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ACVIM Specialty: Ettinger - MS 2023 > Haemolymphatic and Immunology > Flashcards

Haemolymphatic and Immunology Flashcards

1
Q

What TH cells are most often implicated in IMDz

A

TH2 as they result in humoral responses and antibody production towards self antigens

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2
Q

What are the key steps involved in formation of the platelet plug?

A
  1. Adhesion of platelets to vWF - this is mediated via the Gp1b receptor
  2. Activation of platelets - platlets release compounds usch as ADP, TxA and PAF which activates further platelets
  3. Platelet aggregation (fibrin clot formation)
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3
Q

What is the rate limiting step in the coagulation cascade?

A

Activation of prothrombin activator

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4
Q

Outline the extrinsic pathway of coagulation

A
  1. Tissue factor (III) is released from damaged endothelium. This activates and combined with VII and caclium to activate factor X
  2. Factor Xa combines with factor V and calcium along with platelet phospholipids to form the prothromin activator complex
  3. This, in turn, converts prothrombin to thrombin (II)
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5
Q

Outline the intrinsic pathway of coagulation

A
  1. Factor XII is activated via trauma or contact with subendothelial collagen
  2. Factor XIIa activates XI in the presence of HMW-K and is accellarated by prekallikrien
  3. Factor XIa activates IX
  4. Factor IXa combines with platelet phospholipids, factor VIII and thrombin (II) to activate factor X
  5. Factor X goes on to convert prothrombin to thrombin in the FCP as for extrinsic coagulation
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6
Q

What part of the coagulation cascade does prothrombin time (PT) test?

A

The extrinsic pathway and final common pathway

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7
Q

What part of the coagulation cascade does activated partial thromboplastin time test (aPTT)

A

The intrinsic and final common pathway

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8
Q

What part of the coagulation cascade does activated clotting time test?

A

Intrinsic and final common pathway

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9
Q

What is the mechanism by which anticoagulant rodenticide toxicity occurs?

A

They block the reduction of vitamim K epoxide via inhibition of vitamin K epoxide reductase. This means that clotting factors cannot be refreshed Vitamin K dependent clotting factors at II, VII, IX and XI. PT is prolonged first in rodenticide toxicity due to factor VII having the longest half life

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10
Q

Factors in the extrinsic pathway

A
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11
Q

Factors in the intrinsic pathway

A
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12
Q

Factors in the final common pathway

A
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13
Q

Factor I

A

Fibrinogen

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14
Q

Factor II

A

Prothrombin

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15
Q

Factor III

A

Tissue factor

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16
Q

Factor IV

A

Calcium

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17
Q

Factor V

A

Proaccelerin

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18
Q

Factor VI

A

Doesn’t exist?

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19
Q

Factor VII

A

Serum prothrombin conversion accelerator

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20
Q

Factor VIII

A

Antihaemophilic factor

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21
Q

Factor IX

A

Christmas factor

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22
Q

Factor X

A

Stuart factor

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23
Q

Factor XII

A

Hageman factor

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24
Q

Factor XIII

A

Fibrin stabilising factor

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25
Q

What does an increased PT and normal aPTT suggest

A

Early rodenticide toxicity

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26
Q

What may a normal PT and increased aPTT suggest

A
  • Lack of factor XII (Hagemen deficiency)
  • Lack of factor IX (Haemophilia B)
  • Lack of factor VIII (Haemophilia A)
  • Lack of factor I (Haemophilia C)
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27
Q

What may increased PT and aPTT suggest?

A

Rodenticide toxicity
Hepatic disease
DIC
Dysfibrigenaemia

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28
Q

when are FDPs produced and what do they indicate, what are the DDx for increases?

A

FDPs are produced when plasmin lyses fibrin. Therefore, they are a marker of plasmin activity.

DDx: DIC, rodenticide toxicity, hepatic or thrombotic disease

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29
Q

What are D-dimers and therefore what do they indicate?

A

FDP that only occurs from cross linked fibrin. due to their short T1/2 they can only indicate recent fibrinolysis (<5h). Therefore,

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30
Q

What are the components of virchows triad?

A

Vascular stasis
Hypercoaguability
Vascular endothelial activation

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31
Q

What is the most common reason for PTE?

A

Neoplasia

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32
Q

What neoplastic disease is particularly assocaited with prolonged clotting times?

A

Mammary carcinoma

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33
Q

When would PT be expected to be prolonged with rodenticide toxicity?

A

After 36 - 72 hours

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34
Q

What testing can demonstrate DIC?

A

Compensated phase - hypercoaguable
Decompensated phase - hypocoacuable

  • PT/aPTT
  • Thrombocytopenia
  • Increased FDPs/D-dimers
  • Fibrinogen (will be low)
  • Antithrombin (will be low)
  • RBC shear injury may be seen
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35
Q

How can DIC be treated?

