Haemostasis and common coagulation abnormalities

Question 1

What is hypoplastic anaemia, and how does it differ from aplastic anaemia?

Answer 1

Hypoplastic anaemia is a form of anaemia characterized by reduced cellularity in the bone marrow, specifically a decrease in erythroid precursors. Aplastic anaemia is a more severe condition where all three hematopoietic lineages (erythroid, myeloid, and megakaryocytic) are markedly diminished or absent.

Question 2

Define the terms “erythroblast” and “precursor” in the context of haematopoiesis.

Answer 2

Erythroblast refers to a nucleated precursor cell in the erythrocyte (red blood cell) lineage. Precursor, in the context of haematopoiesis, is a general term for cells that give rise to more specialized cells, such as erythroblasts giving rise to erythrocytes.

Question 3

Differentiate between normocytic and normochromic erythrocytes.

Answer 3

Normocytic refers to normal cell size, and normochromic refers to normal hemoglobin content. Normocytic, normochromic erythrocytes have a size and hemoglobin concentration within the normal range.

Question 4

Explain the terms “myeloid” and “cytotoxic” in the context of bone marrow disorders.

Answer 4

Myeloid refers to cells derived from the bone marrow, including erythrocytes, granulocytes, and monocytes. Cytotoxic implies a destructive effect on cells. In the context of bone marrow disorders, cytotoxic conditions may lead to reduced production or destruction of blood cells.

Question 5

What is the distinction between aplastic anaemia and pure red cell aplasia?

Answer 5

Aplastic anaemia involves a severe reduction in all hematopoietic lineages (erythroid, myeloid, and megakaryocytic). Pure red cell aplasia is a subtype where only the erythroid lineage is affected, leading to a significant decrease in red blood cell production.

Question 6

Describe bicytopenia and pancytopenia, providing an example of each.

Answer 6

Bicytopenia involves a reduction in two blood cell lineages (e.g., red blood cells and platelets). Pancytopenia involves a reduction in all three blood cell lineages (red blood cells, white blood cells, and platelets). An example of bicytopenia is anemia and thrombocytopenia. An example of pancytopenia is aplastic anaemia.

Question 7

What characterizes non-regenerative anaemias, and why is reticulocytosis absent in these cases?

Answer 7

Non-regenerative anaemias are characterized by a lack of a proper reticulocyte response, indicating inadequate bone marrow response to the anemia. Reticulocytosis is absent due to impaired or insufficient erythropoietic activity in the bone marrow.

Question 8

How does pre-regenerative anaemia differ from non-regenerative anaemia in its early stages?

Answer 8

In pre-regenerative anaemia, the bone marrow responds appropriately to anemia by releasing reticulocytes. In the early stages of non-regenerative anaemia, the bone marrow fails to produce an adequate number of reticulocytes.

Question 9

Discuss the infectious origins of non-regenerative anaemia, focusing on feline and canine parvoviruses.

Answer 9

Feline and canine parvoviruses can cause non-regenerative anaemia by infecting and destroying rapidly dividing cells in the bone marrow, particularly affecting the erythroid lineage.

Question 10

List the primary categories of primary bone marrow disorders, and provide examples of each.

Answer 10

Primary bone marrow disorders include aplastic anaemia (e.g., idiopathic aplastic anaemia), myeloproliferative disorders (e.g., polycythemia vera), and myelodysplastic syndromes (e.g., refractory anemia).

Question 11

Explain how Feline Leukaemia Virus (FeLV) can lead to pure red cell aplasia and its impact on blood typing.

Answer 11

FeLV can lead to pure red cell aplasia by suppressing erythropoiesis. FeLV-infected cats may develop autoantibodies against blood type antigens, impacting blood typing and transfusion compatibility.

Question 12

What are cytotoxic origins of bone marrow disorders, and how do they affect red cell production in dogs and cats?

Answer 12

Cytotoxic origins involve toxins or drugs that can suppress bone marrow function, leading to decreased red cell production in both dogs and cats.

Question 13

What is the difference between PIMA and IMHA?

Answer 13

PIMA involves immune-mediated destruction of early erythroid precursors, while IMHA involves the destruction of mature red blood cells by the immune system.

Question 14

How do neoplastic origins contribute to anaemia, and what factors may be involved in cancer-related anaemia?

