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ACVIM Generals Revision > Haematology and Immunology: Clinical COPY > Flashcards

Haematology and Immunology: Clinical COPY Flashcards

1
Q

What type of immune response is immune mediated disease generally caused by?

A

TH2 responses (antibodies against a self antigen)

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2
Q

What percentage of dogs will have bacteria when on immunosuppressive treatment?

A

30%

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3
Q

Why is PT often prolonged first in disorders of coagulation?

A

Factor VII from the extrinsic pathway has the shortest half life of all the factors so is often consumed first.

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4
Q

Prothrombin time:

  • Test characteristics
  • What it tests
  • Point at which the test is considered complete
A
  • Plasma is added to a medium containing calcium chloride and tissue factor within a lipid membrane.
  • Tests the extrinsic and final common pathway
  • The PT finishes when fibrin strands form
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5
Q

aPTT

  • Test characteristics
  • What it tests, what it does not test
A
  • Plasma is incubated with a contact activator (e.g. kaolin, celite) which will activate XII and the pathway continues.
  • Tests the intrinsic pathway and final common pathway.
  • The fibrin stabilising complex (XIII) and the extrinsic pathway (VII) are not tested.
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6
Q

What Ddx could you have for:

  1. Increased PT but normal aPTT?
  2. normal PT but increased aPTT?
A
  1. Early rodenticide toxicity
  2. Factor XII (Hageman) deficiency, Factor XI (haemophilia C), Factor IX (Haemophilia B) or Factor VIII (Haemophilia A), heparin therapy.
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7
Q

ACT
- Test characteristics

A

Whole blood is used and a contact activator is added. The platelets acts as their own membrane for the tests. Therefore, visible clot formation is the end point.

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8
Q

How is fibrinogen measured?

A

The Clauss method: fibrinogen is exposed to a large amount of thrombin.

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9
Q

Reasons for reduced fibrinogen concentrations

A

Anticoagulant use
Elevated FDPs
Decreased albumin
XIII deficiency (as the fibrin is not stabilised)
Amyloidosis

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10
Q

How is thrombin clot time measured?

A

By adding lots of thrombin to citrated plasma. It is measuring the function/levels of fibrinogen.

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11
Q

What is FDP measurement testing and what are some Ddx if this is normal?

A

FDPs are produced when plasmin lyses fibrin clots. Therefore, elevations may occur in:

  • DIC
  • Rodenticide toxicity
  • Hepatic disease
  • Thrombotic diseases
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12
Q

What are D-dimers?

A

These are specific FDPs that are only produced from cross-linked fibrin. They have a very short T1/2 so can indicate recent fibrinolysis.

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13
Q

TEG parameters and alterations with hyper and hypocoaguable states.

A

R = the time to onset of fibrin formation

K = time for the deviation of the needle by 20mm (this is a measure of speed of clot formation)

alpha angle = speed of clot formation

MA = maximum strength of the clot

The LA30 and LA60 = the amount (%) of clot that has undergone lysis by 30 minutes and 60 minutes, respectively.

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14
Q

Which TEG parameters indicate:

  1. Coagulation factors
  2. Platelet number and function
A
  1. This is generally indicated by the reaction time (time to fibrin formation)
  2. This is indicated more by the rate of fibrin formation (e.g. alpha angle, k etc.)
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15
Q

How much of a reduction in clotting factor activity is required before PT/aPTT are prolonged?

A

50-70%

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16
Q

What will the following alterations result in on TEG testing?

a) low PCV
b) Increased fibrinogen
c) Thrombocytopenia

A

a) + b) will appear hypercoaguable
c) will appear hypocoaguable

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17
Q

What percentage of mortality in IMHA is likely due to thromboembolic disease?

A

up to 50%

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18
Q

What is the incidence and survival of ATE in cats with cardiac disease?

A

33% incidence and 35% survival

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19
Q

What percentage of dogs with PLN will suffer thromboembolic complications?

A

14-27%

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20
Q

What is the most common cause of pulmonary thromboembolism in dogs?

A

Neoplasia

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21
Q

In what neoplasias is DIC a common problem?

A

Haemangiosarcoma
Mammary carcinoma
Pulmonary adenocarcinoma

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22
Q

How long does it typically take for clinical bleeding to occur following rodenticide toxicity?

A

2-5 days

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23
Q

What are PIVKAs

A

Proteins induced by vitamin K abscence. This test will be prolonged if vitamin K is deficient in some way.

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24
Q

Which factor is increased in DIC and is thought to be a major contributor to its development?

A

Increased expression of tissue factor.

The extrinsic pathway is then activated and there is consumption of coagulation factors. Therefore, there are two phases:

  1. Compensated = hypercoaguable
  2. Uncompensated = bleeding
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25
Q

What are the diagnostic criteria for DIC?

n.b. there may be some actual criteria here but this is what I have noted from Ettinger

A

PT/aPTT alterations

Thrombocytopenia

Increased FDPs/D-dimers

Hypofibrinogenaemia

Decreased antithrombin

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26
Q

Treatment of DIC

A

Compensated phase = anticoagulants

Uncompensated = FFP transfusion

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27
Q

What are acquired anti-coagulants?

