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Midterm 2 Flashcards

0
Q

Clinical symptoms for Polycythemia Vera are

A

Hematemesis
Hematachezia
Epistaxis

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1
Q

Polycythemia is

A

Increase in either the RBC count, total hemoglobin or hematocrit

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2
Q

Polycythemia Vera is diagnosed how

A

High PCV and RBC parameters

Bone marrow

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3
Q

Polycythemia Vera is treated by

A

Phlebotomy

Chemotherapy

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4
Q

Polycythemia is classified in two ways, they are

A

Absolute and relative polycythemia

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5
Q

Absolute polycythemia can be broken down into two parts they are

A

Primary and secondary

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6
Q

Absolute Polycythemia (primary) is

A

A neoplastic condition
Bone marrow increases the production of all cell mainly RBC
Decreased erythropioten

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7
Q

Absolute Polycythemia (primary) is also known as

A

Polycythemia Rubra Vera

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8
Q

Absolute Polycythemia (secondary) is

A

Developed in response to hypoxemia and erythropoietin

Seen in higher elevations

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9
Q

Absolute Polycythemia (secondary) can be seen in animals with these conditions

A

Heart failure

Renal arterial thrombosis

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10
Q

RBC production in the bone marrow takes how long

A

3-6 days

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11
Q

Relative Polycythemia is also known as

A

Hemoconcentration

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12
Q

Relative Polycythemia is

A

RBC body mass remians the same but there is a decrease in blood fluid (plasma) level.

Most common and clinically significant

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13
Q

This classification of Polycythemia is most common and clinically significant

A

Relative

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14
Q

Where are WBC storage pools present

A

Bone marrow & walls throughout the blood stream

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15
Q

Between 50-75% of Neutrophils are not circulating they are adhered along the vessel walls. This is called

A

Margination or pavementing

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16
Q

Marginated Neutrophils make the majority of this

A

Marginal pool

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17
Q

Circulating Neutrophils last how long in circulation and how long in tissue

A

6-7 hours circulation

4 days in tissue

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18
Q

What is Neutrophilia

A

The increase in circulating neutrophils

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19
Q

What is a left shift

A

Increase number of band cells in circulation

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20
Q

What causes Neutrophilia

A

Epinephrine (stress and anxiety)
Corticosterioid (medication)
Tissue damage (phagocytic)

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21
Q

Neutropenia is

A

The decrease in circulating Neutrophils

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22
Q

Neutropenia is caused by

A

Overwhelming tissue damage (infection)
Granulopoietic hypoplasia
Shock (sequestration netropenia )

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23
Q

Sequestration Neutropenia (shock) is caused by

A

Anaphylactic shock or endotoxemia

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24
Q

Granulopentic Hypoplasia Neutropenia is caused by

A

Diminished bone marrow production
Band cells in blood stream
Infection

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25
Q

Lymphocytosis is

A

An increase in circulating lymphocytes

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26
Q

Lymphopenia is

A

Decrease in lymphocytes

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27
Q

Causes of Lymphocytosis are

A

Epinephrine induced
Chronic infection
Virus infection

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28
Q

Causes of Lymphopenia

A 
Stress/steroid related 
Loss of lymph (chylothorax)
Cancer chemotherapy
Irradiation 
T-cell immunodeficiency
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29
Q

Monocytosis is

A

An increase in circulating monocytes

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30
Q

Moncytopenia is

A

Decrease in circulating monocytes

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31
Q

Causes of monocytosis

A

Stress/steroid
Chronic inflammation
Granulomatous disease

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32
Q

Causes of monocytopenia

A

Pancytopenic conditions

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33
Q

Eosinophilia is

A

Increase circulating eosinophils

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34
Q

Eosinopenia is

A

Decrease circulating eosinophils

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35
Q

Causes of Eosinophilia

A

Parasitism

Immediate hypersensitivity disorders

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36
Q

Causes of Eosinopenia

A

Stress
Steroids
Pancytopenic

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37
Q

Signs for a Stress Leukogram

A 
Increased WBC: (15,000-35,00) 
Neutrophilia no left shift
Moncytosis 
Eosinophenia
Lymphopenia
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38
Q

Sign of Infammatory Leukogram

A 
Increased WBC: (20,000-35,000)
Neutroohilia with left shift 
Moncytosis 
Eosinophenia
Lymphopenia
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39
Q