Answer 14

Neoplastic origins contribute to anaemia by infiltrating the bone marrow, disrupting normal hematopoiesis. Cancer-related anaemia may result from chronic inflammation, tumor-produced cytokines, and direct invasion of the bone marrow by cancer cells.

Question 15

What are the necrotic origins of bone marrow disorders, and what conditions can lead to vascular occlusion in the bone marrow?

Answer 15

Necrotic origins involve conditions causing cell death in the bone marrow. Vascular occlusion in the bone marrow can be caused by thrombosis or embolism, leading to ischemia and necrosis.

Question 16

Explain the significance of erythropoietin in stimulating erythropoiesis and its association with hypothyroidism.

Answer 16

Erythropoietin is a hormone that stimulates erythropoiesis. In hypothyroidism, reduced metabolism can lead to decreased erythropoietin production, contributing to anemia.

Question 17

Discuss nutrient deficiencies, particularly iron deficiency, and how it affects erythropoiesis.

Answer 17

Iron deficiency impairs hemoglobin synthesis, leading to microcytic, hypochromic red blood cells. It is a common cause of nutritional anemia.

Question 18

What is the process of bone marrow sampling, and what are the common sites for bone marrow aspiration?

Answer 18

Bone marrow sampling involves aspirating a small amount of marrow for examination. Common sites include the iliac crest and sternum. The procedure is done using a needle, and samples are typically obtained from the posterior iliac crest.

Question 19

List the equipment required for bone marrow aspiration, and describe the procedure.

Answer 19

Equipment includes a syringe, needle, and anticoagulant. The procedure involves inserting the needle through the skin and cortex of the bone, aspirating marrow into the syringe.

Question 20

What is primary hemostasis, and what triggers its initiation?

Answer 20

Primary hemostasis is the initial response to vascular damage, involving platelet adherence and formation of a loose platelet plug. It is triggered by exposure of the subendothelial matrix due to vascular damage.

Question 21

Describe the role of von Willebrand factor in primary hemostasis.

Answer 21

Von Willebrand factor mediates platelet adherence to the collagen surface during primary hemostasis, essential for the assembly of the platelet plug.

Question 22

What happens to platelets following adherence in primary hemostasis?

Answer 22

After adherence, platelets activate, changing their form to a more amorphous shape with multiple projections, increasing their total surface area.

Question 23

Explain the significance of platelet degranulation in the hemostatic process.

Answer 23

Platelet degranulation involves the release of chemical messengers and expression of fibrin receptors, contributing to the formation of a mesh-like structure from aggregated platelets held together by strands of fibrin, known as the platelet plug.

Question 24

Define secondary hemostasis and its role in the hemostatic process.

Answer 24

Secondary hemostasis involves the sequential activation of clotting factors, creating a chain of biochemical and cellular events to increase the stability and structural rigidity of the blood clot formed during primary hemostasis.

Question 25

How does fibrin contribute to the stability of the blood clot in secondary hemostasis?

Answer 25

Fibrin binds to the loose thrombus formed during primary hemostasis, creating a more stable clot and increasing its longevity.

Question 26

Explain the role of vitamin K in the coagulation cascade.

Answer 26

Vitamin K is a cofactor required for the formation of functioning clotting factors II, VII, IX, and X. It is essential for the activation of these factors in the coagulation cascade.

Question 27

Differentiate between the extrinsic and intrinsic pathways in the coagulation cascade.

Answer 27

The extrinsic pathway is activated by damage to endothelial tissue and involves clotting factors III (tissue factor) and VII. The intrinsic pathway is activated by factors in the blood and involves clotting factors XII, XI, IX, and VIII. Both pathways feed into the common pathway.

Question 28

Describe the final steps of the common pathway in the coagulation cascade.

Answer 28

The common pathway starts with Factor X and ends with the conversion of fibrinogen to fibrin. It involves the activation of factor Xa, which, along with other factors, leads to the formation of a stable fibrin clot.

Question 29

What is fibrinolysis, and how does it relate to tertiary hemostasis?

Answer 29

Fibrinolysis is the process of clot dissolution initiated at the time of endothelial damage. Tertiary hemostasis refers to the processes that follow the formation of the definitive blood clot, including clot dissolution. Fibrinolysis involves the release of tissue plasminogen activator (tPA) and the conversion of plasminogen to plasmin, which degrades fibrin.

