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Immune Mediated and Hematology > Immune Mediated Ettinger > Flashcards

Immune Mediated Ettinger Flashcards

1
Q

What are 5 mechanisms of loss of self tolerance?

A
  1. Release of sequestered antigen or expression of developmental antigen
  2. Abnormal tolerance (changes in T reg)
  3. Molecular mimicry, cross reactivity to foreign antigen
  4. Alterations in self proteins (haptenization - sulfas in dobies)
  5. Oxidation damage
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2
Q

What % of normal dogs and cats have a + ANA?

A

Dogs: 20%
Cats: 10%

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3
Q

What is the platelet factor 3 test?

A

Patient plasma with normal platelets and then check PT

If PT shortened, Igs injured plts and released phospholipids = coag activation

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4
Q

Which 2 infectious diseases can results in antiplatelet antibodies?

A

RMSF and Ehrlichia (+ based on flow)

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5
Q

How do you diagnose SLE?

A

Need Class I +2 of class 2 or 3+ of Class 2/3
Class 1: ANA +
Class 2: Polyarthritis, nephropathy, proteinruia, IMHA, dermatopathy, petechia, pleuritis-pericarditis, cutaneous lesions
Class: 3 LN, anemia, fever

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6
Q

What is the LE Cell test?

A

Test for SLE
Clotted mashed blood (release nucleoproteins), incubated with neutrophils
If Abs - neuts will phagocytze the material

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7
Q

What is the prognosis for SLE?

A

Unknown!!

Make to monitor renal function in these patients

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8
Q

What are autoantigens in primary IMHA?

A

RBC glycoproteins
RBC anion channel band 3
Cytoskeletal protein spectrin

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9
Q

What are the most common Ig in IMHA?

A

IgG >IgM
Most only IgG, some IgG and IgM, rare to have IgM only
1 report of IgA

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10
Q

What happens if you have IgG in IMHA?

A

Extravascular hemolysis from phagocytes of RES, partial internalization = spherocytes

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11
Q

What happens if you have IgM in IMHA?

A

Intravascular hemolysis that is complement mediated and also Extravascular hemolysis

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12
Q

What is the most common form of IMHA in cats?

A

Secondary

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13
Q

What % of dogs with IMHA get TED?

A

About 30-50%

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14
Q

Why are IMHA dogs hypercoaguble?

A

Increased in TF (esp MP)
Increased fibrinogen
Increased platelet response (75% have activated platelets, increased P-selectin)
Decreased anticoags (AT, thrombomodulin, Protein C, plasminogen activators)

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15
Q

What are the risk factors for TED in IMHA?

A 
Severe thrombocytopenia
Hypoalb
Neg Coombs
IV catheter
Increased ALP
Hyperbilirubinemia
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16
Q

What are the hallmarks for dx of IMHA?

A

Marked regenerative anemia - 42-85%
Spheocytosis - 52-95%
Autoagglutination (Anti-RBC Abs)

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17
Q

What are options if there is a ineffective erythroid regeneration?

A
  1. IM destruction and erythroid precursor
  2. Anemia of inflammation
  3. Paraneoplasia
  4. Lack of EPO (CKD)
  5. BM disease (myelophtisis, myelofibrosis, myeloproliferative disease)
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18
Q

Can Anti RBC Abs be seen in ITP dogs too?

A

YES

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19
Q

What is contained in the Coomb’s antiserum?

A

Species specific Antiserum - IgG, IgM, C3

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20
Q

How often is IMHA coomb’s negative?

A

23-63%

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21
Q

Is Ig isotype associated with survival in IMHA?

A

No, but bilirubin is!!

If you have >2 Ig isotypes (IgG/IgM) = More severe anemia, spheocytosis, and autogluttination

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22
Q

Is the # of transfusions a predictor of survival in IMHA?

A

Yes it has been noted

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23
Q

What is the thought behind HIGH dose pulse steroid tx for IMHA?

A

Nongenomic effects that result in PROFOUND supression

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24
Q

What is the cytotoxic component of azathioprine?

A

Thioguanines Resulting in impaired RNA, DNA, and protein synthesis

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25
Q

How much more potent is mycophenolate to azathioprine?

A

10X

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26
Q

When would clodronate have the most benefit in IMHA dogs?

A

It results in MP depletion (spleen) - Most benefit if IgM or C3 = Intravascular hemolysis (?)

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27
Q

What is the long term survival in IMHA?

A

About 40%

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28
Q

What is the mortality rate with IMHA?

A

About 30-70% - High early moratality in first 2 months

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29
Q

Which cytokines are related to poor outcome in IMHA?

A

IL-15, IL-18, GM-CSF, MCP-1

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30
Q

Can feline IMHA be nonregnerative?

