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VET377B SPAM Second Half > Haematology > Flashcards

Haematology Flashcards

1
Q
  • What is the source of Bilirubin?
  • Where does the body get its Iron from?
A
  • From the destruction of Haemoglobin
  • 90% of the bodies Iron is recycled from Haemoglobin, only 10% is from the diet
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2
Q
  • What is Haemoglobinemia?
  • What is Haemoglobinuria?
A
  • Presence of excessive haemoglobin in the blood plasma
  • Abnormally high concentrations of free haemoglobin in urine
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3
Q

What is Thrombocytopenia?

A

A decreased number of circulating platelets

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4
Q
  • Explain Thrombopoiesis
  • What hormone kicks off Thrombopoiesis and where is it made?
  • What stimulates Thrombocoiesis?
  • When is this increased and what is the risk?
A
  • Production of Platlets
  • Thrombopoietin (TPO) - made in Renal tubular epithelial, hepatocytes
  • IL6
  • IL6 is released uring inflammatory conditions which increases the risk of thrombosis
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5
Q

What is the cell life span for RBC?

Where does aged RBC go?

What happens to them here?

A
  • Average 2-3 months
  • Goes to the Spleen where it is phagocytosed by Macrophages
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6
Q

Explain how Neutrophils Neutralize bacteria?

A
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7
Q

What are the consequences of Acute Blood Loss Anaemia?

A
  • Hypovolemic shock and death - Rapid loss of more then 20-30% of Blood Volume
  • Rapid loss of up to 20% of the blood volume
    • Immediately after - hypovolemia without anaemia, thrombocytopenia and hypoproteinmia (balanced loss of erythrocytes and plasma)
    • After several hours - Normovolumia (due to compensatory systems) pre-regenerative, normocytic, normaochromic anaemia, thrombocytosis, hypoproteinemia.
    • After 3-4days = regenerative, macrocytic, hypochromic anaemia
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8
Q

What is the functions of Monocytes?

What is the half-life of monocytes?

A
  • Phagocytosis (Including erythrophagocytosis)
  • Antigen presentation to T lymphocytes
  • Immunomodulation
  • Half-life
    • IN the Blood 0.5days - 3days (Species dependent)
    • Migrated to tissues - Macrophages upto 3months
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9
Q

Explain Iron metabolism

A
  • only 3% of our iron comes from Gastro-Intesinal absorbtion
  • The rest is recycled within the spleen predomantly by Macrophages phagocytosing old RBC’s (120days old)
  • Iron as Ferritin (and hemosiderin) is stored within macrophages inside the macrophages
  • This Iron then is coupled with Transferrin (plasma protien) which then transfers the iron to the BM for use in Erthopoiesis
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10
Q

Anaemia

  • Regenerative Anaemia means what is happening?
    • What could be causing this to happen?
  • Non-Regenerative Anaemia means what?
    • What can be a cause of this?
A
  • Regenerative Anaemia - Reticulocytes are in the peripherial blood
    • Caused by Haemoloysis or Haemorrage
  • Non-Regenerative Anaemia - the RBC are not being replaced
    • This is a problem with production, either with the bone marrow or with EPO production in the kidney
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11
Q

What is Polycythemia vera?

A
  • Hypervolemia due to a neoplastic condition causing an increase in RBC
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12
Q

What is the main functions of Neutrophils?

A
  • Defence against invading microorganisms, primary Bacteria :
    • Recognize inflammatory signals
    • Leave the blood (via Diapedies)
    • Migrate through tissue to a site where bacteria are present and phagocytose them
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13
Q

If we gave an animal too much estrogen and caused an exodogenous Estrogen Toxicity what would we expect to see and how long would it take?

A
  • Thrombocytopenia and Neutrophilia 10-20days after administration
  • Mild but progressive non regenerative anaemia in the first 3 weeks leading to pancytopenia with BM aplasia between 3 and 4 weeks
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14
Q

If we have Macrocytic, Hypochromic Anaemia what could be some differentials?

A
  • Regenerative Anaemia
    • This is because the Cells are bigger (Macrocytic) and the same haemoglobin content but spread over more cytoplasm would make them lighter in colour.
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15
Q

What could cause a chronic Iron Deficiency?

A
  • Gastrointestinal ulcers
  • Blood-sucking parasites
  • Fleas
  • Ticks
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16
Q

What does Aplasia mean?

What does Hypoplasia mean?

A
  1. Aplasia = Completly lacking of eg no bone marrow
  2. Hypoplasia = Reduced quantity of.
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17
Q

If you have Microcytic, hypochromic anaemia what would your differentials be?