A

Compensated phase may benefit from anticoagulants (e.g. heparin)
Plasma transfusion to replace clotting factors.

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36
Q

What is the pathomechanism of the development of acquired anticoagulants and the potential causes?

A

Develop due to autoantibody formation against coagulation factors. This has been reported with:
- IMHA
- Drug reactions
- Lymphoproliferative diseases and neoplasia
- Antiphospholipid antibody protein (lupus anticoagulant)

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37
Q

How are acquired anticoagulants tested for?

A

By mixing patient and control plasma. Coagulation times will remained prolonged after mixing due ot the presence of antibody in the patien plasma.

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38
Q

Which factors are present in the following blood products:
- FFP
- Cryoprecipitate
- Cryosupernatent
- Stored plasma

A
  • All of them
  • VIII and XIII, vWF, fibrinogen and fibronectin. The advantage over FFP is that it is a smaller volume
  • Contains II, VII, IX and XI
  • Stored plasma has lower levels of V and VIII
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39
Q

What heritable hypocoaguable state are GSDs prone to, what is this and how is it diagnosed and treated?

A

Scott syndome
Autosomal recessive trait which is due to a defect of procoagulant activity on the platelet surface
Diagnosis is through a prothrombin consumption assay or flow cytometry for a lack of phosphatidylserine on platelet surface
Treatment = cryopreserved PRP

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40
Q

Which is the more common haemophilia?

A

A & B

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41
Q

What is the inheritance pattern of haemophilia A & B

A

Autosomal x-linked

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42
Q

Haemophilia A

A

Factor VIII deficiency

43
Q

Haemophilia B

A

Factor IX deficiency

44
Q

Haemophilia C

A

FActor XI deficiency

45
Q

How is afibrinogenaemia tested for?

A

Clauss test

46
Q

What breed might you suspect NOT to have rodenticie toxicity in if you note prolonged PT?

A

Devon Rex - reported to have vitamin K gamma glutamyl carboxylase deficiency.

47
Q

How are coagulopathies treated?

A

Plasma transfusion is never wrong in a case that has haemorrhage to replace clotting factors.

48
Q

How long does it take for precursor RBCs to mature to RBC and then how long until these are released into the circulation and lose their RNA?

A

5 - 7 days for maturation
Stored in BM for 2 -3 days
Residual RNA is lost within 24 - 48 h of being in the circulation

49
Q

Calculation for corrected Rt% and normal values for dogs and cats

A
50
Q

Osmotic fragility test:
- How is it performed
- How is it interpreted
- What does it indicate?

A
  1. Incubate two tubes with RBCs, one in 0.9% NaCl and the other in 0.55% NaCl
  2. Centrifuge for 5 minutes
  3. Look at the tubes

Positive = 0.55% has more haemolysis
Negative = both tubes look the same

The OFT indicates whether or not there has been RBC membrane damage (e.g. with IMHA)

51
Q

Approximate sensitivity and specficity for DAT (Coombs) in dogs and cats

A
  • Dog: 61 - 82, 94 - 100%
  • Cat: 62, 95 - 100%
52
Q

What Babesia spp. have anti-erythrocyte antibodies been demonstrated in?

A

B. gibsoni and vogeli (not canis!)

53
Q

How is babesia diagnosed simply?

A

Blood smear, using buffy coat and/or an ear prick sample can increase sensitivity

54
Q

Breed predispositions and heritability patterns of the following:
- Pyruvate kinase deficiency
Phosphofructokinase deficiency

A

Both are autosomal recesive disorders
- PK: Abysinnian, Somali, DSH, Basenji, Beagle, Cairn Terrier, Chihuahua, Dachshund, Pug, Labrador, Toy American Eskimo Dog, WHWT
- PPK: ESS, American Cocker, Whippet, Wachtelhund

55
Q

What bone marrow abnormality may occur in PK deficiency?

A

Myelofibrosis

56
Q

What does this picture indicate?

A

A stomatocyte, reported in certain breeds

57
Q

Negative prognositic indicators for canine IMHA

A
  • Icterus
  • Petechiation
  • Increased BUN
  • Increased aPTT
  • Thrombocytopenia
  • Left shift and monocytosis
  • Increased cytokines
58
Q

What is the pathogenesis of feline alloimmune haemolysis?

A

Type B cats develop type A autoantibodies in the first frew weeks of life. Therefore, if a type A or AB kitten consumes colostrum from a type B cat it may lead to feline neonatal isoerythrolysis.

