Midterm 2 Flashcards
0
Q
Clinical symptoms for Polycythemia Vera are
A
Hematemesis
Hematachezia
Epistaxis
1
Q
Polycythemia is
A
Increase in either the RBC count, total hemoglobin or hematocrit
2
Q
Polycythemia Vera is diagnosed how
A
High PCV and RBC parameters
Bone marrow
3
Q
Polycythemia Vera is treated by
A
Phlebotomy
Chemotherapy
4
Q
Polycythemia is classified in two ways, they are
A
Absolute and relative polycythemia
5
Q
Absolute polycythemia can be broken down into two parts they are
A
Primary and secondary
6
Q
Absolute Polycythemia (primary) is
A
A neoplastic condition
Bone marrow increases the production of all cell mainly RBC
Decreased erythropioten
7
Q
Absolute Polycythemia (primary) is also known as
A
Polycythemia Rubra Vera
8
Q
Absolute Polycythemia (secondary) is
A
Developed in response to hypoxemia and erythropoietin
Seen in higher elevations
9
Q
Absolute Polycythemia (secondary) can be seen in animals with these conditions
A
Heart failure
Renal arterial thrombosis
10
Q
RBC production in the bone marrow takes how long
A
3-6 days
11
Q
Relative Polycythemia is also known as
A
Hemoconcentration
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
13
Q
This classification of Polycythemia is most common and clinically significant
A
Relative
14
Q
Where are WBC storage pools present
A
Bone marrow & walls throughout the blood stream
15
Q
Between 50-75% of Neutrophils are not circulating they are adhered along the vessel walls. This is called
A
Margination or pavementing
16
Q
Marginated Neutrophils make the majority of this
A
Marginal pool
17
Q
Circulating Neutrophils last how long in circulation and how long in tissue
A
6-7 hours circulation
4 days in tissue
18
Q
What is Neutrophilia
A
The increase in circulating neutrophils
19
Q
What is a left shift
A
Increase number of band cells in circulation
20
Q
What causes Neutrophilia
A
Epinephrine (stress and anxiety)
Corticosterioid (medication)
Tissue damage (phagocytic)
21
Q
Neutropenia is
A
The decrease in circulating Neutrophils
22
Q
Neutropenia is caused by
A
Overwhelming tissue damage (infection)
Granulopoietic hypoplasia
Shock (sequestration netropenia )
23
Q
Sequestration Neutropenia (shock) is caused by
A
Anaphylactic shock or endotoxemia
24
Granulopentic Hypoplasia Neutropenia is caused by
Diminished bone marrow production
Band cells in blood stream
Infection
25
Lymphocytosis is
An increase in circulating lymphocytes
26
Lymphopenia is
Decrease in lymphocytes
27
Causes of Lymphocytosis are
Epinephrine induced
Chronic infection
Virus infection
28
Causes of Lymphopenia
```
Stress/steroid related
Loss of lymph (chylothorax)
Cancer chemotherapy
Irradiation
T-cell immunodeficiency
```
29
Monocytosis is
An increase in circulating monocytes
30
Moncytopenia is
Decrease in circulating monocytes
31
Causes of monocytosis
Stress/steroid
Chronic inflammation
Granulomatous disease
32
Causes of monocytopenia
Pancytopenic conditions
33
Eosinophilia is
Increase circulating eosinophils
34
Eosinopenia is
Decrease circulating eosinophils
35
Causes of Eosinophilia
Parasitism
| Immediate hypersensitivity disorders
36
Causes of Eosinopenia
Stress
Steroids
Pancytopenic
37
Signs for a Stress Leukogram
```
Increased WBC: (15,000-35,00)
Neutrophilia no left shift
Moncytosis
Eosinophenia
Lymphopenia
```
38
Sign of Infammatory Leukogram
```
Increased WBC: (20,000-35,000)
Neutroohilia with left shift
Moncytosis
Eosinophenia
Lymphopenia
```
39
Bone marrow is the site of
The production of most blood cells
40
Marrow is present in this bone cavity
Medullary
41
In extreme cases these two areas con produce blood cells
Liver and spleen
42
What happens to the bone marrow as animals age
Active marrow decreases and is replaced with fat (yellow marrow)
43
Marrow remains active where
In long bones (ribs, sternum, pelvis, skull)
44
The development process for a RBC is
Rubriblasts -> prorubicyte -> rubricyte -> metarubicyte -> reticulocyte -> RBc
45
The development process for granulocytes is
| Neutrophil,basophil,enosinophil
Myeloblast -> promyelocyte -> myelocyte -> metamyelocyte -> granulocyte
46
The development of Monoblast is
Monocytes
47
The development of lymphoblast are
Lymphocytes (T or B)
48
The development of platelets is
Megakaryoblast -> megakaryocyte -> platelets
49
3 reasons to examine bone marrow
Non- regenerative anemia
Abnormal cells found on blood smear
Culture in cases of osteomyelitis
50
Bone marrow collection sites
Proximal humerus
Proximal femur
Wing of ilium
51
Bone marrow collection needles
Rosenthal bone marrow aspiration needle
| Jamshidi needle for biopsy (bone marrow core)
52
Infectious agents for bone marrow
Erhlichosis
FeLV virus
FIP virus
53
Chemicals and toxins that cause bone marrow infections
Chemotherapy and radiation
54
Immune mediated disease that cause bone marrow infection