A
  • Iron Deficiency (low iron = decreased haemoglobin = decreased size and colour of RBC) (99% of Microcytic,Hypochromic Anaemic cases)
  • Anaemia of inflammatory disease (Can only be mild anaemia)
  • Normal for Akita or Shiba dogs.
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18
Q

Classify the Anaemia of Inflammatory Disease using the Wintrobes erythrocyte indicies

A
  • Mild to Moderate
  • Non regenerative
  • Normocytic (rarely microcytic)
  • Normochromic
  • Anaemia after 3-10 days
  • and inflammatory leukocytosis
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19
Q

What are some differential diagnosis for thrombocytosis

A
  • Physiologic
    • Splenic contraction
    • Epinephrine
  • Drug-Induced
    • Epinephrine
    • Vincristine
  • Reactive
    • Inflammation
    • Infection
    • Neoplasia
    • Trauma
    • Rebound from Thrombocytopenia
    • Iron Deficiency-related
  • Essential Thrombocytemia
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20
Q

If we have a Moderate non-regenerative anaemia, normocytic, normochromic with neutropenia and thrombocytopenia

What kind of Anaemia would it likely be?

A

Chronic Aplastic Anaemia

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21
Q

According to the cell based model what are the main phases of the secondary haemostasis?

A
  • Initiation
    • Extrinsic pathway
    • Tissue factor
    • Cell surface : Fibroblasts
  • Amplication
    • Intrinsic pathway
    • Thrombin
    • Cekk surface : Platelets
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22
Q

What is the order proliferation of Red Blood Cells?

(Erythropoiesis)

A
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23
Q

What is Leukaemia?

A

Neoplasitic diseases characterized by the clonal proliferation of malignant hematopoietic progenitor cells in the bone marrow. This creates more leukocytes that are not fully developed. (Myeloid or Lymphoid cells)

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24
Q

Explain the pathogenisis for DIC

A
  • DIC is always secondary to an underlying disease :-
    • Severe inflammation
      • Sepsis
      • Heat Stroke
      • Pancreatitis
      • Viral Infection
      • IMHA
    • Neoplasia
    • Other
      • Snake Venom
  • Initiation via Tissue Factor
    • Widespread/severe endothelial injury: exposes TF
    • Severe organ injury : releases TF or cytokine storm
    • Inflammatory Cytokines : Induce TF expression on monocytes +/- endothelial cells (no endothelial injury)
    • Cancer: Aberrant TF expression
  • Amplication: Intrinsic Pathway
    • Thrombin activating factors XI, VIII and V, Thrombin inhibiting fibrinolysis
    • DIC contained or compensatedby inhibitors = non-overt DIC
      • Antithrombin ATIII - prevent fibrinogen converting to fibrin
      • Protein C (PC) - vitamin K dependant anticoagulant and pro-fibrinolytic protein activated by thrombin -> inactivates factors Va and VIIIa
  • Dissemination
    • DIC dysregulated or uncompensated = overt DIC
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25
Q

What % of cases of IMHA are Intravascular compared to Extravascular?

A
  • Intravascular - 20%
  • Extravascular - 80%
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26
Q

What can be secondary to Haemoglobinuria?

A

Kidney damage

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27
Q

What changes in the blood would we see with Mild or Chronic inflammation?

A
  • Neutrophilia - increased peripheral demand for neutorphils is met by release of marginal pool
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28
Q

What are some clinical signs of IMHA?

What would be the first test you would do if you have these clinical signs?

A
  • Weakness
  • Lethargy, Exercise intolerance
  • Pallor mucous membrane
  • Icterus –> pre hepatic hyperbilirubinemia
  • Tachypnoea, Tachycardia –> Hypoxia secondary to severe anaemia
  • Hepatosplenomegaly –> increased erythrophagocytosis
  • Check for Auto-Aggulation - positive in ~60% of IMHA. If Autoaggulation present = IMHA
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29
Q

What are the pathogenesis for Primary and Secondary Aplastic Anaemia?

A
  • Primary
    • Idiopathic
  • Secondary
    • Infectious agents
    • Chemical/Physical Agents
    • Drugs
    • Toxins
    • Immune-Mediated
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30
Q
  • What are some consequences of Chronic Blood Loss Anaemia
  • What is the pathogenesis of Chronic Blood Loss Anaemia
A
  • Main cause of Iron deficiency anaemia
  • Pathogenesis
    • Parasites (eg Hookworms, Flease etc)
    • Gastrointestinal Ulcers (eg administration of NSAID and glucocorticoids, mast cell tumors)
    • Neoplasia (eg. bleeding into body cavities and tissues
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31
Q

What is the Marginating pool : Circulating Pool of Neutrophils in Dogs and Cats

A
  • Dogs - 1:1
  • Cats - 3:1
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32
Q
  • When looking at CBC what does MCV stand for?
  • What does an increased number tell you?
A
  • Mean Corpuscular Volume - the size of the erythrocytes
  • The average size of the RBC are bigger meaning that they are Macrocytic.
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33
Q

What is the pathogenesis of Haemolytic Anaemia

A
  • Hemolytic anaemias occur as a result of increased erythrocyte destruction in the following ways :-
    • Intravascular Haemolysis - Haemoglobinemia and haemoglobinuria
    • Extravascular Haemolysis - phagocytosis by cells of the mononuclear phagocyte system (**Common). Increased total bilirubin and icterus
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34
Q

If we have Infections (++Bacteria), tissue injury or a immune mediated disorder what kind of leukogram would we expect?

