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118 Cards in this Set
- Front
- Back
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3 categories of defense of innate immunity include: mechanical, chemical, and microbiological. Name components of each.
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Mechanical --> Mucus, tears, tight junctions between epithelial cells
Chemical --> Antimicrobial peptides, fatty acids, low pH, enzymes Microbiological --> Microflora |
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How is complement activated?
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There are 3 pathways (Lectin, Classical, Alternative) that all lead to generation of C3 convertase, which cleaves C3 into C3b (which is left bound on pathogen's surface) and C3a (which is released).
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What are the functions of complement?
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Neutralization - C3a recruits phagocytic cells to the site of infection and promotes inflammation.
Opsonization - Phagocytes with receptors for C3b will engulf the pathogen. Cell lysis - Formation of MAC complex to destroy cell membranes. |
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What are T cell receptors composed of?
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Majority of TCRs is made up of alpha and beta chains. A minority is made up of gamma and delta chains.
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What are B cell receptors composed of?
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BCRs are made up of either heavy chain and kappa chain OR light lambda chain.
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What are the 2 signals needed for T cell activation?
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1) TCR interacts with MHC. CD8+ T cells interact with MHC1, and CD4+ T cells interact with MHC2.
2) Co-stimulation: CD28 receptor on T cell interacts with CD80+CD86 proteins on APC. 3) A third signal flavors the T cell response. |
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What are the 2 signals needed for B cell activation?
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1) BCR interacts with antigen. B cells can recognize naive antigen, so MHC presentation is not required.
2) Co-stimuation: CD40 on B cell interacts with CD40L on activated T cell. |
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Where are naive T cells found?
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They are exported from the thymus and circulate between the blood and secondary lymphoid organs (LNs and spleen). They have limited range.
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Where are effector T cells found?
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They have a wider range of mobility. They circulate between blood and cutaneous mucosal sites, depending on where they are programmed to hone to.
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Once B cells are activated, they undergo clonal expansion in either an extrafollicular foci or a germinal center. What's the difference?
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Extrafollicular foci --> Happens in the red pulp of spleen and medullary cords of LNs. B cells rapidly differentiate into plasma cells to make lots of antibodies. These plasma cells are short lived (3-5 day lifespan).
Germinal center --> Happens in LN follicles. Part of the adaptive immune response. The B cells undergo affinity maturation, and memory B cells are produced; they migrate to the bone marrow or spleen. They can be quickly activated upon re-infection with a pathogen. |
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True or False:
A large fraction of immature B cells are selected to go into the mature B cell pool. |
FALSE. A small fraction of immature B cells survive to go into the mature B cell pool.
Immature B cells leave the bone marrow; if they make it to the spleen without showing any strong affinity to self-antigen, the immature B cell becomes a transitional B cell. If the TBC makes it through periphery without any strong affinity to self-antigen, it goes to the pool of mature B cells. The mature B cells have central and peripheral tolerance. Self-reactive B cells go into anergy, and will likely die. |
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What are the primary lymphoid organs, and what happens there?
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Primary lymphoid organs include hymus and bone marrow. Lymphocytes are produced and develop here.
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What are the secondary lymphoid organs, and what happens there?
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Secondary lymphoid organs include the spleen and lymph nodes. Lymphocytes respond to antigen here.
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What are the tertiary lymphoid organs?
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MALT, GALT, etc. Can be diffuse or organized.
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How does a hyperplastic lymph node differ from a neoplastic lymph node?
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A hyperplastic LN maintains an intact architecture, while a neoplastic one (i.e. lymphoma) has effaced architecture.
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What is the role of the spleen?
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It monitors blood-borne antigens.
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Describe the components of the spleen.
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White pulp - Lymphatic nodules located here.
Marginal zone - Region b/t white and red pulp. Antigens from blood get trapped in this area; they're presented to splenic lymphocytes here. Red pulp - Lymphocytes, RBCs, and macrophages located here. |
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Describe a type 1 hypersensitivity.
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Type 1 hypersensitivities are IgE (and mast cell) mediated. They are immediate, developing seconds to minutes after exposure to an allergen. Individuals can be genetically predisposed to developing type 1 hypersensitivities.