59
Q

IMHA consensus criteria for:
a) Diagnosis of IMHA
b) Support of IMHA
c) Suspicious of IMHA
d) Not IMHA

A

a) - ≥2 signs of immune destruction + ≥1 sign of haemolysis
b) - ≥2 signs of immune destruction without signs of haemolysis
- 1 sign of immune destruction with one sign of haemolysis
c) 1 sign of immune destruction without signs of haemolysis
d) No signs of immune destruction or haemolysis

Signs of immune desctruction: Spherocytes, positive ISAT without or without washing (with washing counts as 2x sigsn of immune destruction), positive DAT or FC (flow cytometry)

Signs of haemolysis: hyperbilirubinaemia or hyperbilirubinuria, haemoglobinaemia, haemoglobuinuria, ghosts.

60
Q

What percentage of dogs with IMHA may be non-regenerative at presentation?

A

30%

61
Q

Sensitivity and specificity of spherocytosis in diagnosis of IMHA

A

≥5/HPF = 63% sensitive, 95% specific = supportive of a diagnosis
≥3-4/HPF = 74% sensitive, 81% specific = suspicious for a diagnosis

62
Q

What is the specificity of iSAT for diagnosis of IMHA?

A

1:4 dilution with saline is 100% specific

63
Q

What degree of bilirubinuria is sufficient to suggest haemolysis in dogs vs. cats?

A

> 2+ on dipstick for dogs
Any reaction for cats

Care when interpreting in haemolysed blood samples

64
Q

How can haemaglobinuria be confirmed if red urine is noted?

A

Cetrifugation should not clear haemoglobinuria but may rebove RBCs

65
Q

Which babesia species has proof of concept for causing IMHA in dogs?

A

B. gibsoni

66
Q

Which drugs are noted to cause IMHA in dogs and cats?

A

Cefazedone - dogs
Polythiouracil - cats

67
Q

What imaging is reccomended in the IMHA consensus statement?

A

Abdominal radiography to rule out zinc toxicity, interestingly the other imagings are ‘at the discretion of clinician’

68
Q

What infectious disease testing is reccomended in the IMHA consensus statement?

A

Babesia gibsoni (PCR and serology)
Other testing (e.g. heartworm)
Mycoplasma haemofelis PCR, ideally the others
Babesia felis in endemic areas PCR
B. conradae (PCR) in californian and coyote hunting dogs

69
Q

Treatment algorithm for IMHA
- What is the ‘2nd line therapy’

A

If glucocortcoids + second agent fail to control IMHA then IVIG is the next step, followed by either a third immunosupressive agent or splenectomy.

70
Q

What dose of prednisolone is reccomended for dogs >25kg?

A

50 - 60mg/m2

71
Q

Which immunosupressive agent is NOT reccomended as a second agent in the treatment of IMHA?

A

Cyclophosphamide

72
Q

How quickly can prednisolone be tapered in IMHA

A

every 2 -3 weeks if a second agent is being used. Otherwise if no second agent every 3 weeks and only by 25%

73
Q

Monitoring reccomended for azathioprine

A

CBC and biochemistry every 2 weeks in the first 2 months of treatment thenevery 1 - 2 months therafter

74
Q

Monitoring reccomendation for ciclosporin

A

Biochemistry every 2 - 3 months due ot the risk of hepatotoxicity

75
Q

Monitoring for mycophenolate

A

CBC every 2 -3 weeks in the first month then every 2 -3 months therafter

76
Q

Monitoring for leflunomide

A

CBC and liver enzymes every 2 weeks for the first 2 months then every 1 -2 months

77
Q

When should G-CSF be considered when managing drug induced neutropenia>?

A

If neutropenia occurs for >1 week or an overdose of a myelosupressive agent is given

78
Q

If a relapse occurs during treatment for IMHA what should the tapering interval be increased to after re-evaluating for trigger factors etc.

A

Should be doubles

79
Q

What percentage decrease in PCV can occur in cats undergoing general anaesthesia?

A

25%

80
Q

What is the normal lifespan of a red blood cell in the dog vs. cat?

A

Dog = 100 days
Cat = 72 days

81
Q

What is the mechanism by which hypotoxia triggers EPO release and erythropoisis?

A

Renal hypoxia results in reduced degradation of hypoxia inducible factor-1 (HIPF-1). HIPF-1 binds to hypoxia response elements and stimulates EPO transcription.

82
Q

What is the mechanism by which hepcidin reduces iron?

A

It leads to downregulation of ferroportin 1 so cells do not take up as much iron.

83
Q

What is the mechanism by which reduced vitamin B12 may reduce erythropoisis?

A

B12 is required for purine and thymidylate synthesis.

84
Q

What would be expected of serum EPO levels in primary vs. seconday polycythemia?

