Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ACVIM SAIM (2023) > Hemolymphatics | Immunology | Coagulation > Flashcards

Hemolymphatics | Immunology | Coagulation Flashcards

1
Q

What is the definition of a true autoimmune disease?

A

Loss of immune tolerance to your own tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are some immunoprotective properties of skin?

A

Sebum
Low pH
Secretion of enzymes
Periodic desquamation
Normal flora
Dendritic cells
Gamma-delta T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the inflammatory mediators of the innate immune system?

A

Chemokines and cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which pathway of the complement system involves the innate immune system?

A

Alternate pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Fever is mediated by what pyrogenic cytokines?

A

IL-1
IL-6
TNF-alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is central tolerance and when is it acquired?

A
  • Inability to pathologically respond to self
  • Acquired during B and T cell ontogeny
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is peripheral tolerance?

A

Inability of mature T and B cells to pathologically respond to self

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is an alloantigen?

A

Tissue from genetically dissimilar individuals of the SAME species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a xenoantigen?

A

Tissue from genetically dissimilar individuals of a DIFFERENT species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is an autoantigen?

A

A component of the host’s body that becomes antigenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is a superantigen?

A

Bacterial or retrovial products that bind directly to MHC II outside the antigen binding groove

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Superantigens bind the T cell receptor outside the conventional binding site with specificity for what chain?

A

Beta chain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is an epitope?

A

The part of an antigen that is capable of inducing an immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is a hapten?

A

Small chemical groups that are generally not antigenic but can induce an immune response by binding to a larger protein molecule (carrier protein)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What immunoglobulin is the major serum immunoglobulin?

A

IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where is IgG found?

A

Blood and ECF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are IgG’s two main functions?

A

Opsonization
Virus neutralization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the first immunoglobulin produced during humoral responses?

A

IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How many immunoglobulin units does IgM have? This translates to how many antigen binding sites?

A

Five - it’s a pentamer; the five Ig units are joined by a J chain

Translates to ten antigen binding sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

IgM is INTRAVASCULAR or EXTRAVASCULAR only?

A

Intravascular - its size precludes it from leaving the bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Elevated levels of IgM suggest what?

A

Recent infection or exposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the function of IgM?

A

Activates complement system (specifically classical pathway)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where is IgA produced?

A

Mucosal sites (respiratory and intestinal tracts)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How many Ig chains does IgA have?

A

Two - it’s dimeric with a J chain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where in the body is IgD found?

A

Blood and lymph fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

On the surface of what cells is IgD predominantly found?

A

Immature B lymphocytes - functions as an antigen-specific binding site on these cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

IgE is largely bound to surface receptors on what cells?

A

Mast cells and basophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

IgE is found at HIGH/LOW levels in serum

A

Low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are IgE’s main functions?

A

Allergies
Protection against parasites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Is antigen-antibody binding noncovalent or covalent?

A

Noncovalent. Still a strong bond b/c of hydrophobic bonding, hydrogen bonds, Van Der Waals forces, and ionic interactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the most abundant Ig in the body?

A

IgG - makes of 75% of all antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Which Ig is least abundant in the body?

A

IgD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the largest Ig?

A

IgM - pentamer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Which Ig are secretory (found on mucous membranes)?

A

IgA and IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Which Ig can cross the placenta?

A

IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

J chains of Ig are needed for what?

A

Secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Which Ig have J chains?

A

IgA and IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What Igs are neutralizing Igs?

A

IgG 1-4 and IgA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the three mechanisms of antibody action?

A

Neutralization (particularly effective with viruses)
Opsonization
Activation of complement system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

The Ab-Ag complex binds to what complement protein to start the complement cascade?

A

C1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

The classical complement pathway is triggered by what first step?

A

Antibody binding antigen which then binds C1 protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Is the alternative complement pathway part of the innate or adaptive immune system?

A

Innate - acts in the absence of Ig

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the common end product of the classical and alternative complement pathways?

A

C3b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What does C3b initiate?

A

Terminal pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What does the terminal pathway result in?

A

Formation of the membrane attack complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

C3b can form an immune complex with what CD?

A

CD21

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

T cells express

A

TCR and CD3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

B cells express

A

Surface membrane Ig and CD79

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Are NK cells found in the thymus?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

NK cells survey for cells with

A

Altered MHC I (aka stressed or damaged cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Where do NK cells develop?

A

Bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

NK cells express what two key cell surface molecules?

A

CD16 and CD56

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Ab-ag complexes will bind which CD on NK cells to trigger cytotoxicity?

A

CD16

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

NK cells kill via what two pathways?

A

Perforins/granulysin/NK-lysin
CD95L (also known as Fas ligand)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Perforins/graulysin/NK-lysin are expressed constitutively in granules of NK cells but are upregulated by which two immunocytokines?

A

IL-2 and IL-12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What two cytokines enhance cytotoxicity of NK cells?

A

IL-2 and IL-4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What cytokine enhances survival of NK cells?

A

IL-3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What cytokine promotes rapid differentiation of pre-NK cells and activates macrophages?

A

INF-gamma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are the primary cytokines of NK cells?

A

INF-gamma (type 2 interferon involved in cell-mediated immunity and Th1 T helper responses)

TNF-alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the three types of antigen presenting cells?

A

Macrophages
Dendritic cells
B lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

The term histiocytes refers to what two types of cells?

A

Dendritic cells and macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Macrophages express which MHC class?

A

BOTH - MHC I and II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Ingestion of antigens by macrophages causes what effects?

A

Increased lysosomal and bactericidal activity

Upregulates inducible nitric oxide synthase gene which enhances release of NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Macrophages secrete what cytokine to activate naive T-cells (Th1)

A

IL-12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What two compounds secreted by macrophages downregulate immune response?

A

IL-10 and TNF-beta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

From what bone marrow precursor are dendritic cells derived?

A

CD34 BM precursor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Where are Langerhans cells located?

A

Epidermis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

How long do neutrophils circulate before entering tissues, and then how long do they survive?

A

~10 hours
Survive for a few days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What are three categories of cell adhesion molecules?

A

Selectins
Integrins
Ig Superfamily Adhesion Molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the function of selectins?

A

Function as lectins which bind CHO moieties expressed by endothelial cells or other WBCs —> helps WBC rolling along vascular endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What selectin is found on neutrophils?

A

L-selectin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What selectins are found on the endothelium?

A

E-selectin and P-selectin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is the function of integrins?

A

Bind through protein-protein interactions to stop WBC rolling

Mediate aggregation and transendothelial migration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What are some examples of integrins?