Ex: Urticaria, asthma, anaphylaxis, atopic dermatitis. |
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Describe a type 2 hypersensitivity.
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Type 2 hypersensitivities are IgG, IgM, or compliment mediated. Usually, the offending antigen is a cell-surface molecule.
Ex: Autoimmune hemolytic anemia (AIHA), drug-induced AIHA, transfusion reactions, neonatal isoerythrolysis. |
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Describe a type 3 hypersensitivity.
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Type 3 hypersensitivities are immune complex mediated. The 3 major elements are soluble antigen+antibody complexes, complement fixation by classical pathway, and neutrophils attracted by complement.
Ex: Arthus reaction, bird breeder's DZ, purpura hemorrhagica. |
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Describe a type 4 hypersensitivity.
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Type 4 hypersensitivities are mediated by sensitized T cells. These are delayed type hypersensitivities.
Ex: TB skin test, poison oak reaction, allergic contact dermatitis. |
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How do we avoid a type 2 hypersensitivity, blood transfusion reaction?
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Test recipient's serum using a major cross match (donor cells + recipient serum).
Test donor's serum using a minor cross match (recipient cells + donor serum). |
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What is a neonatal isoerythrolysis?
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Neonatal isoerythrolysis is a type 2 hypersensitivity reaction. It's a type of immune-mediated hemolytic anemia from ingesting maternal colostral antibody directed against surface antigens on the neonate's RBCs.
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How can you differentiate a type 1 atopic dermatitis from a type 4 allergic contact dermatitis?
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Atopic dermatitis is associated with face, nose, eyes, feet, and perineum. We can see urticaria and pruritis. It is associated with food, fleas, and inhaled allergens. Upon pathology, we see eosinophilic infiltration and edema.
Allergic contact dermatitis is associated with hairless areas of the animal's body (like ventral abdomen and feet). We can see alopecia and vesiculation. It is associated with reactive chemicals and dyes that contact the skin. Upon pathology, we see mononuclear cell infiltration. |
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What is a primary immunodeficiency?
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Primary immunodeficiencies always manifest in YOUNG animals. They include inherited defects and gene mutations.
Ex: SCID; BLAD/CLAD; cyclic neutropenia |
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What is a secondary immunodeficiency?
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Secondary immunodeficiencies are often seen in OLDER animals. The animal's immune system develops normally, but some secondary factor (eg, infectious, nutrition, cancer, stress) impairs one or more immune function.
Ex: FIV |
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What is BLAD? What type of immunodeficiency is it?
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BLAD stands for bovine leukocyte adhesion deficiency. It is a primary immunodeficiency. Neutrophils are attracted to the site of infection, but cannot get there b/c the neutrophils can't adhere to the vessel walls - the animal is deficient in a leukocyte integrin!
(In dogs, it's called CLAD.) |
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What is FIV? What type of immunodeficiency is it?
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FIV stands for feline immunodeficiency virus. It is a secondary immunodeficiency. The virus infects CD4+ T cells, leading to increased infections by opportunistic organisms and increased tumor growth.
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How do calcium anticoagulants work?
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Calcium anticoagulants chelate Ca2+, inhibiting the conversion of prothrombin to thrombin + fibrinogen to fibrin.
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What are 2 examples of calcium anticoagulants?
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EDTA - Used in collecting CBC samples
Citrate - Used in coagulation panels and in blood used for transfusions. |
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How do heparin anticoagulants work?
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Heparin activates antithrombin 3, which inhibits thrombin formation.
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When would you use heparin instead of EDTA?
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Heparin can be used to collect blood samples for CBC and chem panels. But unlike with EDTA, the plasma in the heparinized sample can be analyzed, not just the RBCs.
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Let's say you've spun a blood sample down in a hematocrit tube. List the layers, starting from bottom of the tube to the top.
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Starting from the bottom of the tube:
Clay sealant (not part of the blood sample) RBCs Buffy coat (WBCs + platelets) Plasma |
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How is a PCV (packed cell volume) obtained?
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We centrifuge the blood sample in a hematocrit tube to separate it into layers. PCV is the % of the blood that the RBCs make up.
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How is a HCT (hematocrit) obtained?
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HCT is calculated by a machine. It takes into account the average cell size (MCV) and the total # of RBCs (RBC count) in the sample.