A

Leukocytosis with Neutrophilia with Acute inflammation with regenerative left shift.

= The peripheral demand for neutrophils is greater than the storage and marginal pools, therefore bone marrow release young neutrophils as well.

Regenerative left shift = mature neutrophils are more numerous than band nuetrophils

When leukocytosis is marked (>50000/uL) is called Leukemoid reaction because it resembles the blood pattern seen in chronic myeloid leukaemia

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35
Q

What are some causes of Haemolytic Anaemia? (Differential Diagnosis)

A
  • Immune-Mediated erythrocyte destruction
    • Primary
    • Neonatal isoerythrolysis
    • Incompatable Blood Transfusion
    • Drug Induced
  • Erythrocyte Parasite (may have an immune mediated component)
  • Other infecginos agents (may have an immune mediated component)
  • Oxidant compounds of other chemicals and plants compounds
  • Fragmentation (mechanical process)
  • Hereditary erythrocyte defects
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36
Q

What is the difference between Regenerative left shift and a Degenerative left shift?

A
  • Regenerative left shift = More mature neutrophils than Bands
  • Degenerative left shift = More Bands than mature neutrophils
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37
Q

How long after blood loss would we see signs of regeneration?

eg how long till we would see reticulocytes in the peripheral blood?

A

3-4days

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38
Q

What is Thrombocytopenia

A

Condition where there is low blood platelet count.

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39
Q

What are the 2 reasons we could have abnormalities in Heme synthesis?

A
  • Iron and/or Copper deficiency
  • Lead Toxicity
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40
Q

With Extravascular IMHA what happens in the spleen?

A

The Macrophages can either

  • Erythrophagocytose the RBC or
  • They can take a bite out of the cytoplasm of the RBC, leaving Spherocytes (Smaller RBC with more concentrated haemoglobin content.) Which can go back into the peripheral blood.
  • As soon as you see Spherocytes you dont need further tests you can straight away start on Immunosuppressive drugs.
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41
Q

If we had a mild to moderate, non-regenerative, normocytic, normochromic anaemia with basophilic stippling and nucleated RBC’s what would be the cause of this?

A

An abnormality in the Heme synthesis either due to :-

  • Iron and Copper deficiency
  • Lead Toxicity (Basophilic stippling)
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42
Q

What is happening if we have a non-regenerative anaemia without an accompanying leukopenia or thrombocytopenia in the blood?

A

This means we have a reduced erythropoiesis and it may be secondary to

  • EPO deficiency
  • Anaemia of inflammatory disease
  • immune-mediated anaemia
  • Pure Red Cell Aplasia (PRCA)
  • Abnormalities in heme synthesis
  • Disorders of nucleic acid synthesis

This is the most common cause of non-regenerative anaemia in all species

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43
Q
  • On a CBC what does MCHC indicate?
  • What is it called when the numbers are above reference range?
  • What is it called when the numbers are below reference range?
A
  • The colour of the RBC
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44
Q
  • How long does it take for a Myeloblast to become a Neutrophil?
  • What is the half life of a Neutrophil?
A
  • 6-9 days
  • 5-10 hours
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45
Q

How can we tell a reticulocyte from a erythrocyte?

A
  • You can see small fragments of RNA in the cell. (with special stain)
  • Or with a normal H&E stain you can see slightly larger and more basophilic cell as in this picture
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46
Q

What is anaemia?

Before deciding that your patient is anaemic what else must you check?

A
  • Decreased Erythrocyte mass within the body
  • You must check hydration status of the patient before deciding if your animal is Anaemic.
  • Remember Anaemia is a condition not a diagnosis.
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47
Q

How do we classify Anaemia? (3 steps)

A
  1. Assess the Severity
  2. Assess the Regenerativity
  3. Classify using erythrocyte indices
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48
Q

Differentiate the clinical pathological changes associated with intra and extravascular haemolysis

A
  • Intravascular IMHA - RBC destroyed within the blood vessels with contents being released into the blood stream. Haemoglobin will then be seen in the plasma in a clasic red colour
  • Extravascular IMHA - This is where in the spleen macrophages take bites out of the RBC creating Spherocytes, which then return to the peripheral blood
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49
Q

How long ia an Erythrocyte’s cell lifespan for a

  • Dog
  • Cat
  • Horse
A
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50
Q

What are the Vitamin K dependant Coagulation Factors?