A

Very Late Antigen (VLA)
Leukocyte function-associated antigen (LFA)
MAC-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is the function of Ig Superfamily Adhesion Molecules?

A

Stop WBC rolling

Mediate aggregation and transendothelial migration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What are some examples of Ig Superfamily Adhesion Molecules?

A

Intercellular Adhesion Molecules (ICAM)
Vascular Cell Adhesion Molecules (VCAMs)
LFA-2
LFA-3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What are the stages of WBC emigration during inflammation?

A

Activation
Margination of neutrophils
Rolling/sticking
Stopping/adhesion
Aggregation
Transmigration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What molecules are involved in stopping/adhesion during WBC emigration?

A

VLA-4
ICAM
VCAM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What molecules are involved in aggregation during WBC emigration?

A

MAC-1
LFA-1
P-selectin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What molecules are involved in transmigration during WBC emigration?

A

ICAM
VCAM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What happens during the margination step of WBC emigration?

A

Leukocytes move to periphery of vessels due to vasoconstriction and slowing of blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What cell adhesion molecules mediate the rolling phase of WBC emigration?

A

Selectins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What compounds expressed on neutrophils are involved in firm adhesion/aggregation during WBC emigration?

A

CD11-CD18
VLA-4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What happens during the transmigration/diapedesis step of WBC emigration?

A

Neutrophils extend a pseudopod between endothelial cells, digest a small portion of the basement membrane, and emigrate from the vasculature into tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Neutrophils follow what to the site of infection? What factors are involved?

A

Chemotactic gradient

Chemotactic factors: C5a, C3b, fibrin, kinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What part of the endothelium helps initiate the migration of leukocytes into tissues?

A

P and E selectin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What are two Opsonization that bind the Fc receptor?

A

IgG and C3b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Via what two processes do neutrophils destroy ingested bacteria?

A

Respiratory burst
Release of lyric enzymes and anti microbial peptides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Respiratory burst is O2 ____ and release of lyric enzymes/anti microbial peptides is ____.

A

Respiratory burst = oxygen dependent

Release of lyric enzymes/antimicrobial peptides = oxygen independent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

How does respiratory burst work?

A

NADPH oxidase enzyme complex results in formation of potent bactericidal oxidants (H2O2, hypochloride ions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What are differences between perforins and defensins?

A

Perforins:
-Released by granules of cytotoxic T cells and NK cells
-Form a hole in the target cell membrane that allows granzyme to enter and degrade the cell’s DNA, which results in apoptosis

Defensins:
-Act as direct chemoattractants for immature dendritic cells
-Some are opsonic
-They target any organism with a cholesterol-free negatively charged membrane (bacteria, fungi, many viruses)
-Can compromise 50% of protein in azurophil (primary) phagocytic granules
-Found within neutrophil granules and epithelial cells to assist in killing phagocytized bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Where are defensins found?

A

Primary granules of neutrophils and epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What are characteristics of defensins?

A

-Highly cytotoxic
-Arginine-rich cationic proteins
-Form voltage-gated ion channels in bacterial cell membranes resulting in increased permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What are two examples of defensins?

A

Defensin-alpha (DEFA)
Defensin-beta (DEFB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Pathogen associated molecular patterns and damage associated molecular patterns are recognized by what receptors?

A

Pattern recognition receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What portion of the cell wall is recognized by PRRS in Gram-positive bacteria?

A

Peptidoglycans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What portion of the cell wall is recognized by PRRs in Gram-negative bacteria?

A

Lipopolysaccharide (LPS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What portion of the cell wall is recognized by PRRs in acid fast bacteria?

A

Glycolipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What portion of the cell wall is recognized by PRRs in yeast?

A

Mannan- or B-glucan rich cell wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What portion of the cell wall is recognized by PRRs in viruses?

A

Nucleic acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is the most significant family of pattern recognition receptors?

A

Toll like receptors (TLRs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

On what cells are TLRs found?

A

Sentinel cells of the innate immune system:
Macrophages
Neutrophils
Mast cells
Dendritic cells

T and B cells of the adaptive immune system

Non-immune cells (epithelial cells that line respiratory and GIT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What happens when toll like receptors are activated?

A

Turn on genes for production of pro inflammatory factors = INFLAMMATION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Name the TLR that recognizes LPS? Flagellin? DsRNA? Where are they located in the cell (extra vs intracellular)

A

LPS - 4, Flagellin - 5, dsRNA - 3; TLR-4 and TLR 5 are cell surface, TLR-5 is intra-cellular (recognizes viruses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

High mobility group box protein-1 binds which two TLRs?

A

TLR-2 and TLR-4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What are the functions of TNF-A?

A

Adherence, migration, attraction and activation of leukocytes; causes heat/pain/swelling/redness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Which interleukin increases hepcidin in the body? How does this impact blood levels in the body?

A

IL-6 (and IL-1); hepcidin inhibits Fe transport by binding to the iron export channel ferroportin which is located in the basolateral plasma membrane of gut enterocytes and the plasma membrane of reticuloendothelial cells; this will result in anemia of chronic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Give the differences between initiation of the complement system in the classical, alternate, and lectin pathway?

A

Classical - antigen/antibody activates C1
Alternate - bacterial LPS/yeast has C3 undergo spontaneous hydrolysis and combine with Factor B
Leptin - mannose-binding leptin complex binds to mannose-containing carbohydrate on infectious agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

The three complement pathways (classical, alternative, leptin) all end in activation of which complement molecule?

A

C3 convertase, which cleaves C3 > C3a and C3b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Which two complements result in opsonization?

A

C3b and C4b

111
Q

Brittany Spaniels are associated with deficiency in which complement?

A

C3

112
Q

IFN-gamma is the primary activator of which white blood cell?

A

Macrophage

113
Q

CD45+CD3+CD8+ receptors are specific for which type of lymphocyte?

A

Cytotoxic T cell (CD45 -all leukocytes; CD3 - T cell; CD 8 - cytotoxic)

114
Q

IgA functions primarily where, and in what way?

A

Respiratory tract (also GI); neutralization of pathogens and/or products; particularly good against viruses

115
Q

Which interleukin is a hematopoietic growth factor and stimulates growth of neutrophils, eosinophils, and macrophages?

A

IL-3

116
Q

IL-10 promotes growth of what type of T cell?

A

Treg

117
Q

Difference between TNFa, TNFb, and TGFbeta?

A

alpha - pro-inflammatory; beta - anti-inflammatory; TGF-beta - immunosuppressant

118
Q

Th2 CD4 lymphocytes are known for what physiologic function?