A

In primary polycythemia there is erythropoiesis independent of EPO so EPO should actually be reduced. However, secondary polycythemia can result from abherrant EPO production or production in response to hypoxia so in these conditions EPO would be expected to be increased.

85
Q

How do the following hormones stimulate erythropoiesis?
a) Thyroid hormones
b) Glucocorticoids
c) GH

A

a) Increases EPO porduction and erythroid progenitors
b) syergise with HIF
c) direct and indirect (through IGF-1/PRL) stimulator of erythropoiesis

86
Q

What testing can be employed in the diagnosis of primary polycythemia?

A
  1. Rule out altitude related
  2. Identify any cardiac, renal or respiratory disease
  3. Consider a PaO2 to assess whether there is hypoxia
  4. EPO measurement
87
Q

What are the myelosuppressive treatment options of polycythemia vera?

A
  1. Hydroxyurea
  2. Chlorambucil - although this risks leukaemic transformation
  3. Radiophosphorus treatment
88
Q

What are the potential complications of treatment of polycythemia vera?

A

Irone deficiency
Hypoalbuminaemia
Leukaemia and thrombocytopenia

89
Q

What is the lifespan of a platelet in the circulation?

A

7 - 10 days

90
Q

What are the events that occur following binding of the platelet to vWF and the results. N.b. for this card I have outlined events into 4 main processes.

A
  1. Platelet Adhesion and Aggregation
    vWF is present in circulation and binds to damaged endothelium through interaction with subendothelial collagen. Initially it binds to GP1b/V/XI complex which results in the platelet exposing GBIIb/IIIa (the target of clopidogrel). This receptor bings to fibrin in the presence of vWF to allow platelet activation.
  2. Platelet activation occurs through the interaction of many molecules such as thrombin, TXA2, ADP etc. This results in intracellular calcium release through the DAG/IP3 pathway. These cause protein phosphorylation.
  3. Phosphatidylserine is exposed on the platelet surface through this activation process and this acts as a scaffold for tenase and prothrombin (final common pathway).
  4. Finally, platelts produce molecules through the AA pathway (such as TXA2) to activate more platelets.
91
Q

Why might NSAIDs impact on coagulation?

A

They antagonise the production of prostaglandins which are released by the endothelium to inhibit platelet reactivity.

92
Q

What drugs have been particularly implicated in the development of IMTP?

A

Sulfonamides and cephalosporins

93
Q

Which second agent has been used as a sole treatment in IMTP?

A

Mycophenolate

94
Q

What are the three types of vWD?

A
  1. Type 1 = partial quantitative deficiency of all vWD multimers. The total vWF will be reduced but multimers can be present so bleeding tendancies are variable.
  2. Type 2 = this is characterised by a lack of HMW multimers of vWF so these will be reduced whilst the total plasma vWF can be normal. They have a higher risk of bleeding
  3. Type 3 = the most severe and is characterised by a lack of all vWF so bleeding risk is high.
95
Q

Outline the expected vWF, vWF multimers and bleeding risk as well as testing for the three types of vWD.

A

T1 and T3 can be tested with quantitative vWF assay (vWF:Ag) but type 2 needs to have a qualitative assay performed.

96
Q

What is the minimum PCV and platelet count for which a BMBT can be performed?

A

PCV >30% and PLT >100x10e9/L

97
Q

What are the normal ranges for VWF:Ag assay?

A

Normal = 70 - 180%
Borderline = 50 - 69%
Abnormal = 0 - 49%

98
Q

How does the qualitative vWF assay work?

A

The functional assay works by measuring the collagen binding of activity of vWF to bovine collagen using an ELISA. Gel electrophoresis to seperate the VWF multimers is also possible.

99
Q

What breeds are affected by vWD and the different types?
n.b. that T2 and T3 are a more limited list of breeds.

A
100
Q

What is the inheritance of vWF disease types?

A

T1 can be dominant or recessive
T2 and T3 are autosomal recessive

101
Q

What is the definition of SLE?

A

≥2 signs of autoimmunity + the presence of ANA or ≥3 signs of autoimmunity present

102
Q

What breed is SLE noted in?

A

NSDTR

103
Q

What are the most common clincal signs of SLE in dogs vs. cats (top 3)

A

Dogs:
1. Polyarthritis
2. Pyrexia
3. Renal disorders
Cats:
1. Dermatologic/CNS
2. Pyrexia
3. Renal disorders

104
Q

What are the four types of hypersensitivity reaction?

A

Type I: reaction mediated by IgE antibodies.
Type II: cytotoxic reaction mediated by IgG or IgM antibodies.
Type III: reaction mediated by immune complexes.
Type IV: delayed reaction mediated by cellular response.

ACVIM Specialty: Ettinger - MS 2023 (12 decks)

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