A

Spontaneous development of antibodies to a coagulation factor, anti-phospholipid antibodies (lupus anticoagulant) is another type.

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28
Q

How are acquired anti-coagulants tested for?

A

By the ‘plasma mixing test’ which is where patient and control plasma is mixed. Coags would remain prolonged following mixing due to the presence of antibody in the patients plasma.

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29
Q

Which clotting factors are contained in the following blood products:

  1. FFP
  2. Cryoprecipitate
  3. Cryosupernatent
  4. Stored plasma
A
  1. FFP = contains all the factors
  2. Cryoprecipitate is primarily VIII, XIII, vWF, fibrinogen and fibronectin (less than FFP but small volume required)
  3. Sufficient coagulation factors other than those in cryoprecipitate
  4. Lowe levels of V and VIII but has adequate VitK dependent factors.
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30
Q

Which blood products should be used for rodenticide toxicity?

A

FFP or stored plasma are best for this.

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31
Q

Pathophysiologic and genetic basis for Scott syndrome

Diagnosis

A

Deficient procoagulant activity (phosphatidylserine) on the platelet surface.

Autosomal recessive trait of GSD

Diagnosis:

  • Prothrombin consumption assay
  • Flow cytometry for the PTS on the platelet surface
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32
Q

What breed of cat has vitamin K gamma-glutamyl carboxylase deficiency been documented in?

A

Devon-Rex

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33
Q

Which factors are deficient in the following diseases?

  • Haemophilia C
  • Haemophilia A
  • Haemophilia B
  • Stuart-powell deficiency
  • Christmas disease
A

C = XI

B = IX (aka. christmas disesase)

A = VIII

  • X
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34
Q

What is the mode of inheritance of haemophilia A & B?

A

Autosomal X-linked recessive.

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35
Q

What factor can potentially be increased with desmopressin therapy?

A

Factor VIII is increased in people but not dogs.

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36
Q

If haemorrhage is suspected in a cat with Hageman’s trait, what should be evaluated for next?

A

A concurrent haemophilia as Hageman trait should not result in clinical bleeding.

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37
Q

Why might Rts be falsely increased soon after haemorrhage?

A

Due to release from bone marrow storage pools

38
Q

How is the OFT performed and interpreted?

A

Two tubes with RBCs (0.9% saline and 0.55% saline) are incubated and centrifuged for 5 minutes

If 0.55% is haemolysed to a greater degree this indicates increased fragility.

39
Q

Why does hypophosphataemia result in haemolytic anaemia?

A

It reduced RBC ATP stores which will then destabilise the membrane.

40
Q

In which Babesia species infection do anti-RBC antibodies develop?

A

B. gibsoni and B. vogeli

41
Q

Which markers may differentiate histiocytic proliferation from haemophagocytic histiosarcomas?

A

CD11/CD18

42
Q

Which breeds are predisposed to haemophagocytic HS

A

Golden Retriever, Bernese Mountain Dog, Golden Retriever, Flat-Coat

43
Q

What are the major targets of Ig binding in IMHA?

A

Anion-exxhange molecule, erythrocyte membrane glycoproteins

44
Q

What are the poor prognostic indicators for canine IMHA?

A
  • Icterus
  • Petechiation
  • Increased urea
  • Increased aPTT
  • Thrombocytopenia
  • Left shift and monocytosis
  • Increasing cytokines
45
Q

What is the pathomechanism of feline alloimmune haemolysis?

A

Type B cats develop type A autoantibodies in the first few weeks of life.

Therefore, if a type B cat has A or AB kittens their antibodies are passed on in the colostrum.

(Also explains why you should never give a type A cat type B blood)

46
Q

Which reticulocytes are counted by haematology analysers?

A

Aggregate

47
Q

Normal lifespan of canine and feline RBCs

A

100 days, 72 days

48
Q

factors known to reduce EPO production

A

Renal disease
PTH
Low albumin
Ferritin and transferritin

49
Q

Hormones known to facilitate EPO release/production

A

ACTH
Cortisol
ANG II
TSH and thyroxine

50
Q

Cells that produce EPO

A

Peritubular interstitial cells of inner cortex and outer bmedulla

51
Q

Which IL is responsible for increased hepcidin production?

A

IL-6

52
Q

Reason for anaemia in copper deficiency?

A

Copper is required for haemoglobin synthesis but is an uncommon cause of anaemia in veterinary species

53
Q

What is the expected EPO level in primary polycythemia (polycythemia vera)?

A

Should be low due to negative feedback mechanisms.

54
Q

What treatment stragies are there for polycythemia vera?

A

Hydroyxurea
Chlorambucil
Radiophosphorus treatment

55
Q

What is the lifespan of platelets in circulation?

A

6-10 days

56
Q

What is the role of vWF in clotting?