A

Defense against helminths/parasites, allergic response; recruit IgE, mast cells, eosinophils

119
Q

Chronic asthma is an examine of what type of hypersensitivity reaction?

A

Type 4 (delayed)

120
Q

What is the mechanism of action of cyclosporine?

A

Calcineurin inhibitor = cannot phosphorylate NFAT > resulting in less IL-2 (and less IL-3, IL-4, TNFa)

121
Q

Why is azathioprine contraindicated in cats? What dog breed shouldn’t you use azathioprine in?

A

Cats lack thiopurine methyl-transferase (TMPT), which is the detoxification pathway. Giant schnauzer (same reason)

122
Q

Azathioprine and mycophenolate inhibit production of what aromatic compound? How do they work differently?

A

Purines; azathioprine is converted to 6-MP, purine analog that is taken up and thus inhibits S phase of DNA cycle | mycophenolate inhibits inosine monophosphate dehydrogenase, which is an enzyme needed for purine synthesis

123
Q

Which immunosuppressant specifically targets pyrimidine synthesis?

A

Leflunomide

124
Q

Most immune-mediated diseases are from dysregulation of which immune cell?

A

Th2 (Ettinger 8th ed, p 2046)

125
Q

Which antibody class is most commonly involved in canine IMHA?

A

IgG

126
Q

A young GSD presents for hemoabdomen following its spay. Coagulation testing is normal. If all surgical steps were followed correctly, what clotting disorder could still be a differential for this dog? What would be the best treatment for this dog?

A

Scott’s syndrome - platelet procoagulant disorder (platelets cannot externalize phosphatidylserine, which is needed for fibrin formation); give platelets

127
Q

Marked peripheral neutrophilia and hypersegmented neutrophils are consistent with what disease? What breed is known to develop this?

A

Leukocyte adhesion deficiency. European Irish Setter.

128
Q

Breeds associated with X-linked severe combined immunodeficiency? What IL receptor is deficient?

A

Cardigan Welsh Corgis and Basset Hounds; IL-2

129
Q

You see a Jack Russell Terrier puppy for fever following vaccination. There is severe lymphopenia and decreased serum globulin concentrations. This is consistent with what process?

A

Autosomal recessive severe combined immunodeficiency.

130
Q

What breed is associated with cyclic neutropenia?

A

Gray Collie (insertional mutation in the AP3B1 gene)

131
Q

Miniature Dachshunds with lymphocyte function deficits can get pneumonia from what organism? What lymphocyte do they tend to lack?

A

Pneumocystis carinii. Absent B cells.
Cavies have also been reported.

132
Q

Causes of secondary dysmyelopoiesis in dogs

A

IMT and IMHA, myelofibrosis, pure red cell aplasia, and lymphoma; drugs, including chemotherapeutic
agents, chloramphenicol, estrogens and phenobarbital; endogenous overproduction of estrogens; heavy metal
toxicoses; iron deficiency; adenocarcinoma; and leishmaniasis

133
Q

Causes of secondary dysmyelopoiesis in cats

A

immune-mediated hemolytic anemia and thrombocytopenia, pure
red cell aplasia, lymphoma, glomerulonephritis, feline infectious peritonitis, and feline immunodeficiency
virus (FIV) infection

134
Q

Neutropenia is seen in what percentage of cats presenting with FeLV-related illness?

A

50%

135
Q

Most common type of bacteria causing septic arthritis (aka Gram positive/negative; anaerobic/aerobic)

A

Gram positive aerobe

136
Q

Transient polyarthritis in kittens is associated with:

A

calicivirus

137
Q

Most common manifestation of systemic lupus erythematosus in dogs is

A

Polyarthropathy

138
Q

Most common manifestation of systemic lupus erythematosus in cats is

A

Dermatologic lesions (erythema, ulceration, crusts, and depigmentation of the face, ears, and paws) [CNS signs are more common in cats - 24%, than in dogs - 5% but is not the most common overall]

139
Q

Criteria for diagnosis of SLE?

A

Two autoimmunity disorders + positive ANA; or three autoimmunity disorders

140
Q

The ACVIM consensus statement on IMHA describes three infections that can cause Coomb’s positive anemia. What are those three?

A

Heartworm, Leishamiania, Bartonella

141
Q

The ACVIM consensus statement on IMHA describes three infections that can cause Coomb’s positive anemia in dogs. What are those three?

A

Heartworm, Leishamiania, Bartonella

142
Q

IMHA is more prevalent in which breeds?

A

Cocker and Springer Spaniels, Old English Sheepdogs, Bichon Frises, Bearded and Rough-coated Collies, Poodles, and Flat-coated Retrievers

143
Q

ACVIM recommendations for tapering prednisone/immunomodulatory drugs?

A

Taper pred by 25% q3w if single agent, taper pred by 25-33% q3w OR q2w if using second agent [for first taper: they say can drop pred by 25-50%]

144
Q

A dog on glucocorticoids should have UA checked how frequently accordingly to ACVIM consensus on IMHA tx?

A

Every 8-12w

145
Q

Bloodwork monitoring on azathioprine? (according to IMHA consensus)

A

CBCs and relevant serum biochemical variables (especially alanine aminotransferase [ALT] activity) be monitored every 2 weeks during the first 2 months of treatment, and then every 1-2 months until treatment is discontinued.

146
Q

Of the two blood groups Kai 1 and Kai 2, most dogs fall into which group?

A

Kai 1, 94% of dogs, JVIM 2016

147
Q

Dogs with severe pulmonary hypertension had higher values of what variable on a hemogram compared to normal dogs?

A

RDW (related to tricuspid regurgitation pressure gradient), JVIM 2016

148
Q

Which two gram negative bacteria are most likely to be involved as contaminants in blood bags?

A

Serratia and Pseudomonas, JVIM 2016

149
Q

Blood transfusions associated with what in cats receiving dialysis?

A

increased number of treatments (NOT death - this is only the case in dogs), JVIM 2016

150
Q

Significance of phosphatidylserine in RBC?

A

Normally on the inside, but moves to the outside in aged RBC and can be indicator for cell removal by phagocytic cells

151
Q

Three dog breeds associated with Dal-?

A

Dalmatians, Dobermans, Shih Tzus, JVIM 2017

152
Q

Of the following, decreases in which two were associated with well-controlled IMHA? Serum Thymidine Kinase 1, Canine-C-Reactive Protein, Haptoglobin, and Vitamin D Concentrations

A

TK-1 and c-CRP, JVIM 2017

153
Q

What is the biological half-life of cell-free DNA?