ITP
| IMHA - immune mediated hemolytic anemia
55
Myelophistic disease is
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
56
Hemostasis is the
Process the body uses to stop the flow of blood when the vascular system is damaged
57
3 ways to prevent blood loss after a blood vessel ruptures
Vascular spasms
Platelets plug formation
Clot formation/coagulation
58
2 functions of platelets
Initial plug at the site if hemorrhage
| Release active chemical which initiate the clotting process
59
What are platelets attracted to in broken blood vessels
Exposed collagen fibers
60
After platelets attaches to a broken blood vessel they degranualte and release a chemical that does what
Attract other platelets and initiate the clotting process
61
What is the end product of clot
Fibrin
62
What is the clotting process
Complex series of enzyme activations which ultimately leads to the formation of fibrin (clotting cascade)
63
Name the 2 pathways a clotting cascade can be preformed
Intrinsic or extrinsic
64
The intrinsic pathway of the clotting cascade is formed how
```
Endothelial wall damage which attracts platelets
calcium (IV)
common path way (X)
Prothrombin (II)
Thrombin
Fibrinogen (I)
Fibrin or clot
```
65
The Extrinsic pathway for the clotting cascade is formed how
```
Skin wound
Tissue thromboplastin (III)
common path way (X)
Prothrombin (II)
Thrombin
Fibrinogen (I)
Fibrin or clot
```
66
How is the intrinsic pathway activated
Endothelial lining of a blood vessel ruptures
67
How is the extrinsic pathway activated
A membrane factor that is not a component of circulation (skin wound)
68
The release of this clotting factor initiates the extrinsic pathway
Factor (III) thromboplastin
69
The release of this clotting factor initiates the intrinsic pathway
Factor (IV) calcium
70
Both clotting factor cascade pathways meet up at this factor
Factor X stuart power factor
71
Clotting factor I (1) is known as
Fibrinogen
72
Clotting factor II (2) is known as
Prothrombin
73
Clotting factor III (3) is known as
Tissue thromboplastin
74
Clotting factor IV (4) is known as
Calcium
75
Clotting factor X (10) is known as
Stuart power factor
76
Clotting factors are generally hereditary, 4 of those are
Hemophilia A,B,C
| Type 3 Von Willebrands disease
77
Van Willebrands disease is caused by
Lack of function of platelet adhesion at a site of vessel injury
(Dobermans, akita, cockers, German shepherds)
78
Clinical signs for Von Willebrands disease
Mucous membrane hemorrhage
Bruising
Epistaxis
Bleeding from teeth
79
Van Willebrand disease is diagnosed by
Prolonged buccal membrane bleeding time (BMBT) >5min
| vWF antigen assays (elisa test) <50%
80
Treatment for Van Willebrand
Plasma cryoprecipitate transfusion
| Desmopressin
81
Thrombocytopenia is
Low platelets
82
Platelet problems can be categorized as
Quantitative
| Qualitative
83
Quantitative platelet problem is
Decreased numbers of platelets
84
Causes of quantitative platelet problems are
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
Qualitative platelet problem is
Adequate number of platelets but they don't function properly
86
Causes of qualitative platelet problems are
Hereditary hemophilia
| Drugs (aspirins or NSAIDS)
87
Which color blood collecting tube is used to test for clotting
Light blue
88
Different coagulation test are used to evaluate 3 things, they are
Intrinsic pathway
Extrinsic pathway
Platelet formation
89
When anticoagulation of blood is needed which anticoagulant is used
Sodium citrate
90
What is ACT (Activated Clotting Time)
Procedure used to shorten the normal clotting time. If it clots with in 2mins good if it clots >5min not good
91
What does ACT (activated clotting time) use as an agent
Diatomaceous earth
92
Bleeding time can be affected by
Platelet defects
| Buccal mucosal bleeding
93
What can prolong an ACT test
Thrombocytopenia
| Intrinsic coagulation cascade
94
Activated Partial Thromboplastin Time requirers submission of this
Citrated plasma
95
The normal range for a Activated Partial Thromboplastin Time test is
14-20 seconds
96
The Activated Partial Thromboplastin Time test evaluates
Intrinsic cascade
97
The Prothrombin Time test evaluates
Extrinsic cascade
| Platelet formation
98
Prolonged Prothrombin Time test can be associated wit
Liver disease
Hereditary defects in clotting factor
Vitamin K deficiency
99
(PIVKA) Protein Induced by Vitamin K Absence determines the rodenticide toxicity from
Hemophilia
100
Increase in (PIVKA) Protein Induced by Vitamin K Absence can be a sign of
Poison ingestion within 6hour window
101
D-Dimer and Fibrin Degradation Factor (FDP) is primarily used to determine
If DIC
102
High levels of D-Dimer and Fibrin Degradation Factor (FDP) are seen in these 3 states
Hemangiosarcoma
Trauma
Liver Failure
103