A

vWF binds to exposed subendothelial collage and facilitates PLT binding through GP1b/V/IX

Conformational changes then expose the GPIIb/IIIa receptor, vWF binds here to allow plalet aggregation and binding with fibrinogen.

57
Q

Which drugs has IMTP been more often associated with (compared to others)

A

Cephalosporins and sulfonamides

58
Q

How can anti-platelet antibody be tested?

A

Through flow cytometric techniques.

59
Q

How much quicker (approximately) are vincristine treated dogs likely to have

A

approx 2 days

60
Q

Which second agent monotherapy does ettinger cite as being effective for treatment of IMTP?

A

Mycofenolate mofetil

61
Q

Is there a benefit to the use of lyphophylised canine platelets in IMTP?

A

Not shown to be of benefit in a prospective study.

62
Q

How do plasma vWF levels, vWF multimers and bleeding risk vary with vWB types?

A
63
Q

To what degree of platelet reduction and anaemia can a BMBT be performed without concern for an impact on results?

A

PLT > 1000x10e9/L and PCV >30%

64
Q

In which type of vWD might PFA be appropriate?

A

Type 1

65
Q

In which type of vWD is the vWF quantification (vWF:Ag) assay not going to be beneficial?

A

Type 2 since vWF can be normal in this type.

66
Q

Which vWD type is the qualitative assay used in?

A

Type 2, this is the case as a functional assay is required to demonstrate that the multimers are not present.

The factor binding to collaen is compared to the amount of VWF (vWF antigen). If this ratio is high then this is consistent with T2 vWD.

67
Q

What are the treatment options for vWD?

A

Desmopressin
FFP or cryoprecipitate (the latter may be preferred due to needing less volume)

68
Q

In what cases has acquired vWF deficiency been documented in dogs?

A

MMVD
Tetrastarch administration
Angiostronglus

69
Q

What breed has P2Y12 disorder been documented in?

A

Greater Swiss Mountain Dogs

70
Q

Ciclosporin MoA

A

Inhibition of calcineurin which results in the inability to phosphorylate NFAT therefore reducing cytokine production, particularly IL2 (also 3, 4, TNFa)

71
Q

Azathioprine MoA

A

Thiopurine (purine analogue = adenine, guanine).

72
Q

Mycofenolate mofetil MoA

A

Also a purine analogue but inhibits inosine monophosphate dehydrogenase (IMPDH) which is required for de novo purine synthesis

73
Q

Leflunomide MoA

A

Pyrimidine synthesis inhibitor (inhibits dihydro-orotate dehydrogenase which is a de-novo synthesis of pyrimidines inhibitor)

74
Q

Chlorambucil MoA

A

Alklating agent – DNA cross-linking

75
Q

hIVIG MoA

A

Binds to the Fcg receptors on macrophages which prevents them taking up opsonised components.

76
Q

How are the polyarthritides classified?

A
77
Q

Which rickettsial diseases can cause a polyarthritis?

A

Borrelia
Ehrlichia
Anaplasma
Ricketsia ricketsii

78
Q

What scenario might promt you to look for a bacterial L-form arthritis?

A

If you have cutaneous abscessation or draining tracts.

79
Q

What neoplasia’s have reactive polyarthropathies been reported in?

A

Carcinomas

Seminomas

Sertoli cell tumours

Leiomyomas

80
Q

What is the most common manifestation of SLE in dogs vs. cats?

A

Dogs: Polyarthropathy

Cats: dermatological and CNS signs

81
Q

Which breed, other than the Shar-Pei, has a breed associated non-erosive polyarthritis been described in?

A

Akita

82
Q

What percentage of dogs with IMPA have pyrexia?

A

50%

83
Q

How many joints does Ettinger suggest tapping to make a diagnosis of IMPA?

A

>/= 4

84
Q

What is rheumatoid factor?

A

It is a collection of autoantibodies that form against IgG (Fc region) and their normal role is to facilitate their clearance through opsonisation.

85
Q

What are the diagnostic criteria of SLE in veterinary medicine?

A

The presence of 2 or more signs of autoimmunity along with the presence of ANA antibodies.

or

The presence of 3 or more signs of autoimmunity with or without ANA antibodies

86
Q

Breed(s) predisposed to having a large spleen

A

GSD

87
Q

Breed(s) predisposed to having a caudal spleen

A

Miniature schnauzer
Cocker spaniels
Greyhounds

88
Q

What is the characteristic appearance of splenic torsion on abdominal ultrasound?

A

Swiss cheese appearance

89
Q

Which sedative/anaesthetic drug does not tend to cause splenic enlargement?

A

Propofol

90
Q

What is the pathomechanism behind X-SCID?

A

A mutation in the gamma chain of IL-2 resulting in a T-lymphocyte deficiency in affected breeds (Welsh Corgi and Basset hound)

91
Q

Lipaemia effect on TP measurement?

A

Will increase TP measurement with refractometer reading, but will not effect machine measured TP.

ACVIM Generals Revision (32 decks)

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