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What is the difference between plasma and serum?
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Plasma contains fibrinogen, while serum does not.
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What cell types fall under the category of "granulocytes"?
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Granulocytes = Neutrophils, eosinophils, basophils
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What happens in bone marrow when the demand for blood cells is high?
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Hematopoiesis happens in the bone marrow - specifically, in the red marrow at the ends of long bones. If demand is great enough, the yellow marrow (fat) that would normally occupy the center of long bones becomes red and becomes hematopoietic. Sites of fetal hematopoiesis can also reactivate (spleen, liver, lymph nodes, kidneys); this is called extramedullary hematopoiesis.
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What trends do we see as young blood cells develop?
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1. Cell size and nucleus size decrease (except for megakaryocytes).
2. Nuclear : Cytoplasmic ratio decreases. 3. Cytoplasm becomes less basophlic. 4. Specific cytoplasmic contents accumulate. 5. Nucleoili disappear. 6. Chromatin condenses. |
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What is a megakaryocyte?
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Megakaryocytes are bone marrow cells that grow larger as they develop. They fracture to form many platelets / thrombocytes.
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Describe the structure of hemoglobin.
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Hemoglobin is a tetramer of 2 alpha and 2 beta chain subunits. Each chain has its own heme, which consists of a porphyrin ring and Fe2+ (ferrous iron). The ferrous iron is what binds O2 in the lungs and releases it into the tissues.
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What is methemoglobin? Why is it important?
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Methemoglobin is what we call hgb that has heme molecules containing Fe3+ (ferric iron) instead of Fe2+. This is important because Fe3+ CANNOT bind O2. Some drugs (like acetaminophen in cats) cause methemoglobin to be formed at a more rapid rate than hemoglobin.
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What is the Embden-Meyerhof pathway?
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The Embden-Meyerhoff pathway is the basic metabolic pathway of RBCs:
Glucose → Lactate |
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What is the Methemoglobin Reductase pathway?
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The methemoglobin reductase pathway is antioxidizing; it turns methemoglobin into hemoglobin by reducing the Fe3+ in heme to Fe2+.
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What is the Rapaport-Lubering pathway?
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The Rapoport-Luebering pathway produces 2,3-DPG, which is a molecule that's important for regulating hemoglobin's affinity for O2.
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What is the pentose phosphate shunt?
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The pentose phosphate shunt is responsible for regenerating the reducers, NADP+ and NADPH.
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RBCs do not have mitochondria, but still must undergo metabolism! List the 4 major metabolic pathways that occur in RBCs.
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1. Embden-Meyerhof pathway
2. Methemoglobin reductase pathway 3. Rapoport-Luebering pathway 4. Pentose phosphate shunt |
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Why is acetaminophen toxic to cats?
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Acetaminophen is a potent oxidant for cats. It oxidizes Fe2+ (ferrous) to Fe3+ (ferric), so that 30-40% of the hemoglobin ends up being in the methemoglobin state. As methemoglobin, hgb cannot bind O2, and the cat becomes cyanotic. The cat's body cannot reduce the Hgb back to the O2-capable state bc of the overwhelming amount.
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How does a low pH / low O2 / high CO2 environment (i.e., in actively metabolizing tissues) affect Hgb's affinity for O2?
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Hgb has lower affinity for O2 in metabolizing tissues (low pH; low O2). These conditions prompt Hgb to unload their O2 in the tissues, where it's needed.
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How does a higher pH / high O2 / low CO2 environment (i.e., in the lungs) affect Hgb's affinity for O2?
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Hgb has higher affinity for O2 in the lungs, where O2 is high, pH is higher, and CO2 is low. This facilitates the loading of Hgb with O2.
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How does concentration of 2,3-DPG affect Hgb's affinity for O2?
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2,3-DPG binds with greater affinity to deoxy-hemoglobin, and with less affinity to oxy-hemoglobin. It is an allosteric effector, promoting the release of O2 from Hgb.
When 2,3-DPG is high, Hgb's affinity for O2 is low; when 2,3-DPG is low, Hgb's affinity for O2 is high. |
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How does temperature affect Hgb's affinity for O2?
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When temperature is low, Hgb's affinity for O2 is high. When temperature is high, Hgb's affinity for O2 is low.