A

5.64 hours. JVIM 2018

154
Q

Congenital methemoglobinemia in Pomeranians can be caused by a variant in what gene?

A

nonsynonymous variant in the CYB5R3 gene. JVIM 2018

155
Q

A major crossmatch should ideally be performed in a transfusion naive cat. T/F?

A

False - no change in hemolytic reaction between those cross-matched or not cross-matched in transfusion naive cats. JVIM 2018

156
Q

Cyclosporine increases which eicosanoid involved in coagulation in normal dogs?

A

Thromboxane A2, JVIM 2018

157
Q

What were the characteristics of hemostasis in a study that induced experimental E. canis infection in dogs?

A

Hypercoagulable (increased MA) and hypofibrinolytic (lower Ly30 and Ly60), JVIM 2018

158
Q

Dogs with AKI have a phenotype similar to what type of hemostatic disease?

A

VWF type 2, JVIM 2019

159
Q

Indications for membrane-based TPE?

A

Immune-mediated disease, hyperviscosity syndrome, toxicity from highly protein bound substances

160
Q

What percentage of dogs had complications from TPE? What percentage died from complications?

A

34%, 2/34 died from complications, JVIM 2019

161
Q

Prolongation of which values resulted in correlation with therapeutic levels of factor 10a reached from rivaroxaban?

A

1.5-1.9x delay in PT and R values of TEG 3 hours after rivaroxaban administration, JVIM 2019

162
Q

What might be a good biomarker to differentiate survivors vs nonsurvivors in SIRS patients?

A

Angiopoetin-2, JVIM 2019

163
Q

A strong correlation between fibrinogen clauss and what value on rotational thromboelastometry?

A

Maximum clot firmness, JVIM 2019

164
Q

What ultrasonographic findings of the spleen were associated with malignant/suppurative inflammation on FNA?

A

nodules 1-2 cm, peritoneal fluid, >1 target lesions

165
Q

What percentage of non-ITP thrombocytopenic animals were positive for anti-platelet antibody?

A

20% JVIM 2020

166
Q

Dogs on prednisone (2 mg/kg/d) and clopidogrel were how many times more likely to have an excessive effect on platelet function?

A

11 times JVIM 2020

167
Q

Dilution at what ratio of saline to blood results in a specificity of 97% (and diagnostic accuracy of 95%) for saline agglutination suggestive of IMHA?

A

49 (saline) : 1 JVIM 2020

168
Q

How many dogs became neutropenic when administered vincristine in a study involving dogs with ITP?

A

19/127, JVIM 2021

169
Q

Which feline erythrocyte antigens are most prevalent? Which was associated with higher risk of naturally occurring auto-antibody?

A

1 (84%) and 5 (95%); 1 was associated; JVIM 2021

170
Q

Which breeds more frequently presented for nonregenerative immune mediated anemia?

A

Whippets, Miniature Dachshunds, Lurchers (JVIM 2021)

171
Q

MST for nonregenerative immune mediated anemia?

A

277d (JVIM 2021)

172
Q

What percentage of dogs with immune-mediated disease treated with membrane TPE survived to discharge?

A

82% (JVIM 2021)

173
Q

What percent of blood donor bags from Canada tested positive for blood-borne pathogen?

A

1.1%, JVIM 2021

174
Q

RBC IgG and phosphatidylserine is more likely to be expressed in IMHA dogs rather than non-IMHA. T/F?

A

True JVIM 2021

175
Q

3 breeds that represented 50% of primary splenic torsion

A

GSD, Bulldogs, Danes (JAVMA 2016)

176
Q

What breed had the highest risk of aortic thrombosis? What was the most common disease? How many had no underlying disease?

A

Shetland. Most common disease (in all dogs, not just Shelties) - PLN. 1/3 had no underlying disease (JAVMA 2017)

177
Q

What RBC abnormality was noted more frequently in dogs with lymphoma than IBD?

A

Eccentrocyte (JAVMA 2019)

178
Q

What other physical exam finding is noted in cats with osmotic fragility syndrome? (What breeds are generally affected?)

A

Splenomegaly (Abyssian, Somali, although this study found that DSH cats and other breeds can also present) - JFMS 2016

179
Q

What were most common signs of primary erythrocytosis?

A

Seizures and mentation changes (10/18 cats for each) - JFMS 2018

180
Q

What are expected changes can be seen with on a CBC post-splenectomy for at least up to 2w weeks following procedure?

A

Thrombocytosis. Also hypercoagulability (JAVMA 2019)

181
Q

What is the most common cytological diagnosis for a cat with a honey-comb like spleen? What was the prevalence of lymphoma?

A

Lymphoid hyperplasia (64%); 24% of cats with honeycomb pattern had lymphoma - JFMS 2020 (two different papers)

182
Q

Percentage of cats that developed transfusion-related reaction after receiving FFP?

A

14.8% (JFMS 2020)

183
Q

Allo-antigen on type A cats? B cats?

A

N-glycolyl-neuraminic acid - Type A
N- acetyl-neuraminic acid - Type B
AB has both

184
Q

Breeds of cats more known to have type B?

A

British Shorthair, Birman, Devon Rex

185
Q

Why is it recommended to cross-match all cats?

A

Due to presence of Mik antigen

186
Q

Feline type I hypersensitivity reactions tend to have clinical signs related to which body system?

A

Respiratory (upper resp edema, bronchoconstriction) - particularly of relevance in transfusions [but other signs are more likely to happen b/c transfusion reactions are not necessarily hypersensitivities]

187
Q

Virchow’s triad consists of what?

A

alterations in blood flow, endothelial damage, and the existence of hypercoagulable states

188
Q

What is advantage of tissue plasminogen activator compared to other thrombolytic agents (such as urokinase?)

A

More specifically targets FIBRIN-bound plasminogen as compared to free-circulated plasminogen

189
Q

Initial use of warfarin can actually result in a hypercoagulable state - why?

A

Faster drop in protein C levels initially

190
Q

What populations of dogs/cats are at high risk of thrombosis (according to CURATIVE)

A

High risk of thrombosis includes: dogs with IMHA or PLN or PLE or heartworm, cats with cardiomyopathy and associated risk factors, dogs or cats with more than 1 disease/risk factor for thrombosis [severe pancreatitis, steroid, HAC, cancer, liver dz, ]

191
Q

The importance of selectins in the endothelial glycocalyx? What are the two main ones? How are they different?