Question 30

What is the cell-based model of coagulation, and how does it differ from the coagulation cascade model?

Answer 30

The cell-based model describes coagulation through phases of initiation, amplification, propagation, and stabilization. Unlike the simple cascade model, it considers the interaction between various coagulation factors and their regulation to control the coagulation process.

Question 31

How is hyperfibrinolysis associated with clinical situations in veterinary patients?

Answer 31

Hyperfibrinolysis, causing premature clot dissolution and bleeding, has been associated with trauma, cavitary effusions, hepatic disease, and Angiostrongylus infection in veterinary patients.

Question 32

What is the purpose of primary hemostasis, and what does the thrombogram measure?

Answer 32

Primary hemostasis aims to rapidly form a platelet plug at the site of endothelial damage. The thrombogram measures platelet number and size, including platelet count, PDW, MPV, and PCT.

Question 33

What precautions should be taken to avoid platelet clumps during coagulation testing, and what is the most common cause of platelet clumps?

Answer 33

Precautions include gentle sampling techniques, hair clipping, and avoiding excessive negative pressure. The most common cause of platelet clumps is vessel trauma and platelet activation during blood sampling, particularly in cats.

Question 34

What is the purpose of the Buccal Mucosal Bleeding Time (BMBT), and how is it performed?

Answer 34

The BMBT is a screening test for primary hemostasis disorders. It measures the time for a platelet plug to form after a buccal mucosal incision. The patient’s upper lip is reflected, a standard incision is made, and the time until bleeding stops is recorded.

Question 35

What are the parameters measured in platelet function analysis, and how does the Platelet Function Analyser (PFA) 100® work?

Answer 35

Parameters include closure time. The PFA 100® mimics high shear vessel trauma by drawing platelets through a membrane coated with collagen and activators, assessing platelet adherence and aggregation.

Question 36

What does Viscoelastic Testing (VET) assess, and how is shear modulus determined in direct assessment methods?

Answer 36

VET assesses the time to form a blood clot and clot properties. Direct assessment measures shear modulus by observing pin displacement in methods like thromboelastography (TEG®) and rotational thromboelastometry (ROTEM® delta).

Question 37

Describe the components and purpose of the Viscoelastic Coagulation Monitor (VCM) VetTM.

Answer 37

The VCM VetTM is a cartridge-based analyzer for veterinary patients, measuring clot firmness at 10 and 20 minutes (a10, a20) and clot lysis at 45 minutes (LI45) using whole blood.

Question 38

What are the normal ranges for Closure Time in Platelet Function Analysis for dogs and cats?

Answer 38

For dogs, the normal range is 47 to 98 seconds, and for cats, it is 43 to 176 seconds.

Question 39

How does Thromboelastography (TEG®) work, and what is its role in transfusion therapy?

Answer 39

TEG® measures shear modulus by observing pin displacement in response to clot formation. It guides blood product administration, preventing unnecessary transfusions and optimizing resource use.

Question 40

What coagulation factors do Activated Partial Thromboplastin Time (aPTT) and Prothrombin Time (PT) primarily assess, and how are they performed?

Answer 40

aPTT assesses the intrinsic and common pathways, while PT assesses the extrinsic and common pathways. Both are plasma-based tests using activators to mimic coagulation factors.

Question 41

List some conditions or situations that may affect coagulation, according to the provided information.

Answer 41

Conditions include anticoagulant rodenticide toxicity, envenomation, DIC, heatstroke, hypothermia, sepsis, and various hereditary and acquired disorders affecting clotting factors.

Question 42

What are hereditary disorders, and how is Mendelian genetics related to the inheritance of characteristics?

Answer 42

Hereditary disorders are conditions passed from one or both parents to their offspring through genetic material. Mendelian genetics, proposed by Gregor Mendel, outlines the mechanisms controlling the inheritance of characteristics.

Question 43

What is the significance of deciduous teeth in identifying hereditary clotting disorders in veterinary patients?

Answer 43

The first opportunity to discover a clotting disorder in cats or dogs is often when they lose their deciduous teeth or are presented for neutering.

Question 44

How does the nature of mutations contribute to the continuous occurrence of new factor deficiencies in certain dog populations, and how can control be achieved?