A

Factors II, VII, IX, X

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51
Q

How long does it take for a Rubriblast to change to a Metarubricyte?

A

4-5 days

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52
Q

What does Porphyrias mean?

A

Accumulation of porphyrin compounds in cells, tissues, and body fluids

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53
Q

Rank in order of size, Erythrocytes, Leukocytes and Platlets

A
  • Smallest to Largest
    • Platlets
    • Erythrocytes
    • Leukocytes
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54
Q

If we have a Leukopenia - with a Neutropenia what would be the cause of this?

A

The demand on the Neutrophils is too large and all compensatory abilities have been exhaused including the increased myelopoiesis.

Causes of this are:-

Acute Necrisis

Septicaemia

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55
Q

What is the mechanism of IMHA blood transfusion reactions?

A

Transfusion Reactionns occur when plasma of the recipient contains antibodies against one or more antigens on the surface of donor erythrocytes.

  • Antibody formation results from prior exoposure to different erythrocyte antigens via transfusion or pregnancy
  • Severe haemolytic transfusion reactions generally do not occur at the time of the first blood transfusion
56
Q

How can you tell if there is a regenerative anaemia?

A

Reticulocytes are in the circulating blood pool.

Nucleated RBC = >0

57
Q

If we have a Normocytic, normochromic anaemia what would be some of the Differentials?

A
  • Pre-Regenerative Anaemia
  • Chronic Renal Disease
  • Selective erythoid hypoplasia
  • Aplastic or hypoplastic bone marrow
58
Q

What is the most common cause of non-regenerative anaemia in all species?

  • What is the pathogenesis of this?
A

Erythroid hypoplasia/aplasia

Secondary to

  • EPO deficiency
  • Anaemia of inflammatory disease
  • immune-mediated anaemia
  • Pure Red Cell Aplasia (PRCA)
  • Abnormalities in heme synthesis
  • Disorders of Nucleic acid synthesis
59
Q

What would be some pathogenesis of Acute Blood Loss?

A
  • Trauma
  • Coagulation Disorders (eg rodenticide toxicity, DIC, etc)
  • Platelet disorfers (eg. thrombocytopenia and inherited platelet function test)
60
Q

What are the main molecules required for Erythropoiesis?

A
  • Iron
  • Copper
  • Vitamin B12 (Cobalamin)
  • Folate
  • Proteins
61
Q

What are these called?

When would you see them?

A
  • Leptocyte
  • Iron Deficency

Moderate, non-regenerative, microcytic, hypochromic, anaemia

62
Q

What is Leukopenia?

What is the name of the sub-population involved?

Neutrophils

Lymphocytes

Eosinophils

Monocytes

A

Leukopenia = decreased leukocytes

What is the name of the sub-population involved?

Neutrophils = Neutropenia

Lymphocytes = Lymphopenia

Eosinophils = Eosinopenia

Monocytes = Monocytopenia

63
Q

What is Thrombocytopenia?

A

Abnormally low numbers of platlets in the blood

64
Q

What are these blue dots called? And why would they be here?

A
  • Basophilic Stippling
  • Specific for Lead Toxicity
65
Q

If we have an acute inflammation without left shift what could be some differentials?

A
  • Increased peripheral demand for neutrophils is met by the release of the marginating pool and storage pool.
  • Causes
    • Haemorrhage
    • Haemolysis
    • Necrosis
    • Chemical and drug toxicities
    • Malignancy
66
Q

What is the limitation of automated assays for platlet counts?

A
  • Platlets are counted as small cells however platlets regularly aggregate which the computer doesnt take into account so does not count these
  • In cats they have a unique structure M loop region of B1-tubulin which may contribute to the size of the platlets again the machine wont count these as they are seen to be too big to ba a platlet.
67
Q

How does your body respond to Hypovolemia?

A

Kidneys detect the GFR is reduced - Releases Renin etc

68
Q

List the Heriditary Coagulation disorders

A
  • Scott Syndrome
  • Haemophilia A & B
69
Q

If you have Macrocytic, Normochromic Anaemia what would be your differentials?

A
  • FeLV infections
  • Poodle macrocytosis
  • Spurious with persistent hypernaturemia
70
Q

What are the available tests to classify Leukemia?