A

Allow for adhesion of WBC to endothelial cells (and platelets). P selectin and E selectin. E selectin ONLY on endothelial cells and is inducible. P selectin is on endothelial cells and platelets and is stored (aka readily available).

192
Q

Delayed hemolytic transfusion reaction occurs only in what scenario reported in dogs/cats?

A

None in dogs; xenotransfusion of canine blood to cats - 64% incidence

193
Q

Negative prognostic factors for IMHA in cats?

A

Age and TBili (JVIM 2016)

194
Q

Critically ill dogs seem to have significantly decreased respiratory burst capacity despite an increase in monocytes expressing which TLR receptor?

A

TLR 4 (JVIM 2018)

195
Q

Prednisone and cyclosporine affected IL-2 and what other cytokine?

A

IFN gamma. Azathioprine, mycophenolate, leflunomide did not have effects on IL-2 or IFN gamma. JVIM 2020

196
Q

What percentage of dogs on mycophenolate develop GI effects? What was overall incidence of adverse effects? Was this dose dependent?

A

24%, 26%, not dose dependent. JVIM 2021

197
Q

In a study of 13 dogs, what % had erosive IMPA? Where were these lesions? More common in what signalment?

A

16%; ALL carpal joints; more common in middle-aged small breed JAVMA 2016

198
Q

Increased/decreased cell-free DNA, increased/decreased mean platelet component, and progressively increasing/decreasing IL-17 was associated with death in IMHA.

A

Increased, decreased, progressively decreasing JVIM 2017, JAVMA 2018, JVIM 2020

199
Q

What is a characteristic finding in most (92%) of dogs with PIMA on bone marrow cytology (be specific)?

A

Rubricytophagocytosis (JAVMA 2019)

200
Q

The median time for PIMA dogs to go into remission (if they did) was how long?

A

29 days (About 1 month) JAVMA 2019

201
Q

Major difference between PIMA and non-regenerative IMHA on bone marrow cytologies in cats?

A

PIMA - erythroid hypoplasia or aplasia
nonregen IMHA - erythroid hyperplasia or maturation arrest (JFMS 2016)

202
Q

Cyclosporine is not recommended for cats with what diseases?

A

Probably any kind of infectious lol, But also FIV, FeLV, diabetic, past history of malignant neoplasia (JFMS 2017)

203
Q

Retrovirus infected cats had the same response to panleukopenia virus vaccine as did normal individuals. T/F?

A

True - JFMS 2019

204
Q

Signs and finding typical for pulmonary Langerhans cell histiocytosis in cats?

A

Mixed restrictive dyspnea, diffuse nodular pattern to lungs, histiocytic infiltration JFMS 2020

205
Q

E-cadherin biomarker staining on a histiocytic cells confirms that cell as what?

A

Langerhans cell

206
Q

Which two coagulation factors are released by DDAVP?

A

vWF and Factor 8c

207
Q

Function of IL-8? Who secretes them?

A

Pro-inflammatory. Attracts neutrophils and other granulocytes, induces angiogenesis, stimulates phagocytosis. Secreted by macrophages and epithelial cells.

208
Q

what is major acute phase protein in cats?

A

Serum amyloid A (JFMS 2017 looking at heartworms that noted increase in inflammation)

209
Q

Polycythemia vera (primary erythrocytosis) - treatment options?

A

Rpx phlebotomy
Chemo agents (e.g. hydroxyurea)
Hirudotherapy (medicinal use of
leeches)
Onion powder (induce hemolysis) - case report in a cat

210
Q

Polycythemia vera (primary erythrocytosis) - CSx and pathogenesis?

A

Cats: CSx common - congested MM, neuro signs. +/- GI signs.
Patho - as in humans, gain-of-function mutation in exon 12 of the JAK2 gene
leading to erythrocytosis only. But true underlying cause unknown.

211
Q

Define leukoreduction.

A

Methods of preserving blood to optimize its characteristics and limit degradation during storage are required. In particular, the metabolites of leukocytes such as cytokines, histamine, elastase, and acid phosphatase
seem fundamental to the development of storage lesions and post-transfusion reactions.
In humans, the leukoreduction of the human blood units reduces number of WBCs (about 1-5 x 10^6 per blood unit). The prestorage filtration, soon after the blood donation,
reduces the lesions of RBCs during the storage period by removing the leukocytes before their fragmentation and avoiding the accumulation of cytokines of leukocyte origin in stored blood and blood components.

212
Q

1) Why are RBCs susceptible to oxidative injury? Esp cats?
2) What mechanisms do RBCs have to prevent oxidative injury?
3) Clin path findings with RBC oxidative injury?

A

1) Risk factors for oxidative injury: ubiquity, proximity to oxygen, lack of
nuclear material, high iron content.
Cats - feline Hb contains 8 instead of 2 oxidizable sulfhydryl groups. Also feline spleen is inefficient at removing HB. So low numbers (<10%) single, small Heinz bodies may be seen on RBCs in healthy cats.

2) Most impt mechanism = glutathione pathway. Glutathione is a tripeptide produced from cysteine,
glycine & glutamate, and is primarily formed and stored by the liver,
but RBCs have intracellular glutathione as a major antioxidant
defense. Glutathione exerts its antioxidant effect through neutralizing ROS. Glutathione, in the presence of ROS is oxidized and the interaction of free radicals and enzymes like glutathione peroxidase form oxidized glutathione (GSSG). Oxidized glutathione can be recycled through the function of enzymes (eg, glutathione reductase) and cofactors (eg, vitamin C, vitamin E, and selenium), to be reduced to its original form (reduced glutathione, GSH).

3) Heinz bodies, eccentrocytes

213
Q

Heinz bodies
a) Formation process?
b) DDx in cats?
c) DDx in dogs?
d) Which stain to differentiate?

A

a) HBs are produced when the sulfhydryl groups in the globin part of the Hb molecule undergoes oxidation, causing the molecule to become unstable –> damaged Hb molecules coalesce. Usually removed from RBCs by the spleen.

b) DKA > DM, hepatic lipidosis, drugs (acetaminophen), hyperT (with/without anemia), lymphoma, renal failure, propylene glycol (semi-moist food - can see up to 50% HBl; usually not anemic but reduced RBC lifespan), salmon based diets.

c) Onions/garlic, Zn, paracetamol (< cats)

d) New methylene blue (HB stain dark blue, RBC pale aqua)

214
Q

Cat RBCs. Abnormality?

A

Heinz bodies

215
Q

Lifespan of RBCs in dogs vs cats?