Bone marrow is the site of

A

The production of most blood cells

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40
Q

Marrow is present in this bone cavity

A

Medullary

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41
Q

In extreme cases these two areas con produce blood cells

A

Liver and spleen

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42
Q

What happens to the bone marrow as animals age

A

Active marrow decreases and is replaced with fat (yellow marrow)

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43
Q

Marrow remains active where

A

In long bones (ribs, sternum, pelvis, skull)

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44
Q

The development process for a RBC is

A

Rubriblasts -> prorubicyte -> rubricyte -> metarubicyte -> reticulocyte -> RBc

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45
Q

The development process for granulocytes is

Neutrophil,basophil,enosinophil

A

Myeloblast -> promyelocyte -> myelocyte -> metamyelocyte -> granulocyte

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46
Q

The development of Monoblast is

A

Monocytes

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47
Q

The development of lymphoblast are

A

Lymphocytes (T or B)

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48
Q

The development of platelets is

A

Megakaryoblast -> megakaryocyte -> platelets

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49
Q

3 reasons to examine bone marrow

A

Non- regenerative anemia
Abnormal cells found on blood smear
Culture in cases of osteomyelitis

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50
Q

Bone marrow collection sites

A

Proximal humerus
Proximal femur
Wing of ilium

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51
Q

Bone marrow collection needles

A

Rosenthal bone marrow aspiration needle

Jamshidi needle for biopsy (bone marrow core)

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52
Q

Infectious agents for bone marrow

A

Erhlichosis
FeLV virus
FIP virus

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53
Q

Chemicals and toxins that cause bone marrow infections

A

Chemotherapy and radiation

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54
Q

Immune mediated disease that cause bone marrow infection

A

ITP

IMHA - immune mediated hemolytic anemia

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55
Q

Myelophistic disease is

A

Components of marrow are being crowded out of abnormal cells. Most often due to neoplasia of one or more of the cells in the normally exist in the marrow

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56
Q

Hemostasis is the

A

Process the body uses to stop the flow of blood when the vascular system is damaged

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57
Q

3 ways to prevent blood loss after a blood vessel ruptures

A

Vascular spasms
Platelets plug formation
Clot formation/coagulation

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58
Q

2 functions of platelets

A

Initial plug at the site if hemorrhage

Release active chemical which initiate the clotting process

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59
Q

What are platelets attracted to in broken blood vessels

A

Exposed collagen fibers

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60
Q

After platelets attaches to a broken blood vessel they degranualte and release a chemical that does what

A

Attract other platelets and initiate the clotting process

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61
Q

What is the end product of clot

A

Fibrin

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62
Q

What is the clotting process

A

Complex series of enzyme activations which ultimately leads to the formation of fibrin (clotting cascade)

63
Q

Name the 2 pathways a clotting cascade can be preformed

A

Intrinsic or extrinsic

64
Q

The intrinsic pathway of the clotting cascade is formed how

A 
Endothelial wall damage which attracts platelets
calcium (IV)
common path way (X) 
Prothrombin (II)
Thrombin
Fibrinogen (I)
Fibrin or clot
65
Q

The Extrinsic pathway for the clotting cascade is formed how

A 
Skin wound
Tissue thromboplastin (III)
common path way (X) 
Prothrombin (II)
Thrombin
Fibrinogen (I)
Fibrin or clot
66
Q

How is the intrinsic pathway activated

A

Endothelial lining of a blood vessel ruptures

67
Q

How is the extrinsic pathway activated

A

A membrane factor that is not a component of circulation (skin wound)

68
Q

The release of this clotting factor initiates the extrinsic pathway

A

Factor (III) thromboplastin

69
Q

The release of this clotting factor initiates the intrinsic pathway

A

Factor (IV) calcium

70
Q

Both clotting factor cascade pathways meet up at this factor

A

Factor X stuart power factor

71
Q

Clotting factor I (1) is known as

A

Fibrinogen

72
Q

Clotting factor II (2) is known as

A

Prothrombin

73
Q

Clotting factor III (3) is known as

A

Tissue thromboplastin

74
Q

Clotting factor IV (4) is known as

75
Q

Clotting factor X (10) is known as

A

Stuart power factor

76
Q

Clotting factors are generally hereditary, 4 of those are

A

Hemophilia A,B,C

Type 3 Von Willebrands disease

77
Q

Van Willebrands disease is caused by

A

Lack of function of platelet adhesion at a site of vessel injury
(Dobermans, akita, cockers, German shepherds)