A
  • Immunohistochemistry
  • Immunophenotyping
  • Cytochemistry
  • PCR
71
Q

What is myelopoiesis

A

Myelopoiesis is the regulated formation of myeloid cells, including eosinophilic granulocytes, basophilic granulocytes, neutrophilic granulocytes, and monocytes

72
Q

Discuss the Diagnostic Approach to Thrombocytopenia

A
  • Blood Smear Confirmation
  • Consider Breed (King Charles Spaniels)
  • Perform Coagulation Panel
    • Abnormal Coagulation Results Consider
      • DIC
      • Vitamin K antagonists
    • Normal Coagulation Results Consider
      • Anitplatelet antibody test
      • Serology, molecular diagnostics for infectious agents
      • Rule out neoplasia (lymphoma, leukemia, myelodyspastic syndrome, hemangiosarcoma
73
Q

Coagulation Test Results

Normal platelet count and PT with prolonged aPTT, and Negative FDP

A

INhibited defect in the intrinsic pathway (= Haemophilia A & B)

74
Q

What is important to remember with horses when traying to ascertain if the anaemia is regenerative or non-regenerative?

A

Horses do not have reticulocytes in the peripheral blood. They stay in the bone marrow and only mature erythrocytes are released.

Important to remember if you need to know what Anaemia it is with a horse do a second blood test in 3-4days or examin the bone marrow.

75
Q

What is the function of Eosinophils and Basophils?

A
  • Eosinophils are an important component of
    • The type 2 cytokine-induced inflammatory response that is critical in the host defence against helminth infections =
      • Hypereosinophilia due to Parasite infections.
    • The type 1 hypersensitivity allergic reaction
      • Hypereosinophilia with Allergic reactions
76
Q

Coagulation Test Results

Normal platelet count with prolonged aPTT, PT and Negative FDP

A

Multiple coagulation defects (=rodenticide toxicity)

77
Q

Explain the Storage pools of Neutrophils

A
  • Neutrophils once mature are stored in the Bone marrow in the Storage Pool
  • Once they are released from the storage pool they adhere to the endothelial cells (Capillaries and veins) in the peripheral blood and spleen this is the Marginated Pool
  • Then you have the neutrophils which are in the Circulating Pool which is free flowing in the peripheral blood. It is only this pool which is colledcted during blood sampling.
78
Q

What is Leukocytosis?

What is the name of the sub-population involved?

  • Neutrophils
  • Lymphocytes
  • Eosinophils
  • Monocytes
A

Leukocytosis = increased leukocytes

What is the name of the sub-population involved?

  • Neutrophils = Neutrophilia
  • Lymphocytes = Lymphocytosis
  • Eosinophils = Eosinophilia
  • Monocytes = Monocytosis
79
Q

What does Polychromasia mean?

A

A disorder where there is an abnormally high number of immature Red Blood Cells (reticulocytes) in the peripheral blood.

Poly = Many

Chromasia = Colour

80
Q

How does recycled Iron get from the spleen to the bone marrow?

A

Coupled with the plasma protien “Transferrin”

81
Q

If you have chronic kidney disease why would you have a anaemia? Classify the Anaemia you would expect.

A
  • With renal insufficiency you would have a reduction in the EPO produced within the kidneys therefor RBC production would slow down and cease.
  • Mild to moderate, non regenerative, normocytic, normochromic anaemia
82
Q

What is the Pelger-huet anomaly?

A

AN inherited condition characterized by the failure of mature granulocyte nuclei (And Eosinophils and Basophils) to lobulate. Therefore they are hyposegmented.

Australian Shepards are over represented by this condition

83
Q

What is the pathogenisis of thrombosis?

A
  • Neoplasia (Haemangiosarcoma)
  • Sepsis, endotoxaemia
  • IMHA (dogs)
  • Heart Disease
  • PLN and PLE
  • Hyperthroidism (Cats)
84
Q

\e the two main reasons for reduced or defective erythropoiesis?

A
  • Deficiency (Fe, Cu, Vit B12, Folate, Protiens)
  • Bone Marrow and Erythroid Hypoplasia or Aplasia
85
Q

What is the pathogenisis of IMHA Neonatal Isoerythrolysis?

A
  • Happens in 10% of Horses
  • And in Cats with type B blood as they have naturally high anti-A antibiodies

Neonatal Isoerythrolysis develops in neonatal animals following ingestion of colostrum containing antibodies against antigens on theirerythrocytes

86
Q

What is Polychromasia?

A

Cell nucleus of differing colours

87
Q

Coagulation Test Results

Normal platelet count and aPTT with prolonged PT and Negative FDP

A

Early anti-coagulant rodenticide toxicity

88
Q

How long after bone marrow injury would we see

  • Neutropenia
  • Thrombocytopenia
  • Anaemia (Cats and Dogs)
A

Remembering the half lifes of these cells.

  • Neutropenia - 5-6hours
  • Thrombocytopenia - 8 - 10 days
  • Anaemia (cats - 60-70days) (Dogs 100-120days)
89
Q

Looking at the whole blood volume How much is Plasma and the Formed Elements?