A

D: 110-120 days
C: 65-76 days

216
Q

Name 2 congenital platelet disorders in dogs.

A

1) Platelet storage pool disease (impaired adenosine diphosphate (ADP) storage in the dense granules of platelets)

2) Glanzmann’s thrombasthenia (impaired expression of platelet integrin αIIbβ3)

217
Q

What is the pathogenesis of Glanzmann’s thrombasthenia?

A

Autosomal recessive congenital platelet disorder caused by qualitative or quantitative defects of platelet GPIIb–IIIa complex (aka fibrinogen receptor), due to mutations within the gene encoding GPIIb.
Leads to impaired platelet aggregation, platelets cannot bind fibrinogen and mediate clot retraction.

218
Q

Clinical manifestations of Glanzmann’s thrombasthenia & findings on platelet function testing?

A

Bleeding diathesis; intermittent hematoma formation and/or petechiae hemorrhage, onset of signs from young.
Whole blood platelet aggregometry - significant impairment in platelet aggregation in response to ADP and AA.

219
Q

Dog & cat breeds affected by Glanzmann’s thrombasthenia?

A

All cases reported involve mutations in gene encoding GPIIb.

Dogs:
- Otterhounds - single nucleotide change in exon 12 –> substitution of a histidine for aspartic acid within the 3rd calcium-binding domain of GPIIb.
- Great Pyrenees (Type 1 GT - severe quantitative decrease in GPIIb–IIIa). 14-base-pair repeat in exon 13 –> frameshift –> premature stop codon
- Mixed breed dogs (case report Haysom JVIM 2016) - SNP in exon 13 –> premature stop codon at codon for arginine.

Cat: case report (non-pedigree) Li JVIM 2020.
ITGA2B gene –> frameshift –> impaired expression of platelet integrin αIIbβ3.

220
Q

Incidence of transfusion reactions in dogs?
Most common type of transfusion reaction?

A

3-28%.
Febrile non-hemolytic reaction.

221
Q

Describe major vs minor cross-matching.

A

Major CM – detects recipient antibodies against donor RBC antigens.
Minor CM test – detects antibodies in the donor serum against recipient RBC antigens.
Presence of agglutination or haemolysis indicates incompatibility.

222
Q

Role of protein C?

Consequences of protein C deficiency?

A

Circulating, vitamin K-dependent protease produced by the liver. Activated form has a role in regulating coagulation - acts as an anticoagulant by inactivating factors Va & VIIIa –> regulates subsequent thrombin generation.

Venous thrombosis (case report in dog)

223
Q

Which other novel erythrocyte antigens have been identified in cats outside of the AB system? What is the prevalence of these antigens (if known)?

What is the clinical significance of knowing antigen status in cats receiving blood transfusions?

A

Binvel JVIM 2020

Mik
FEA 1 - 84%
FEA 5 - 96%
And 3 other FEAs (2-4)

FEA 1-negative status was associated with a higher risk of having naturally occurring alloantibodies (NOAb) - present in 16.7% cats (vs 5.1% of FEA 1-positive cats).

FEA 1 may correspond to the Mik antigen. Some FEA 1 or Mik-negative cats may present anti-Mik or anti-FEA 1 NOAb - may mediate a clinically relevant transfusion reaction despite blood donor and recipient being AB-matched.

224
Q

Platelet P2Y12 receptor:
- Roles?
- Which drugs target this?

A

Crucial role in ADP-mediated generation of thromboxane A2 (another impt platelet activator). Inititates signaling events that potentiate agonist-induced dense granule release and procoagulant activity.

Drugs - clopidogrel, prasugrel, cangrelor, ticagrelor

225
Q

Platelet 𝛼IIb𝛽3 receptor
- Roles?
- Which drugs target this?

A

Integrin receptor. Binds soluble fibrinogen, vWF, fibronectin, and vitronectin&raquo_space; essential for platelet aggregation.

Drugs - abciximab, tirofiban, eptifibatide

226
Q

Aspirin
- MOA?
- Duration of effects?

A

Irreversibly inhibits COX-1 activity in platelets&raquo_space; prevents production of thromboxane (TXA) A2 & PG

~7-10 days (lifespan of platelets)

227
Q

Where is vWF produced & stored?
Differences in amts between dogs & cats?
Physiologic/pathologic factors influencing vWF fluctuations/

A

VWF - produced by endothelial cells & megakaryocytes, stored in platelet alpha granules & endothelial cells (Weibel-Palade bodies)
(NB FVIII produced by hepatocytes)

Dogs have much less vWF in platelets (3%) cf cats (20%)

Fluctuations - day-to-day fluctuations in healthy dogs. Exaggerated with pregnancy, heat (bitches), systemic illness (esp liver disease, inflammatory disorders). Measure ideally during physiologically ‘quiet’ times.

228
Q

Types of vWD, pathogenesis & predisposed breeds?

A

Type I vWD: normal vWD but low concentration. Many breeds - Airedale, Akita, Bernese Mountain Dog, Dachshund, Dobermans, GSDs, GRs, Greyhound, Irish Wolfhound, Manchester Terrier, Schnauzer, Pembroke Welsh Corgi, Poodle, Shetland Sheepdog etc.
Clinical severity variable depending on vWF: Ag & breed. Airedales rarely bleed, Dobers tend to bleed.

Type II vWD: low vWF concentration + abnormal structure. Severe clinical presentation. German Shorthaired Pointer, German Wirehaired Pointer.

Type III vWD: vWF markedly reduced to absent. Severe clinical presentation.
Familial: Chesapeake Bay Retriever, Dutch Kooiker, Scottish Terrier, Shetland Sheepdog.
Sporadic: Blue Heeler, Border Collie, Bull Terrier, Cocker Spaniel, Labrador Retriever, mixed breeds, Pomeranian etc.

229
Q

Describe what information can be obtained from the labelled parameters on the TEG tracing in the diagram. What associations do these parameters have to standard coagulation assays?

A

R (reaction time) = time to initial fibrin formation
- Primarily affected by coagulation factor activity (direct correlation with PT +/- aPTT)

K (clotting time) = time needed to reach a predetermined clot strength
- K dependent on coagulation factor activity + [fibrinogen] + platelets.

Angle (α) = rate of clot formation

Maximum clot strength (MA) = maximum amplitude of tracing (in mm).
- MA can be converted to G = clot strength in units of force (dynes/cm2).
- MA determined primarily by platelet number/function + [fibrinogen].

230
Q

What is the function of P-selectin wrt platelets?