78
Q

Clinical signs for Von Willebrands disease

A

Mucous membrane hemorrhage
Bruising
Epistaxis
Bleeding from teeth

79
Q

Van Willebrand disease is diagnosed by

A

Prolonged buccal membrane bleeding time (BMBT) >5min

vWF antigen assays (elisa test) <50%

80
Q

Treatment for Van Willebrand

A

Plasma cryoprecipitate transfusion

Desmopressin

81
Q

Thrombocytopenia is

A

Low platelets

82
Q

Platelet problems can be categorized as

A

Quantitative

Qualitative

83
Q

Quantitative platelet problem is

A

Decreased numbers of platelets

84
Q

Causes of quantitative platelet problems are

A

Immune mediated thrombocytopenia which autoantibodies attack platelets

DIC: platelets are consumed as millions of tiny clots are formed throughout the body

Infection: agents attack platelets leading to decreased platelets

85
Q

Qualitative platelet problem is

A

Adequate number of platelets but they don’t function properly

86
Q

Causes of qualitative platelet problems are

A

Hereditary hemophilia

Drugs (aspirins or NSAIDS)

87
Q

Which color blood collecting tube is used to test for clotting

A

Light blue

88
Q

Different coagulation test are used to evaluate 3 things, they are

A

Intrinsic pathway
Extrinsic pathway
Platelet formation

89
Q

When anticoagulation of blood is needed which anticoagulant is used

A

Sodium citrate

90
Q

What is ACT (Activated Clotting Time)

A

Procedure used to shorten the normal clotting time. If it clots with in 2mins good if it clots >5min not good

91
Q

What does ACT (activated clotting time) use as an agent

A

Diatomaceous earth

92
Q

Bleeding time can be affected by

A

Platelet defects

Buccal mucosal bleeding

93
Q

What can prolong an ACT test

A

Thrombocytopenia

Intrinsic coagulation cascade

94
Q

Activated Partial Thromboplastin Time requirers submission of this

A

Citrated plasma

95
Q

The normal range for a Activated Partial Thromboplastin Time test is

A

14-20 seconds

96
Q

The Activated Partial Thromboplastin Time test evaluates

A

Intrinsic cascade

97
Q

The Prothrombin Time test evaluates

A

Extrinsic cascade

Platelet formation

98
Q

Prolonged Prothrombin Time test can be associated wit

A

Liver disease
Hereditary defects in clotting factor
Vitamin K deficiency

99
Q

(PIVKA) Protein Induced by Vitamin K Absence determines the rodenticide toxicity from

A

Hemophilia

100
Q

Increase in (PIVKA) Protein Induced by Vitamin K Absence can be a sign of

A

Poison ingestion within 6hour window

101
Q

D-Dimer and Fibrin Degradation Factor (FDP) is primarily used to determine

102
Q

High levels of D-Dimer and Fibrin Degradation Factor (FDP) are seen in these 3 states

A

Hemangiosarcoma
Trauma
Liver Failure

103
Q

D-Dimer and Fibrin Degradation Factor (FDP) are both formed how

A

Formed as clots are broken down and degraded

104
Q

A hematocrit is obtained how

A

Filling a microhematcrit tube at least 3/4 full then centrifuging the tube then reading the paced cell volume

105
Q

Plasma Protein Determination is collected how

A

Breaking the microhematocrit tube just above the Buffy coat and dispensed the plasma from the non-broken side on the refractometer

106
Q

What does DEA stand for

A

Dog Erythrocytic Antigens

107
Q

How many blood group antigens does a dog have

108
Q

DEA 1 antigens are broken down into two subgroups they are

A

DEA 1.1 (40-40% of the dog population)

DEA 1.2 (10-20% of the dog population)

109
Q

DEA 1.1 are the most important antigens because

A

They have strong antigenicity and cause the most serious problems during transfusion

110
Q

Dogs do not have naturally occurring antibodies to other blood groups

111
Q

Is it safe for a first time incompatible transfusion to be given to a recipient who has nerve had a previous transfusion