Answer 44

Due to the spontaneity of mutations, new factor deficiencies arise continuously. Control can be achieved through breeding strategies that preclude breeding from affected individuals.

Question 45

What are some common hereditary primary hemostatic disorders in veterinary patients, and name one breed associated with each type?

Answer 45

Von Willebrand Disease (e.g., Airdale, Akita)
Thrombocytopenia (e.g., Greyhound)
Beta1-tubulin Macrothrombocytopenia (e.g., German Shepherd)

Question 46

Describe the three forms of von Willebrand Disease (vWD) and mention some breeds associated with each type.

Answer 46

Type I: Normal structure but inadequate concentration (e.g., Doberman)
Type II: Inadequate concentration affecting large molecules (e.g., German Shorthaired Pointer)
Type III: No detectable vWF (e.g., Scottish Terrier)

Question 47

What are the clinical signs of von Willebrand Disease (vWD), and how is it diagnosed?

Answer 47

Clinical signs include gingival hemorrhage, epistaxis, hematuria, melena, cutaneous bruising, and excessive bleeding post-surgery. Diagnosis involves normal platelet count, coagulation profile, and using tests like BBMT and vWF antigen concentration (ELISAs).

Question 48

What is the treatment approach for von Willebrand Disease (vWD), and why should aspirin or NSAIDs be avoided?

Answer 48

Treatment involves blood products (cryoprecipitate, FFP, whole blood) and desmopressin. Aspirin or NSAIDs should be avoided as they affect platelet function.

Question 49

Explain the genetic basis of Haemophilia A and Haemophilia B and mention some breeds associated with each.

Answer 49

Haemophilia A is a deficiency in Factor VIII, affecting breeds like Golden Retriever and Labrador. Haemophilia B is a deficiency in Factor IX, seen in breeds like Rhodesian Ridgeback and Lhasa Apso.

Question 50

What are the clinical signs and diagnostics of Haemophilia, and what precautions should be taken in the management of haemophiliac patients?

Answer 50

Clinical signs include lameness, hematomas, and prolonged bleeding. Diagnostics involve prolonged aPTT and normal PT. Precautions include avoiding invasive procedures and anticoagulant drugs.

Question 51

How is Factor XII deficiency (Hageman trait) inherited in cats, and what is its significance in terms of bleeding tendencies?

Answer 51

Factor XII deficiency is inherited as an autosomal recessive trait in cats. It does not cause abnormal bleeding but prolongs aPTT. Measurement of individual clotting factors is advisable if a prolonged aPTT is documented.

Question 52

What is the seasonality observed in rodenticide anticoagulant poisoning, and why are small dogs more vulnerable to ingestion?

Answer 52

There is a significant increase in cases during August, September, and October, with a drop from December to April. Small dogs are more vulnerable due to a lower toxic dose, and their size allows them to access bait-hidden areas that larger dogs cannot reach.

Question 53

Name two first-generation anticoagulant rodenticide agents and explain why they are used less commonly than second-generation agents.

Answer 53

First-generation agents include warfarin, coumatetralyl, and diphacinone. They are used less commonly due to lower toxicity levels, requiring repeated ingestion for lethality, unlike the more potent and longer-lasting second-generation agents.

Question 54

What is the mode of action of anticoagulant rodenticides, and how do they affect vitamin K1-dependent clotting factors?

Answer 54

Anticoagulant rodenticides irreversibly bind to and inhibit vitamin K1 epoxide reductase, preventing the formation of active vitamin K1 and stopping the activation of vitamin K1-dependent clotting factors (II, VII, IX, and X).

Question 55

What are the clinical signs of rodenticide toxicity, and which coagulation factors are affected first?

Answer 55

Clinical signs include intra-cavitary bleeding (respiratory most affected), haemoabdomen, haemarthrosis, pericardial bleeding, CNS bleeding, and larger hematomas at injection sites. Factor VII is affected first, with aPTT elevation occurring 24-36 hours post-exposure.

Question 56

How is anticoagulant rodenticide toxicity diagnosed, and what are the limitations of coagulation tests in confirming this toxicity?

Answer 56

Diagnosis involves non-specific early signs or signs of spontaneous hemorrhage. Coagulation tests (aPTT and PT) are affected, but their elevation is not specific to rodenticide toxicity and can occur in other bleeding disorders.