A

YES the majority of them are >58%

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31
Q

What is the prognosis for feline IMHA?

A

Mortality 24-32%

Dt Lower TED

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32
Q

What is the classic presentation of phosphofructokinase def?

A

Persistent compensation hemolytic anemia = CRISIS with exertion
“Alkaline fragile”

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33
Q

What is the prognosis with PK def?

A 
Pyruvate kinase defs = Decrease in ATP = Membrane defect = HEMOLYSIS
IRON Overload (changes in BM and liver)
Dead by 1-5 yrs!!!
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34
Q

How does hypophosphatemia result in hemolysis?

A

Decreased ATP, depleted 2-3DPG, and ecreased glutathione - RBC fragility = Hemolysis

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35
Q

What the compensatory mechanisms dt anemia?

A

From hypoxia from decreased Hbg

  1. Increased 2,3 DPG (only in dogs)
  2. Increased CO
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36
Q

Which breed gets hemophagocytic syndrome?

A

Tibetan Terriers - NOT cancer, but proliferative disorder of MPs = Bi and Panyctopenias

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37
Q

How is vincristine helpful in ITP?

A

Increased platelet count by stimulating megakaryotyes and impairs phagocytosis of opsonized platelets by impairing mirotubules within MP!!!

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38
Q

What results in GI signs with leflunomide?

A

Accumulation of metabolite TMFA

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39
Q

Is the severity of thrombocytopenia prognostic?

A

NO

lowest with sepsis and ITP

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40
Q

How do you obtain a platelet count?

A

plt in HPF and X15-20K = Average platelets

41
Q

Why do CKCS have a macrotrhombocytopenia?

A

Related to a Beta tubulin defect

42
Q

What is the primary antibody in ITP?

A

IgG - Against alpha granules or GPIIb-IIIa

43
Q

What are the 3 main products for platelet replacement?

A
  1. Fresh Whole Blood
  2. Platelet rich plasma
  3. Platelet concentrate
44
Q

What does vWF bind to on platelet?

A

GPIb alpha receptor

45
Q

Are there daily variations in vWF concentrations?

A

Yes, may need to check more than once

46
Q

Is there an association of HypoT4 with vWD?

A

NO!!

47
Q

What is the treatment of vWD and what is the drugs MOA?

A

Desmopressin - Release stores vWF from endothelial cells

Enhanced platelet function independent of vWF

48
Q

What products have vWF if you have a patient that is bleeding?

A
  1. Fresh Whole Blood
  2. FFP
  3. Cryoprecipitate (5-10X vWF in 1/10 volumes)
    NOTE: No improvemetn in Fresh plasma in BMBT
49
Q

Are Hageman Factor Def cats at risk of bleeding and can they undergo procedures?

A

Factor 12 - Prolonged PTT

No bleeding and safe to undergo procedures

50
Q

What factors is stores blood lacking?

A

No factor 8, vwF, or 5

But it has Vit K factors (2,7,9,10)

51
Q

What should you consider if you have low plt count and normal coags?

A

Thrombocytopenia

52
Q

What should you consider if you have normal plt count, and just PTT is prolonged?

A
  1. Intrinsic Factor Defects (8, 9, 11)

2. Contact Pathway Factors: Hageman, prekallikrein, kininogen

53
Q

What should you consider if you have normal plt count and prolonged PT?

A
  1. Extrinsic Factor Defects (7)
54
Q

What should you consider if you have normal plt count and prolonged PT/PPT?

A
  1. Common Pathway (2, 5, 10)

2. Combined Vit K (2,7,9,10)

55
Q

What should you consider if you have normal plt count and prolonged PT/PTT, and low fibrinogen?

A

Fibrinogen def

56
Q

What should you consider if you have normal plt count and normal coags but bleeding?

A

vWD
Platelet defects
Firbinolysis defects
Nonhemostatic defects

57
Q

What are the major factors that result in hypercoagulability?

A
  1. Decreased endogenous anticoagulants (AT, protein C, protein S)
  2. Increased enzymatic activity (increased activity of Factor 8 with Cushing’s)
  3. Increased fibrinogen (inflammation, more firbin clots that are denser and resistant to fibrinolysis)
  4. Increased platelet activity
58
Q

What does PT stand for?

A

Prothrombin time

59
Q

What does PTT stand for?

A

Activated Partial thromboplastin time

60
Q

What is thought to contribute to aspirin resistance in dogs?

A

70% normal dogs have defect in G-protein signaling

61
Q

What factor is increased in Cushing’s that may be a risk for hypercoag?

A

Factor 8

62
Q

How does decreased HCT affect TEG?