A

55% = Plasma - Water & Proteins (7%)

45% = Formed Elements

90
Q
  • What are these called?
  • what are the indicitive of?
A
  • Codocyte (Target Cells)
  • Iron deficiency

Moderate, non-regenerative, Microcytic, Hypochromic, Anaemia

91
Q

What are the functions of the following lymphocytes?

  • T lymphocytes
  • B Lymphocytes
A
  • T lymphocytes
    • responsible for cellular immunity
  • B Lymphocytes
    • involved in the humoral immunity
92
Q

What are globulins?

A

They make up 52% of the plasma proteins and they are mainly inflammatory proteins (these increase when we have inflammation)

93
Q

What is some pathogenisis for Bone marros Hypoplasia or Aplasia?

A
  • Estrogen Toxicity (Dogs and Ferrets)
  • Drug Induced cases of hypoplasia
    • Phenylbutazone (dogs and maybe horses)
    • Trimethoprim-Sulfadiazine administration in dogs
    • Bracken fern poisoning in cattle and sheep
    • Griseofulvin in cats
    • Trichloroethylene-extracted soybeen meal in cattle
    • Immunosuppressive drugs (azathioprine)
    • Radiation
  • Hypoplasia and Aplasia due to infections agents
    • Acute aparvovirus infecctions (transient marrow hypoplasia but not aplastic anemia)
    • FeLV
    • Ehrlichia sanis
    • Theileria parva
  • Immune Mediated
94
Q

What Coagulation factor is deficient in

Haemophilia A

Haemophilia B

A
  • Haemophilia A = Factor VIII
  • Haemophilia B - Factor IX
95
Q

What is it called when there are more than 30% of platelets stored in the spleen?

A

Redistribution thrombocytopenia

96
Q

What would cause Hypercortisolism?

What is the body’s response to this?

What would we see in the blood during this?

What other changes would you see?

What are some causes of this?

A
  • Stress can cause an animal to release cortisol.
  • The response to Glucocortisol is to shift neutrophils from the storagfe and marginating pools into the peripheral blood and also to decrease the egress (diapedies) of neutrophils from blood into the tissues.
  • Due to decreased neutrophil diapedesis and intravascular aging, hypersegmentation can be seen (right shift)
  • You would see a stress leukogram (LEMONS), along with the Neuthropilia, you would have Monocytosis, Eosinopenia and Lymphopenia.
  • Causes
    • Exogenous
      • admin of Glucocorticoids,
    • Endogenous
      • Pain
      • Trauma
      • Prolonged emotional stress
      • intense sustained exercise
      • hyperthermia
      • hyperadrenocorticism
97
Q

What is the half life of Coagulation Factors?

A
  • Factor VII <5hours
  • Factor II and XIII Several days
  • All others range between 1-2days
98
Q

How much % of body weight is an animals Blood Volume?

A

8%

99
Q

What is Polycytemia? (Erythrocytosis)

what causes it?

A
  • Increase in haematocrit, Maemoglobin and RBC count
  • Relative Erythrocytosis
    • Dehydration
    • Splenic Contraction
  • Absolute Erythrocytosis
    • Hypoxemia -> Compensatory EPO production
    • Primary Erythrocytosis: myeloproliferative neoplasm
100
Q

List some drugs and oxadant compounds which can induce IMHA / Haemolytic Anaemia

A
  • Drugs
    • Penicillin (horses)
    • Cephalosporins (Dogs
  • Oxidant Compounds
    • Onions (Cats, Dogs, Horse, Cow/Sheep)
    • Paracetamol (Cats, Dogs)
    • Diabetes mellitus (Cats, Dogs)
    • Lymphoma (Horse)
101
Q

What is the pathogenisis of Anaemia of inflammatory disease?

A
  • Iron deficiency
  • Shortened erythrocyte life span –> secondary to membrane damage caused by endogenous oxidants generated during inflammation
  • Inhibition of erythropoiesis –> secondary to inflammatory mediators
102
Q

A stress Leukogram has what blood results?

A

LEMONS Less Lymphocytes and Eosinophils And More Monocytes and Neutrophils

103
Q

Coagulation Test Results

Thrombocytopenia with prolonged aPTT, PT and positive FDP

A

Consumption of platelets and coagulation factors (=DIC)

104
Q

If we have an Acute inflammation with degenerative left shift. What would we expect to see?

What is the only cause of this?

A
  • Leukocytosis with a degenerative left shift Neutrophilia
    • the peripheral demand for neutrophils is massive and fast. Both the storage and marginating pools are exhausted and bone marrow release young neutrophils (Band and Metamyelocytes)
  • Hyper-Acute inflammatory process
105
Q

When looking at blood results what figure do we look at to assess the severity of Anaemia?