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Where do we get the iron we need for Hgb?
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Animals obtain iron from their diet. Total body iron load is regulated via intestinal absorption, NOT excretion.
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How is iron absorption regulated?
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Iron absorption is regulated via hepcidin, which is made by the liver. Hepcidin regulates ferroportin, which is the portal protein at the basal membrane of enterocytes, that lets iron be absorbed.
More hepcidin = Less intestinal Fe absorption. |
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What is the mechanism behind anemia of chronic inflammation / DZ?
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Inflammation → Increased hepcidin → Decreased intestinal Fe absorption → Decreased erythropoiesis → Less RBCs
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You see target cells on your blood smear. What does this imply?
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Target cells are formed because the RBCs have decreased Hgb content due to Fe2+ deficiency or hepatic DZ. Because of the decreased amount of Hgb, the cells have a decreased ability to reversibly deform as they leave the spleen.
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You see echinocytes on your blood smear. What does this mean?
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Presence of echinocytes is not a specific test. Lots of things can cause this type of RBC shape.
It can be: 1) Artifact from drying or storage of blood in EDTA 2) From splenic sequestration 3) From electrolyte abnormalities 4) From uremia 5) From a snake bite |
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You see spherocytes on your blood smear. What does this imply?
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Spherocytes are seen in patients with immune-mediated hemolytic anemia. Antigen-antibody complexes form on the RBCs' membranes; macrophages take bites out of the RBC's membrane to remove these complexes. When the remaining membrane re-seals around the RBC's cytosol, a spherocyte is formed.
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You see schistocytes on your blood smear. What does this imply?
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Schistocytes form when RBCs get fragmented due to a microangiopathy.
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You see acanthocytes on your blood smear. What does this imply?
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Acanthocytes can lead us down the pathway of hepatic DZ. It may indicate that hypercholesterolemia or abnormal phospholipids are present.
***Acanthocytes are normal in PIGS and CALVES. |
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You see Heinz bodies on your blood smear. What does this indicate?
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Heinz bodies indicate oxidative damage (which can be caused by oxidant drugs, plants, or other chemicals). The bodies consist of denatured hemoglobin. Cats have some normal level of Heinz bodies present bc their Hgb have a higher number of SH groups, making them more prone to oxidizing damage.
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What is a Howell-Jolly body? What does it mean if you see them on a blood smear?
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Howell-Jolly bodies are the remains of an RBC's nucleus. Their presence in RBCs usually means that there is some spleen damage. They are also seen with sickle cell anemia.
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What are the hallmarks of immune-mediated hemolytic anemia?
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1) Spherocytes on blood smear
2) Agglutination (from RBCs cross-linking with anti-RBC antibodies) |
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How do RBCs die?
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1) Failure of metabolism → ATP depletion.
2) Failure of reducing power → Hgb oxidation. 3) Senescence: RBC ages and membrane proteins get altered → Antibodies bind to altered proteins. 4) RBC is engulfed by splenic macrophages. |
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What is the average RBC lifespan in a dog? A cat?
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Dog → 100 days
Cat → 60 days |
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Describe the breakdown and excretion of RBCs.
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In the spleen, old RBCs are phagocytized by macrophages. RBCs get broken down into globin and heme. The heme portion gets broken down into biliverdin, and then unconjugated bilirubin (indirect bilirubin), which is carried by albumin in the plasma to the liver. In hepatocytes, bilirubin becomes conjugated (direct bilirubin), and is excreted into the bile. In the bile, conjugated bilirubin is broken down by bacteria into urobilinogen, then stercobilin. Finally, the heme breakdown products are excreted in urine and feces. Stercobilin gives poop its brown color.
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What does it mean to blood-type a patient? When do you do one?
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When we do a blood typing, we ID the primary RBC surface antigens of the blood donor and recipient.
ALWAYS run a blood-typing before doing RBC or plasma transfusions. |
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What does it mean to run a cross-match?
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When we do a cross-matching, we're trying to determine the compatibility of the donor's blood and the recipient's blood. We can assess what effects donor and recipient antibodies will have on one another.
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How do cats and dogs differ from one another in terms of blood types?