A

Hypercoag

63
Q

How does plt

A

Hypocoag

64
Q

What affects R in TEG?

A

Coag factors

NOTE: Heparin prolongs it

65
Q

What affects K and alpha in TEG?

A

Fibrinogen
Factor 13
Platelets

66
Q

What affects MA in TEG?

A

Fibrin production

Platelet function

67
Q

What dz have been noted on TEG to result in hypercoag?

A 
Parvo virus
Cancer
DIC
PLE
PLN

NOTE: HAC same as controls

68
Q

What dz have been noted on TEG to result in hypocoag?

A

Cancer
DIC (clinical bleeding)
HCM (some cats)

69
Q

What are risk factors for DIC?

A 
Prolonged hypotension
SIRS
Changes in blood flow
Tissue damage
change in vascular integrity 
Hemolysis
70
Q

What is mediator of DIC?

A

Release of TF!!!! From monocytes and endothelial cells

Which activates Factor 7 (extrinsic pathway) = LOTS of thrombin which cleaves fibrinogen to make fibrin

71
Q

What are the components of a diagnosis of DIC?

A
  1. Condition that predisposes to DIC
  2. Prolonged coags
  3. Low Platelets
  4. Increased d-dimers and FDPs
  5. Decreased AT
  6. Evidence of thrombi
72
Q

What is seen on a coag that would EXCLUDE DIC?

A

Normal D-dimers

73
Q

Should heparin be used for DIC?

A

Controversial
Thought to prevent further thrombi BUT no studies in humans that there is a benefit
DOES NOT work if there is NO AT!!!

74
Q

What syndrome is noted in Greyhound with arthritis?

A

Felty’s syndrome (rheumatoid arthritis)

75
Q

What are the two main forms of erosive polyarthritis?

A
  1. Rheumatoid Arthritis

2. Periosteal Proliferative Polyarthritis (CATS)

76
Q

Which breed of young dogs gets polyarthritis that does not respond well to treatment?

A

Adolescent Akitas

77
Q

What are the vaccines that dogs and cats develop polyarthritis with?

A

Cat: Calicivirus
Dogs: Distemper

78
Q

What are the 4 types of IMPA?

A
  1. Primary IMPA
  2. Reactive to infection/inflammation remote from joint
  3. Enteropathic (GI or hepatic disease)
  4. Neoplasia
79
Q

For Type 4 IMPA in cats, what should be considered?

A

Myeloproliferative disease

80
Q

What should normal joint fluid look like?

A
81
Q

What does IMPA joint fluid look like?

A
82
Q

Do repeat joint taps every 3 weeks result in neutrophilic inflammation in the joints?

A

NO!!

83
Q

What is the transit time of neutrophils?

A

About 10 hours

84
Q

What is the transit time of lymphocytes?

A

30 mins

BUT recirculate for years

85
Q

What is the transit time of monocytes?

A

12 hours

86
Q

What is the transit time of eosinophils?

A

30 mins

87
Q

What is the transit time of basophils?

A

30 mins

88
Q

What is found on an iron panel?

A

Serum iron (iron bound to transferrin)
TIBC (serum transferrin concentration
% saturation = % transferrin bound by iron (normal about 30%)
Ferritin = Storage iron in serum = Reflects total body iron

89
Q

What does hepcidin do?

A

Binds to cell surface and internalizes ferroportin (only iron exporter) = NO export of iron (also inhibits DMT1 expression)
Increased with inflammation
Decreased with anemia, hypoxia

90
Q

What would you see in the BM of a nonregenerative IMHA?

A

Erythroid hyperplasia = Expansion of immature erythyroid precursors

91
Q

What are T cell markers?

A

CS 3, CD4, CD5, CD8

92
Q

What are B cell markers?

A

CD21, CD22

93
Q

What does CD34 mark?

A

Immature lymphoid/myeloid precursors

94
Q

What are the difference on PARR Of B and T cells?

A

B cells = V, D, J genes

T cells = V, J genes

95
Q

What type of lymphocytosis can be seen with Chronic E. canis?

A

Lymphocytosis Granular Lymphocytes = Homogenous CD8 Tcells

96
Q

Does involvement of the bone marrow change prognosis of leukemia?

A

NO!

97
Q

What is important for B cell leukemias?

A

Cell size important
Small = BAD (MST 15 DAYS!!)
Large = Better (MST 17 months)

98
Q

What is important for T cell leukemias?

A

is important
>30K Poor prognosis
1K days!

99
Q

What type of lymphocytosis occurs with Addison’s disease?

A

Increased in CD4 T cells, CD8 T cells, and B cells = HETEROGENOUS

Immune Mediated and Hematology (4 decks)

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