Question 57

What is the management approach for acute recent ingestion of anticoagulant rodenticides, and why is prolonged treatment with vitamin K1 necessary?

Answer 57

Management involves inducing emesis, oral activated charcoal, and prolonged treatment with vitamin K1. Prolonged treatment is necessary due to the prolonged half-lives of second-generation agents, ensuring vitamin K1 epoxide recycling resumes after complete metabolization.

Question 58

How should hypocoagulable patients with signs of active hemorrhage due to anticoagulant rodenticide toxicity be treated emergently?

Answer 58

Emergency treatment includes A-B-C assessment, appropriate symptomatic treatment based on bleed location, and immediate transfusion with plasma products (FFP, SP, Cryosupernatant) to provide clotting factors II, VII, IX, and X.

Question 59

What is the preferred route for vitamin K1 therapy, and why is the oral route ideal in treating anticoagulant rodenticide toxicity?

Answer 59

The preferred route is oral, as vitamin K1 is delivered directly to the liver via the portal circulation. Intravenous administration is an alternative, but the oral route is safer and more effective.

Question 60

What is Acute Traumatic Coagulopathy (ATC), and what are the proposed mechanisms for its development?

Answer 60

ATC is associated with severe trauma. Proposed mechanisms include plasma protein C activation, glycocalyx disruption, fibrinogen depletion, platelet dysfunction, and the lethal triad (hypothermia, haemodilution, and acidaemia).

Question 61

How is ATC diagnosed, and what is the recommended early treatment approach for severe trauma patients?

Answer 61

Diagnosis involves abnormal thromboelastometry or thromboelastography traces. Early treatment includes the presumptive provision of blood products within six hours, typically packed red blood cells (PRBC), fresh frozen plasma (FFP), and platelets in a 1:1:1 ratio.

Question 62

Describe the life cycle of Angiostrongylus vasorum and the mechanisms by which it induces coagulopathy in infected dogs.

Answer 62

Angiostrongylus vasorum involves slugs, snails, and frogs as intermediate hosts. Dogs become infected by ingesting the intermediate host. Mechanisms of coagulopathy include hypofibrinogenaemia, acquired von Willebrand syndrome, immune-mediated thrombocytopenia, secretion of anticoagulants, and deficiency of factors V and VIII.

Question 63

What are petechiae and ecchymoses, and how do they relate to bleeding in Angiostrongylus vasorum infection?

Answer 63

Petechiae are tiny pinpoint spots of hemorrhage, while ecchymoses are larger areas of discolouration in the skin. In Angiostrongylus vasorum infection, they result from bleeding into mucous membranes or the skin due to coagulopathy.

Question 64

What conditions are associated with the development of Disseminated Intravascular Coagulation (DIC), and how is DIC managed?

Answer 64

Conditions associated with DIC include sepsis, systemic inflammatory response syndrome (SIRS), heatstroke, trauma, envenomation, immune-mediated hemolytic anemia (IMHA), severe viral infections, pancreatitis, severe parasitic infections, and neoplasia. Management involves supportive care, treating the primary condition, and, if necessary, the transfusion of blood products.

Question 65

How can medications and fluids, such as NSAIDs, haemodilution, and synthetic colloids, impact coagulation?

Answer 65

NSAIDs inhibit COX pathways, potentially affecting platelet aggregation. Haemodilution, especially in hypovolemic shock, can dilute clotting factors. Synthetic colloids may interfere with primary and secondary hemostasis, causing platelet dysfunction, reduced von Willebrand and factor VIII activity, and hypofibrinogenaemia.

Question 66

What unintended consequences can arise from the use of anticoagulants like Heparin, and how does liver disease impact coagulation?

Answer 66

Anticoagulants like Heparin can cause anticoagulation. Liver disease can lead to bleeding disorders due to a lack of clotting factor activation, impacting the synthesis of anticoagulants, fibrinolytics, and haemostatic proteins.

Question 67

How does acidaemia and uremia influence coagulation, and what are some general nursing considerations for patients with clotting disorders?

Answer 67

Acidaemia can reduce coagulation factor activity, and uremia can cause platelet dysfunction. Nursing considerations include careful venepuncture, avoiding invasive procedures, gentle handling, padded kennels, monitoring for bleeding signs, and avoiding medications that negatively impact coagulation.