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Cats have naturally-occurring antibodies against the blood type antigens that they don't have. There is no such thing as a universal blood donor in cat world.
Dogs have naturally-occurring antibodies present for some systems only. Universal donors exist in dog world. |
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What parameters on a CBC describe RBC mass / whether anemia is present?
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RBC count
Hgb HCT (hematocrit) |
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Describe the mechanism of anemia.
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Decreased RBC Mass → Hypoxia → Increased EPO production in kidneys → Stimulation of erythropoiesis → Increased RBC production → Release of reticulocytes → Increased retic count on CBC
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Describe the characteristics of a reticulocyte.
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1) Larger than mature RBCs, so you'll see macrocytosis (↑ MCV).
2) Bluer than mature RBCs bc they have residual RNA and less Hgb, so you'll see polychromasia. 3) They are NOT released in response to an anemia in horses. 4) There is a baseline level of erythropoiesis going on always, so it's normal to find some amount of retics in blood (ref range: 0 - 65,000/ uL). |
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How can you tell if a horse's anemia is regenerative?
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Since horses don't throw retics during an anemia, you'd have to look at their bone marrow, either via biopsy or aspirate.
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What are the different types of anemia?
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Describe hemolysis.
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1) Hemolysis is a type of regenerative anemia.
2) Hemolysis can be intra- or extra- vascular, though extravascular is more common. 3) Hemolysis is caused by: immune-mediated, oxidative damage, infections, metabolic, fragmentation. |
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What is the mechanism of intravascular hemolysis?
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RBC lysis → Free Hgb in vessels → Hemoglobinemia → Hemoglobinuria
Ex: Heinz body anemia from acetaminophen toxicosis in cats |
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What is the mechanism of extravascular hemolysis?
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Extravascular hemolysis occurs in the spleen and other tissues.
The mechanism is similar to what happens normally in the spleen. (This is why our poop is brown.) |
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What lab results would point you in the direction of an intravascular hemolysis?
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1) ↓ RBC count / ↓ HCT / ↓ Hgb (Anemia)
2) ↑ MCH and ↑ MCHC (Falsely raised from hemoglobinemia) 3) Indications of nephropathy 4) Ghost cells on blood smear |
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What clinical signs would point you in the direction of extravascular hemolysis?
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1) ↓ RBC count / ↓ HCT / ↓ Hgb (Anemia)
2) Icterus of mucous membranes AND plasma 3) Splenomegaly |
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Describe hemorrhage.
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1) Hemorrhage can result from hemostasis abnormalities or trauma.
2) Hemorrhage can be acute / chronic & internal / external. 3) Hemorrhage can be regenerative (acute or internal) or non-regenerative (chronic or external). |
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What lab results would point you in the direction of an acute / internal hemorrhage?
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Since whole blood is lost, RBCs and plasma decrease proportionately, and this can mask the anemia. After a few days, though, fluid from interstitium will replace plasma VOLUME and anemia is apparent:
1) ↓ RBC count / ↓ HCT / ↓ Hgb (Anemia) 2) ↓ TP 3) ↑ Reticulocytes (Regenerative anemia. Since blood loss hasn't been going for long / is contained within the body, the body can compensate / recycle the iron lost and produce more RBCs.) |
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What lab results would point you in the direction of a chronic / external blood loss?
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1) ↓ RBC count / ↓ HCT / ↓ Hgb (Anemia)
2) ↓ TP 3) No reticulocytes / Non-regenerative. (Blood loss has been going on for so long / the animal is bleeding outside of its body, so that body cannot compensate / all the iron is lost. New RBCs cannot be made.) 4) ↓ MCV (microcytic) 5) ↓ MCHC (hypochromic - typical of Fe deficiency) 6) +/- ↑ Platelets 7) +/- Parasites of GI or skin |
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What are examples of anemia caused by decreased production?
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Iron-limited erythropoiesis: chronic blood loss; nutritional / functional Fe2+ deficiency.
Anemia of chronic DZ: anemia of inflammation; chronic kidney DZ; chronic liver DZ. Primary bone marrow DZ: leukemia, tick-borne DZ, aplastic bone marrow. |
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Why does chronic inflammation cause anemia?
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Inflammatory cytokines suppress the recycling of Fe2+.