A
  • You can look at RBC, HGB and HCT however in veterinary medicine we usually look at HCT
106
Q

What are these?

A

Heinz Bodies usually seen when Haemolytic Anaemia is caused by Oxaditive compounds like Onions.

(Oxidised Haemoglobin)

107
Q

What is Polycythemia

A
  • Also Called Polyglobulia
  • A diseased state in which the haemocrit (the volume % of red blood cells in the blood) is elevated
  • (The amount of erythrocytes is increased)
  • This can be primary or secondary
108
Q

What would a persistant chronic Hypoxia cause (what changes would be seen in the blood?)

Why

A
  • You would see a polycytemia (Increase in Red Blood Cell %)
  • Kidneys would detect the reduction in Oxygen being carried in the blood and would release erythropoietin which would go to the bone marrow requesting more RBC’s
109
Q

What CBC differences would we see between Chronic Iron Deficiency and Anaemia of Inflammatory Disease?

A
110
Q

What would make Blood Plasma red?

A

Intravascular Haemolysis of RBC

111
Q

At what cell life stage do Red Blood Cells (Erythrocytes) leave the bone Marrow?

A
112
Q

IMHA can be Primary or Secondary, what causes primary? What would be the treatment?

What could be some Causes for Secondary IMHA?

A
  • AutoImmune Haemolitic Anaemia ( Predisposed Factors - Age, genetic, environmental)
  • Treatment would be auto immune suppressant drugs
  • Secondary IMHA - Immune response to :-
    • Anti-drug or microbe,
    • Antibody to RBC determinant modified by drug of microbe,
    • Absorbed immune complex
113
Q
  • What are Von Willerband Factors?
  • What is Von Willerbrand Disease, list the 3 types
A
  • Released from endothelial cells upon injury - these bridge platelets with sub-endothelial matrix which binds platelets with collagen. vWF are chained multimers which can be chained into very long and strong sizes.
  • Von Willerbrand Disease - chains are lost
    • Type 1 - equal decrease in all sizes of multimers = quantitative change
    • Type 2 - Decrease in only the large multimers = qualitative change
    • Type 3 - No detectable vW factor
114
Q

If we have a Moderate to severe, non regenerative, normocytic, normochromic anaemia what would be the cause of this?

A

Immune-Mediated Anaemia

  • Maturation arrest (where the cells are unable to mature)
  • Marrow Hyperplasia (Reticulocytes Cells are destroyed before being released from the bone marrow)
115
Q

What are the clinical pathological changes seen with IMHA?

A
  • Anaemia - Sever (Mean hct 15%)
  • Strongly regenerative or pre-regenerative if onset acute
    • Macrocytic and hypochromic
  • Non regenerative if antibodies against erythroid precursors
  • Hyperbilirubinemia (~75%) = increased erythrophagocytosis
  • Leukocytosis due to neutrophilia and left shift and monocytosis (>80 of cases)
    • probably due to ischemic necrosis within tissues
  • Thrombocytopenia usually not severe
    • If IMHA with Thrombocytopenia = Evans Syndrome
  • Spherocytosis (75%) = due to macrophage pitting
    • if extravascular (80%)
  • Haemoglobinemia and Haemoglobinuria
    • if intravascular (20%)
116
Q

What are the 2 main functions of Albumin?

A
  • Maintaining Oncotic Pressure
  • Binding other Molecules including drugs
    • Transporting Hormones, Calcium etc
117
Q

List the common causes of Thrombocytopenia

A
  • Decreased or defective platelet production -
    • Aquired megakaryocyte hypoplasia
    • aplasia
  • Increased Platelet Loss -
    • Massive truma,
    • Extensive external haemorrhage
  • Accelerated consumption of platelet -
    • DIC,
    • Thrombocytopenic thrombotic purpura
    • Haemolytic uremic syndrome
  • Increased Platelet destruction
    • Primary (Idiopathic)
    • Secondary
      • Infectious agent
      • Neoplasia
      • Drugs
      • Immune-Mediated
  • Abnormal Platelet Distribution
118
Q

What can Estrogen Toxicity Cause?

  • How can Estrogen Toxicity come about?
A
  • Aplastic Anaemia
  • Exodogenous - Given to much Estrogen. Endogenous - Sertolli Cell tumour (Cryptochid Testicle), functional ovarian follicles, Ovarian granulosa tumours
119
Q

7% of Plasma are proteins, What makes up these Plasma Proteins?

A
  • Albumin - 44%
  • Globulins - 52%
  • Fibrinogen - 4%
120
Q

How do we differentiate Leukaemia?

A
  • Origin
    • Myeloid
    • Lymphoid
  • Maturative Stage
    • Acute
    • Chronic
  • Staging
    • Check other organs
121
Q

What are these and what is it cause by?