A

P-selectin = cell adhesion molecule/protein produced by activated platelets & endothelial cells. Mediates rolling of platelets & WBCs on activated endothelial cells. After platelet activation, P-selectin is translocated from intracellular granules to the external membrane. Fibrinogen then aggregates platelets by bridging glycoprotein (GP) IIb/IIIa between adjacent platelets.

231
Q

What is the function of P-selectin wrt platelets?

A

P-selectin = cell adhesion molecule/protein produced by activated platelets & endothelial cells. Mediates rolling of platelets & WBCs on activated endothelial cells. After platelet activation, P-selectin is translocated from intracellular granules to the external membrane. Fibrinogen then aggregates platelets by bridging glycoprotein (GP) IIb/IIIa between adjacent platelets.

232
Q

What is ADAMTS13?
Deficiency results in what condition?

A

Zinc-containing metalloprotease enzyme that cleaves vWf anchored on the endothelial surface, in circulation & at sites of vascular injury.

Deficiency (either autoantibody-mediated destruction or gene mutation) leads to thrombotic thrombocytopenic purpura (TTP).

233
Q

Which coagulation factors are stable vs labile in transfusion products?

A

Stable: II, VII, IX, X
Labile: V, VIII

234
Q

Which dot plot(s) is/are normal vs abnormal? Explain why.

A

(A) is a normal dot plot with distinct separation of cell clusters of all five cell types. Identification of each cell (dot) is indicated by the color code at the bottom (neutrophils, lymphocytes, monocytes, eosinophils, and basophils, respectively). URBC is un-lysed RBC.

**Distinct lines drawn through the middle of a cell cluster is an indication the instrument classified cells incorrectly. A cell cluster should have one cell type and one color. Dividing a cell cluster into two or more colors indicates that cluster of one cell type was classified as more than one type. **

(B) is an abnormal ProCyte dot plot. There is a long oval cluster of cells extending up from the normal neutrophil area, to the right of the true, small cluster of blue lymphocytes and continuing up into the area to the lower right of the true red monocytes. This long oval cluster of neutrophils was classified as neutrophils (violet: lowest part) lymphocytes (blue: middle part) and monocytes (red: upper part).
The blood smear had toxic immature neutrophils which appeared to have increased fluorescence.

** (C) is an abnormal ProCyte dot plot **in which the oval cluster of cells to the far right was actually all eosinophils but about half (lower part with light blue dots) were incorrectly classified as basophils by ProCyte. The sharp line bisecting the distinct cell cluster predicts the instrument error. There was satisfactory separation of neutrophil, lymphocyte, and monocytes clusters.

235
Q

Role of vitamin K in hemostasis?

A

Co-factor for enzyme γ-glutamyl carboxylase, which modifies FII, VII, IX & X&raquo_space; allows binding to Ca2+, then to phospholipid membranes on platelets.
Also needed for activation of anti-clotting factors proteins C, S & Z.
- Protein C inhibits FVIIIa & Va, inhibiting thrombin generationl; protein S = cofactor
- Protein Z inhibits FXa

236
Q

Inherited disorders in Vitamin K-dependent enzymes has been reported in what cat breed? Pathogenesis? Clinical manifestations?

A

Devon Rex.

Pathogenesis: abnormal gamma-glutamyl carboxylase (carboxylase-epoxidase) enzyme, required for activation of vitamin K-dependent factors with vitamin K hydroquinone as a cofactor. Enzyme has abnormally decreased affinity for both vit K hydroquinone & inactive CFs&raquo_space; decreased affinity can be overcome with vitamin K supplementation.

CSx: hematomas, conjunctival hemorrhage, hemarthrosis, massive bleeding into body cavities.
Prolonged PT & aPTT; normal fibrinogen & platelet counts. Reduced activities of CFs (II, IX, X <20% activity, VII <50% activity)

237
Q

What BM & hemogram changes can be observed with estrogen toxicity?

A

Early - myeloid hyperplasia (increased M:E ratio) + peripheral neutrophilia
Also increased BM plasma cells (3%+), aplastic anemia

238
Q

What cut-off % of non-lymphoid blast populations in BM or blood is used to diagnose acute myeloid leukemia?

A

> 20% blasts
(Chronic ML - marked peripoheral left shift)

239
Q

What populations of cats are most commonly diagnosed with MDS?

A

FeLV and/or FIV+

240
Q

What are the normal values in cat/dog BM for the following:
- Plasma cells
- Lymphocytes
- Mononuclear phagocytes
- Granulocytes
- M: E ratio?

A
  • Plasma cells </= 2%
  • Lymphocytes <10% (up to 14% in healthy dogs, 20% in cats)
  • Mononuclear phagocytes </= 2%
  • Granulocytes (myeloblasts, promyelocytes) </= 5%
  • M: E ratio - dogs 0.75-2.5, cats 1-3
241
Q

What hemostatic abnormalities are common in cats with liver disease (cholangitis, HL or neoplasia)?

What is the % of bleeding complications in cats undergoing liver bx? Which cats are most at risk?

A
  • Vit K def (prolonged PT, decr FII, VII, X activities, increased PIVKA)
  • FXIII deficiency (impt in final stabilization of fibrin clot)
  • Decr anti-coagulants (AT, PC)
  • Fibrinogen variable (incr with inflammatory dz, decr with lipidosis)

Minor bleeding 22% (Hct drop <10%), 13% needed major tx.
Cats with obstructive jaundice most at risk for transfusion dependency (though uncommonly have prolonged PT/APTT)

242
Q

What are systemic complications of hyperviscosity syndrome?

A

Common - hemostatic disorders (coating of platelets with Ig etc.) –> petechiae, epistaxis & mucosal hemorrhage
Ocular changes - visual abnormalities
Neuro signs (e.g. seizures), renal failure, CHF

243
Q

What immunohistochemical stain is useful to diagnose lymphangiosarcoma in dogs?

A

Prospero-related homeobox gene 1 (PROX-1). Marker specific to lymphatic endothelial cells.

244
Q

Increased levels of what amino acid may lead to thrombosis? What does this reflect?

A

Homocysteine. HyperHCY reflects B12 or folate deficiency
(observed in 100% healthy Greyhounds, 75% Greyhounds with thrombosis in 1 paper)

245
Q

Which clotting factors does heparin inactivate? What does it activate?

A

At low + high doses - inhibits Xa
At high doses - inhibits FIIa, IXa, XIa, XIIa, XIIIa (fibrin-stabilising), FVa, FVIIIa
Activates tPA (fibrinolytic) & release of tissue factor inhibitors

246
Q

DDx for reticulocytosis without anaemia?

