil NETs

215
Q

Are NETs found in canine blood products?

A

Yes - increase during RBC storage and are higher in non-leukoreduced units on day 42

216
Q

Are FFP transfusions beneficial in cats?

A

Yes - significantly less likely to be coagulopathic afterward

217
Q

What percent of cats experience acute transfusion reactions after receiving FFP?

A

14-16%, depending on the study
- Most commonly increased temp, followed by respiratory signs

ACVIM: SAIM Specialty boards study 2023 (38 decks)

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