Expect to also see an inflammatory leukogram (duh) and high plasma proteins from increased globulins. |
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Why does chronic renal DZ lead to anemia?
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Since 90% of EPO is made in kidneys, when the kidneys aren't functioning properly, there won't be much EPO made to stimulate erythropoiesis. The uremic toxins that accumulate can lead to ECHINOCYTES.
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We have an anemic patient. What lab results could we see that would lead us down the pathway of anemia of primary bone marrow DZ?
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1) Normal MCV
2) Normal MCHC / MCH 3) Concurrent -cytopenias, or even pancytopenia |
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What are the causes of polycythemia (↑HCT; aka, ↑PCV)?
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Most polycythemias are "relative." This means that the increased PCV is due to:
1) Dehydration (in which case, we'd also see ↑TP) 2) Splenic contraction (which causes redistribution of RBCs) 3) Or is epinephrine-induced (which is seen mainly in horses and cats). Rarely, polycythemias are "absolute." This means the increased PCV is due to: 1) Primary RBC neoplasia 2) Increased EPO production in kidneys (secondary polycythemia) due to chronic hypoxia or rare neoplasias |
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What lab results would you expect to see in an iron-deficient animal?
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Microcytic (↓ MCV), hypochromic (↓ MCHC or MCH) anemia.
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What are the indications for doing a bone marrow biopsy/aspirate?
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1) Persistent, unexplained -cytopenias (EXCEPT lymphopenia.)
2) Persistent, unexplained / Extreme increases in blood cell numbers. 3) Presence of atypical cells in blood. 4) To stage hemic neoplasias. 5) Unexplained hypercalcemia (only AFTER you've looked at LNs, neck, and butt). 6) Unexplained monoclonal hyperglobulinemia 7) If you're working up histoplasmosis, leishmania, Fe2+ deficiency, or lysosomal storage DZs. |
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Where and when should bone marrow biopsies+aspirates be taken?
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Where? From flat bones or ends of long bones.
When? At (or close to) the time of concurrent CBC. |
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What is myelophthisis?
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It is the failure of bone marrow to produce cells due to replacement or displacement of marrow by an abnormal proliferation of cells or tissues.
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What is a lymphoblast? What does it mean when we see them in blood smears?
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Lymphoblasts are immature, large lymphocyte precursors. They do NOT normally circulate in blood. If they're present, it points to PRIMARY LYMPHOMA or PRIMARY LYMPHOCYTIC LEUKEMIA.
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What's the difference between acute and chronic lymphocytic leukemia?
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Acute LL → Will see clonal proliferation of immature cells.
Chronic LL → Will see clonal proliferation of mature cells. |
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Which WBCs are granulocytes and which are mononucleocytes?
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What are some things to remember about leukograms?
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1) A leukogram is not as precise as a hemogram bc we're looking at WBCs in blood, when their main location is in tissues.
2) The parameter, "WBC count" is just a count of all nucleated cells in a sample. This means that it includes nucleated RBCs; often, tests will give you a "corrected" version of the parameter. |
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What molecules regulate granulopoiesis (neutrophils + basophils + eosinophils)?
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IL-3, GM-CSF, G-CSF
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Which species have a large storage pool for neutrophils?
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Dogs, cats, pigs
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What is the "marginal pool" in reference to neutrophils?
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Neutrophils can accumulate near the walls of vessels as they roll/adhere/exit out. These neutrophils are NOT measured in leukogram.
Dogs / Horses / Ruminants → Circulating pool = Marginal pool in size. Cats → Marginal pool is 3x the size of Circulating pool. |
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True or False:
Neutrophils are long-lived in tissues. |
False. Neutrophils survive 1-4 days in tissues before undergoing apoptosis and macrophage phagocytosis.
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What will we see if there's an increased demand for neutrophils in the tissues?
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A left shift!
There's a rapid increase in bone marrow production and release of neutrophils. Once all the mature neutrophils are used up, the marrow starts sending out increasingly immature neutrophils (aka, a left shift is seen). Bands are first released, then metamyelocytes, then myelocytes. |
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What does the corticosteroid stress leukogram look like?
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1) MATURE neutrophilia (NO left shift). Glucocorticoids encourage neutrophils to go into the blood; this means more neuts move from storage pool in marrow to marginal pool in vessel walls, to circulating pool in blood.