D-Dimer and Fibrin Degradation Factor (FDP) are both formed how
Formed as clots are broken down and degraded
104
A hematocrit is obtained how
Filling a microhematcrit tube at least 3/4 full then centrifuging the tube then reading the paced cell volume
105
Plasma Protein Determination is collected how
Breaking the microhematocrit tube just above the Buffy coat and dispensed the plasma from the non-broken side on the refractometer
106
What does DEA stand for
Dog Erythrocytic Antigens
107
How many blood group antigens does a dog have
7
108
DEA 1 antigens are broken down into two subgroups they are
DEA 1.1 (40-40% of the dog population)
| DEA 1.2 (10-20% of the dog population)
109
DEA 1.1 are the most important antigens because
They have strong antigenicity and cause the most serious problems during transfusion
110
Dogs do not have naturally occurring antibodies to other blood groups
Kdvkdnknd
111
Is it safe for a first time incompatible transfusion to be given to a recipient who has nerve had a previous transfusion
Yes
112
If a recipient or donor has been transfused before one or both may have developed what
Antibodies with can set up for a transfusion reaction
113
In a transfusion reaction two possible consequences can occur, they are
Recipient has antibodies that attack donors RBCs
| Donor has antibodies which attack the recipients RBCs (minor)
114
Transfusion reactions result in either (2)
Hemolysis (primary reaction)
| Agglutination
115
In a hemolysis transfusion reaction what happen
Breakage of RBCs leading to the release of hemoglobin into the plasma
116
If an animals plasma or serum is red this can be due to what
Hemolysis
117
Free hemoglobin can severely damage this organ and can lead to failure
Kidneys
118
What causes agglutination
Antigens and antibodies clumping together
119
Agglutination can lead to
Blood clots in vessels
120
Acute Hemolytic Transfusion reactions only occur in and why
DEA 1.1/1.2 negative dogs because these dogs do not have naturally occurring antibodies
121
Ideally all transfused blood will be
DEA 1.1 & 1.2 negative
122
This breed of dog has a low frequency of DEA 1.1/1.2 antigens making them suitable as blood donors
Greyhounds
123
This breed of dog is DEA 1.1 positive
Labs
124
A DEA positive dog can receive what type of transfusion
DEA positive or negative
125
A DEA negative dog can receive what type of transfusion
Negative only
126
Cats have three blood antigens they are
A
B
AB
127
Most cats obsess this antigen
A
128
Cats with AB blood can receive this type of transfusion
A or B
129
Cats with B blood that are transfused with A blood will have a reaction. Signs include
```
Apnea
Urination
Defection
Vomit
Neruo depression
```
130
Feline Neonatal Isoerythrolysis is
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
Feline Neonatal Isoerythrolysis can lead to
Jaundice
Brown urine
Rapid death
Tail tip drops off
132
Cats get one blood type from mom and dad. The dominant blood type is
A
133
If a mom is type A and dad is type B the offspring will have
Type A blood
134
Cross matching is done to
Determined if the donor or recipient has antibodies against each others RBCs antigens
135
A major cross match test for
Whether the recipient has antibodies against the donor
136
A minor cross match is
Whether the donor has antibodies against the recipient
137
Crossmatching is not necessary if
Neither dog had had a transfusion
138
Name the phases of the estrous cycle
Anestrus
Proestrus
Estrus
Diestrus
139
Anestrus phase
Characterized by a predominance of intermediate round nucleus with basophilic cytoplasm
140
Proestrus phase
Capillary breakage and leakage of RBCs through uterine epithelium
141
Estrus phase
Predominance of superficial cornified cells
142
Diestrus phase
Decline in the number & reappearance of intermediate and parabasal cells
143
Parabasal cells are
Round small cells with large nucleus to cytoplasm
144
Parabasal cells can be seen primarily during which estrus cycle phase
Anestrus
145
Intermediate cells are
Round irregular cells with small nucleus to cytoplasm
146
Intermediate cells can be seen during which estrus cycle phase
All stages but estrus
147
Superficial cells are
Large irregular shaped with small nucleus and all large cytoplasm
148
Superficial cells can be found during this estrus cycle phase
Estrus
149
During anestrus phase which cells are present
```
Parabasal & intermediate cells
Few RBCs (no neutros)
```
150
During proestrus which cells are present
Intermediate & parabasal
| Large # of RBCs (neutros)
151
During estrus which cells are present
Superficial cells with no RBCs
152
During diestrus which cells are present
Parabasal, intermediate
| Few RBC
153
Epithelial Tumors: benign and malignant are known as
Adenoma and carcinoma
154
Connective Tissue Tumors: benign and malignant
Oma and sarcoma