A

Fragmentation (From RBC’s hitting something)

  • Schistocytes = RBC fragments with pointed extremities
  • Acanthocytes = RBC’s with irregularly spaced, variably sized spicules
    • Due to fragmentation or lipid disorders (Hypercholesterolemia) If you have Acanthocytes by them selves
122
Q
  • When does a Myeloblast stop dividing?
  • At what stage are neutrophils released from the Bone Marrow?
A
  • At the Myelocyte stage
  • Depending on if there is a left shift or not, they should be mature, otherwise they can be released as bands.
123
Q

List the aquired coagulation disorders

A
  • Disseminated intravascular Coagulation
  • Thromboembolism
  • Liver Disease
  • Vitamin K deficiency
  • Snake Envemonation
124
Q
  • What is the main systemic regulator of Iron metabolism?
  • Where is this produced?
  • What does it do?
  • When would the production of this regulator be increased?
A
  • Hepcidin (protien)
  • Produced by hepatocytes (Liver)
  • Hepcidin inhibits iron export from enterocytes, macrophages and hepatocytes.
  • Hepcidin production is increased with
    • Iron Overload
    • Inflammation - independent of body iron requirement
  • Hepcidin production is reduced with
    • Iron Deficiency
    • Increased erythropoiesis
125
Q

What can we see in this Blood Smear?

A

This blood smear contains Reticulocytes (Larger and Bluer RBC) and Metarubricytes (Neucleated RBC)

126
Q

If we had an acute aplastic anaemia what would we see in the CBC

A

Neutropenia and Thrombocytopenia

127
Q
  • What is the correct name for Aplastic Anaemia?
    • What does this actually mean?
  • When we have aplastic anaemia what happens?
A
  • Aplastic Pancytopenia
    • = Anaemia and Thrombocytopenia and Leukopenia - due to the lack of bone marrow all of these cannot be produced
  • Haematopoietic Bone marrow is replaced by adipose tissue
128
Q

What is Evans Syndrome?

A

Its when you have Immune Mediated Haemolytic Anaemia and Thrombocytopenia

129
Q

How can you tell is Anaemia is regenerative of non-regenerative?

A
  • Under the microscope you will see wither nucleated RBC / Metarubricytes and Reticulocytes or you will see larger bluer RBC depending on the stain used
  • The will be a reading of reticulocytes (RET) on the CBC
130
Q

Explain what a left shift or right shift is when talking neutrophils

A
  • Left Shift - Peripheral blood has immature (Band) neutrophils within it
  • Right Shift - Peripheral blood has Hypersegmented (Degenerate) neutrophils within it
131
Q

What is a Coombs test for?

A

The Coombs test checks your blood for antibodies that attack red blood cells.

This is helpful when needing a Blood Transfusion (Indirect Coombs Test) to see if the body will be reject a particular blood type,

Direct Coombs test to see if your RBC have antibodies attached to them like in cases of IMHA and Thrombocytopeania

132
Q

If we see Heinz bodies in a blood smear what has caused these?

A

Oxidative Changes, eg Onion, Paracetamol (in cats)

133
Q

What are these (found in blood smear, and what are they caused by?)

A

Howell-Jolly Body

  • In normal cats and horses (non-sinusoidal spleens): Howell-Jolly bodies are not removed as readily as in dogs or cattle, so low numbers may be seen.
  • Regenerative anemia: All species.
  • Compromised or absent splenic function: Corticosteroids, splenectomy.
  • Erythroid dysplasia: In non-anemic miniature and toy poodles with hereditary macrocytosis, increased numbers of Howell-Jolly bodies (some abnormal and fragmented) may be observed. Similarly, abnormal and increased Howell-Jolly bodies may be seen in myelodysplastic syndrome (primary myelodysplasia).
134
Q

What markers would we need to see in the blood smear to say there is Oxidative Damages? (EG dog has ingested Onions)

A

Diagnosis of an oxidant-induced hemolytic anemia is based on finding a regenerative anemia with characteristic red blood cell morphologic abnormalities of Heinz bodies and eccentrocytes.

135
Q

What are some oxidising agents that could cause Heinz Bodies in animals blood?

A

Garlic, onion, leek, porpofol, paracetamol, lymphoma, diabetes mellitus, zink, bracken fern, red maple leaves

136
Q

What would the pathogenesis be for seeing an anaemia with Acanthocytes and Schistocytes in the blood?

A

Increased RBC destruction due to mechanical damage.

Ddx:

  • Vascular disorders
    • Microangiopathy
    • Haemangiosarcoma
    • Vena cava syndrome
  • DIC
137
Q

What is myelophthisis

A

Anaemia caused by atrophy of the Bone Marrow. Caused by Leukemia, Lymphoma or metastic carcinoma, or Myeloma

VET377B SPAM Second Half (7 decks)

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