2) Lymphopenia 3) Monocytosis (especially in dogs) |
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If we see neutropenia + L shift in a large storage pool species, what does this indicate?
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This indicates an overwhelming infection. Despite having lots of neutrophils in reserve in their large storage pool, the marrow's supply is exhausted. Prognosis is poor.
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If we see neutropenia+ L shift in a small storage pool species, what does this indicate?
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This is common to see during the early phase of marked inflammation. It indicates serious DZ, but not necessarily marrow exhaustion.
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We see toxic neutrophils on our blood smear. What does this mean?
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Marked toxic change in neutrophils is due to bacterial toxins and can indicate sepsis.
We may see dohle bodies, cytoplasmic basophilia, vacuolization, persistent purple granules, or large neutrophils. |
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Name this WBC.
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Eosinophil.
Eosinophilia can mean: Parasitism Allergy / Hypersensitivity Fungal DZ Paraneoplastic DZ Eosinophlic leukemia |
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Name this WBC.
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Basophil.
Basophilia can mean: Lipid disorder Feline heartworm Myeloid neoplasm |
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Name this WBC.
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Lymphocyte.
Lymphocytosis can be caused by: Normal in young animals Epinephrine mediated, esp in cats Persistent inflammation Neoplasia Bovine leukemia virus |
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What are the 3 overlapping stages of hemostasis?
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1) Primary hemostasis → Formation of the initial platelet plug: adhesion to collagen; aggregation of platelets; release of granule contents; viscous metamorphosis to make fibrin clot.
2) Secondary hemostasis → Formation of cross-linked fibrin to stabilize platelet plug (coagulation). Thrombin cleaves Fribrinogen into fibrin; fibrin monomers polymerized into long chains. 3) Tertiary hemostasis → Destruction of clot by fibrinolysis. |
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Describe platelets.
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Platelets are anuclear cells in mammals; thrombocytes are the nucleated equivalent in non-mammals.
Formation: Megakaryoblast → Promegakaryocyte → Megakaryocyte → Platelets. 1/3 of platelets are stored in spleen. Splenic contraction can result in increased circulating platelets. |
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What does PT and PTT on a coag panel tell you?
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Prolonged PT and PTT tells us that it's taking longer for the animal to clot; some coagulopathy is present.
Increased PTT = Something's wrong with intrinsic pathway. Increased PT = Something's wrong with extrinsic pathway. |
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What does fibrinogen on a coag panel tell you?
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Increased fibrinogen means there's inflammation.
Decreased fibrinogen means there might be liver DZ. |
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What does FDP (fibrinogen degradation products) on a coag panel tell you?
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FDPs are cleared by the liver, so if liver DZ is present, can see increased FDP.
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What does D-dimer on a coag panel tell you?
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D-dimers are the most sensitive indicator of fibrinolysis; it only detects insoluble cleaved fibrin, and NOT fibrinogen.
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What is DIC (disseminated intravascular coagulation)?
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DIC is the pathological activations of coagulation, leading to the formation of small blood clots in vessels throughout the body. This pathological process consumes all the animal's coagulation proteins & platelets. Normal coagulation is disrupted, and abnormal bleeding occurs from the skin, GI tract, respiratory tract, and surgical wounds.
DIC is secondary to other DZs. |
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What lab test abnormalities would you see with DIC?
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You need more than 2-3 of these to have DIC:
Thrombocytopenia Prolonged PTT Prolonged PT Shistocytes Decreased ATIII Increased FDPs Increased D-dimers Decreased fibrinogen |
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What is virchow's triad?
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The triad states that there are 3 major factors responsible for development of thrombosis:
1) Changes in vessel wall, making it procoagulant. 2) Changes in pattern of blood flow. 3) Changes in constituents of blood, making it hypercoagulable. |
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What does it mean if a left shift is degenerate?
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It means that the number of immature neutrophils (bands, etc.) is greater than the number of mature neutrophils.
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What does an epinephrine-mediated leukogram look like?
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1) Lymphocytosis
2) Leukocytosis 3) Neutrophilia 4) Thrombocytosis (Splenic contraction) 5) Polycythemia |