112
Q

If a recipient or donor has been transfused before one or both may have developed what

A

Antibodies with can set up for a transfusion reaction

113
Q

In a transfusion reaction two possible consequences can occur, they are

A

Recipient has antibodies that attack donors RBCs

Donor has antibodies which attack the recipients RBCs (minor)

114
Q

Transfusion reactions result in either (2)

A

Hemolysis (primary reaction)

Agglutination

115
Q

In a hemolysis transfusion reaction what happen

A

Breakage of RBCs leading to the release of hemoglobin into the plasma

116
Q

If an animals plasma or serum is red this can be due to what

117
Q

Free hemoglobin can severely damage this organ and can lead to failure

118
Q

What causes agglutination

A

Antigens and antibodies clumping together

119
Q

Agglutination can lead to

A

Blood clots in vessels

120
Q

Acute Hemolytic Transfusion reactions only occur in and why

A

DEA 1.1/1.2 negative dogs because these dogs do not have naturally occurring antibodies

121
Q

Ideally all transfused blood will be

A

DEA 1.1 & 1.2 negative

122
Q

This breed of dog has a low frequency of DEA 1.1/1.2 antigens making them suitable as blood donors

A

Greyhounds

123
Q

This breed of dog is DEA 1.1 positive

124
Q

A DEA positive dog can receive what type of transfusion

A

DEA positive or negative

125
Q

A DEA negative dog can receive what type of transfusion

A

Negative only

126
Q

Cats have three blood antigens they are

127
Q

Most cats obsess this antigen

128
Q

Cats with AB blood can receive this type of transfusion

129
Q

Cats with B blood that are transfused with A blood will have a reaction. Signs include

A 
Apnea
Urination
Defection
Vomit
Neruo depression
130
Q

Feline Neonatal Isoerythrolysis is

A

Kittens have a different blood type from the queen and sucking on her milk cause the moms antibodies to destroy they kittens red blood cells

131
Q

Feline Neonatal Isoerythrolysis can lead to

A

Jaundice
Brown urine
Rapid death
Tail tip drops off

132
Q

Cats get one blood type from mom and dad. The dominant blood type is

133
Q

If a mom is type A and dad is type B the offspring will have

A

Type A blood

134
Q

Cross matching is done to

A

Determined if the donor or recipient has antibodies against each others RBCs antigens

135
Q

A major cross match test for

A

Whether the recipient has antibodies against the donor

136
Q

A minor cross match is

A

Whether the donor has antibodies against the recipient

137
Q

Crossmatching is not necessary if

A

Neither dog had had a transfusion

138
Q

Name the phases of the estrous cycle

A

Anestrus
Proestrus
Estrus
Diestrus

139
Q

Anestrus phase

A

Characterized by a predominance of intermediate round nucleus with basophilic cytoplasm

140
Q

Proestrus phase

A

Capillary breakage and leakage of RBCs through uterine epithelium

141
Q

Estrus phase

A

Predominance of superficial cornified cells

142
Q

Diestrus phase

A

Decline in the number & reappearance of intermediate and parabasal cells

143
Q

Parabasal cells are

A

Round small cells with large nucleus to cytoplasm

144
Q

Parabasal cells can be seen primarily during which estrus cycle phase

145
Q

Intermediate cells are

A

Round irregular cells with small nucleus to cytoplasm

146
Q

Intermediate cells can be seen during which estrus cycle phase

A

All stages but estrus

147
Q

Superficial cells are

A

Large irregular shaped with small nucleus and all large cytoplasm

148
Q

Superficial cells can be found during this estrus cycle phase

149
Q

During anestrus phase which cells are present

A 
Parabasal & intermediate cells
Few RBCs (no neutros)
150
Q

During proestrus which cells are present

A

Intermediate & parabasal

Large # of RBCs (neutros)

151
Q

During estrus which cells are present

A

Superficial cells with no RBCs

152
Q

During diestrus which cells are present

A

Parabasal, intermediate

Few RBC

153
Q

Epithelial Tumors: benign and malignant are known as

A

Adenoma and carcinoma

154
Q

Connective Tissue Tumors: benign and malignant

A

Oma and sarcoma

Clin Path (2 decks)

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