A
  • Drive for erythropoiesis - pulmonary disease most common, CVS disease, renal hypoxia (renal/extra-renal causes)
  • Inappropriate EPO release (renal or hepatic tumors)
  • Ni convincing evidence of iron deficiency associated with blood loss
  • Compensated haemolytic anaemia
247
Q

What causes increase in erythropoietin?

A

Renal cortical hypoxia

248
Q

Reticulocytosis should occur after what amount of time?

A

2-5 (or 7 depending on what chapter of Ettinger you read…) days

249
Q

Patients on cytotoxic drugs should generally have a CBC rechecked within _ to _ days.

A

7-21 days

250
Q

Causes of Heinz body anemia?

A

Onion, zinc, acetaminophen, methylene blue toxicosis

251
Q

Collapse following exercise with evidence of hemolysis in English Springer Spaniel is consistent with what disease? What other breed can have this?

A

PFK deficiency. American cocker spaniels

252
Q

Breeds affected by pyruvate kinase deficiency? Signs are a result of what pathophysiologic process?

A

Beagle, Basenji, West Highland White Terrier, Cairn Terrier, American Eskimo Dog, Dachshund, Pug(Pug is included as breed per UCD); signs due to myelofibrosis and hemolytic anemia

253
Q

What happens to ferritin and transferrin in inflammation? What is transferrin indicated as an iron panel?

A

Ferritin goes up (positive acute phase), transferrin goes down; transferrin listed as TIBC

254
Q

Which anti-epileptic agent can cause dysmyelopoeisis?

A

Phenobarbital

255
Q

Difference between epoetin and darbopoetin?

A

Darbopoetin is more heavily glycosylated, which poses less risk of developing anti-EPO antibodies

256
Q

Other side effects of EPO agents besides development of antibodies

A

Hyperviscosity (hypertension, seizures); Fe deficiency; for epoetin > fever, injection site irritation, mucocutaneous ulceration

257
Q

Causes for secondary inappropriate polycythemia?

A

EPO producing tumor, pyelonephritis, local renal hypoxia, hyperthyroidism, hyperadrenocorticism, acromegaly

258
Q

EPO production in primary polycythemia is

A

Low to normal

259
Q

Low antithrombin III can be secondary to:

A

Reduced hepatic production, consumption, renal or enteric loss

260
Q

What are the laboratory markers of DIC? (There are seven)

A

Thrombocytopenia, prolonged clotting times, elevated FDP, elevated D-Dimer, decreased fibrinogen, decreased anti-thrombin, red blood cell fragmentation

261
Q

Stored plasma is appropriate to administer to a patient with anticoagulant rodenticide intoxication. T/F?

A

True - stored plasma does not have factors 5/8 but does have the others

262
Q

What does cryo-poor plasma not contain?

A

Cryo-poor plasma doesn’t contain factor 5, factor 8, vWF, fibrinogen, fibronectin (aka what cryoprecipitate contains)

263
Q

Factor 13 deficiency will result in what change to PT/PTT/ACT?

A

None

264
Q

Canine breeds associated with Factor 7 deficiency

A

colony-bred mongrels, Beagles, Miniature Schnauzers, Alaskan Malamutes, Boxers, and Bulldogs (eClinPath)

265
Q

Feline breeds associated with Hemophilia B (which factor is this?)

A

British Shorthair cats and Siamese-cross cats (Factor 9).

266
Q

Breeds associated with Factor 11 deficiency(hemophilia C)

A

Springer Spaniel, Great Pyrenees, Weimaraner, and Kerry Blue terrier breeds.

267
Q

Differentiate the three types of vWD

A

Type 1 - low plasma concentration, full array of vWF multimers, mild to moderate bleeding
Type 2 - variable concentration, absence high molecular weight multimers, moderate to severe bleeding
Type 3 - no vWF, severe bleeding tendency

268
Q

Breeds associated with vWD (for which there is DNA testing)

A

Type 1 - Bernese Mountain Dog, Corgi (Cardigan and Pembroke Welsh), Coton de Tulear, Doberman
Pinscher, Dutch Partridge dog, German Pinscher, Goldendoodle, Irish Setter, Kerry Blue Terrier, Manchester Terrier, Papillon, Poodle, Stabyhoun, West Highland Terrier

Type 2 - German Shorthaired Pointer, German Wirehaired Pointer

Type 3 -
Dutch Kooiker,* Scottish Terrier,** Shetland Sheepdog*** [different DNA mutations in all of these]

269
Q

What is Glanzman thrombasthenia and how is it different from CalDAG-GEFI
thrombopathia? Breeds?

A

Both involve fibrinogen receptor, GPIIb-IIIa (this allow platelet activation/connection to vWF and fibrinogen); In Glanzmans’s this is absent or deficient - Otterhounds, Great Pyrenees; in CalDAG this a signal transduction disorder that prevents conformation change that allows binding - BASSETS, Spitz Landseer

270
Q

Ideal PK properties of drugs suitable for clearance by hemodialysis? Examples?

A

Low molecular weight
Low Vd (<1L/kg)
Low plasma protein binding
E.g. Baclofen

271
Q

Types of TPE?

A

1) Membrane based TPE - apheresis based on molecular size

2) Centrifugal TPE - apheresis based on molecular density. Adv - possible for other apheresis techniques e.g. RBC, WBC, platelets. Disadv - require specific machines, only available in few specialized institutions.

272
Q

Hemoperfusion (HP) - definition, indications? complications?

A

Def: direct molecular adsorption by activated charcoal, and can remove any drug or toxin with affinity to charcoal, independent of molecular weight and plasma protein binding, until saturation of the filter is reached.

Common complications: thrombocytopenia, leukopenia, hypocalcemia, hypoglycemia, hypothermia. Mostly eliminated by HP & haemodialysis (HP/HD) - combo therapy where blood is first filtered with HP and then processed through an HD filter before returning to the patient.

273
Q

TPE indications?

A

IMD
Hyperviscosity syndrome
Highly protein-bound toxins

274
Q

Anti-coagulation during TPE - methods & indications?

A

Systemic heparinization (SH) - contraindicated in hemostatic disorders (IMTP, DIC, pulmonary hemorrhage, CNS bleeding).
Regional citrate anticoagulation (RCA) - citrate-Ca complexes accumulate when administration rate > hepatic metabolism –> ionized hypoCa, metabolic alkalosis. Contraindicated for mTPE (humans). Low admin rate with hemostatic disorders (when cannot use SH).

ACVIM SAIM (2023) (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions