Leukocytes

Question 1

neutrophil kinetics

Answer 1

left-shift = younger neutrophils (band, hyposegmented and bigger in size)
right-shift = older neutrophils (hypersegmented)

Question 2

Pelger-Huet anomaly

Answer 2

inherited condition characterised by failure of mature granulocyte nuclei to lobulate, and so the neutrophils nuclei appear hyposegmented. The neutrophils are perfectly functional, so this is just a morphological change. Common in Australian shepherd dogs.

Question 3

causes of mature neutrophilia

Answer 3

catecholamines
glucocorticoids
mild/chronicc inflammation
acute inflammation without left-shift

Question 4

catecholamines

Answer 4

(exercise, fear, excitement) e.g. adrenaline
Immediate effects but short half-life and so short DOA

Question 5

glucocorticoid response

Answer 5

shift of neutrophils from storage and marginal pools and decreased diapedesis

Stress leukogram = at least 2/4 of the following clinical signs; neutrophilia, monocytosis, lymphopenia, eosinopenia

Sources: exogenous administration, hyperadrenocorticism, stress, hyperthermia

Question 6

mild or chronic inflammation

Answer 6

increased peripheral demand for neutrophils is met by release of marginal pools

Likely does not involve bacterial infection, as this would elicit a more severe response – more likely to be sterile inflammation e.g. haemorrhage, necrosis, haemolysis, neoplasia, toxicity

Question 7

neutrophilia with left shift

Answer 7

• Indicated by presence of banded neutrophils (hyposegmented)
• Causes by acute inflammation with either regenerative or degenerative left shift

Question 8

enerative vs degenerative left-shift neutrophilia

Answer 8

regenerative = mature neutrophils more numerous than band neutrophils
degenerative = band neutrophils more numerous than mature neutrophils (demand for neutrophils is massive - indicates severe infection)

Question 9

toxic changes in neutrophils

Answer 9

foamy vacuolation
dohle bodies
increased basophilia

Question 10

neutropenia

Answer 10

one of the most severe signs of life-threatening bacterial infection
- massive consumption of neutrophils

Question 11

leukaemia

Answer 11

presence of neoplastic cells of haematopoietic origin in blood and/or bone marrow
it can be of any haematopoietic cell lineage

Question 12

maturative stages of leukaemia

Answer 12

acute = mutation stopped the maturative process, so the cells are morphologically immature
chronic = mutation occurred after the maturation process was complete, so cells are morphologically mature and cell type can be identified.

Question 13

classification of leukaemia by origin of cells

Answer 13

myeloid = megakaryocytes, granulocytes, monocytes and erythrocytes

lymphoid = lymphocytes

Question 14

distinguishing between myeloid and lymphoid leukaemia cells based on morphology

Answer 14

lymphoid cells are medium-large size, cytoplasm is mildly basophilic, rarely granulations or vacuolations, nuclei are usually round, nucleoli is prominent

myeloid cells are larger, deeply basophilic, often have vacuolisations (rare granulations), and nucleoli are visible).

Question 15

distinguishing between myeloid and lymphoid leukaemia cells based on clinical testing

Answer 15

Lymphoid and myeloid cells can be distinguished based on morphology, however, it is not always straightforward so clinical testing such as PCR is more relied upon.
All tests look for antigen expression on the cell surfaces – some antigens are specific for a specific cell lineage.

Question 16

thrombopoietin

Answer 16

the hormone that stimulates the production of platelets.
is produced by various cells in the body, mainly renal tubular epithelial, bone marrow stromal cells and hepatocytes

Question 17

platelet kinetics

Answer 17

• 30% platelet circulating mass is in the spleen
• Platelets circulate for 5-9 days, as they age they are removed from the circulation by macrophages in the spleen and liver

Question 18

why are errors in platelet enumeration common?

Answer 18

Platelets change shape and aggregate when stimulated and so the instruments miss some of them
-> You must check platelet counts on blood smears to confirm

Question 19

thrombocytopaenia

Answer 19

decrease in circulating platelets
the most common acquired haemostatic disorder in veterinary medicine

Question 20

clinical signs of thrombocytopaenia

Answer 20

petechiation/ecchymosis in tissues or mucosal membranes, epistaxis, melena, hematochezia, haematuria, prolonged bleeding after venipuncture, retinal haemorrhage or hyphema.

Question 21

what can cause decreased production of platelets?

Answer 21

Acquired megakaryocyte hypoplasia or aplasia

Bi- or pan-cytopenia

Infectious agents, chemical/physical agents, drugs, toxins, immune-mediated.

Question 22

differentials for thrombocytopaenia

Answer 22

decreased production = hypoplasia/aplasia, bi or pancytopenia, infectious agents, chemical/physical agents, drugs, toxins, immune-mediated

platelet loss = trauma, haemorrhage

consumption = DIC (very common)

destruction = immune-mediated thrombocytopaenia, evans syndrome (if with IMHA)

distribution = splenomegaly associated

Question 23

Acquired coagulation disorders

Answer 23

DIC
Thromboembolism
liver disease
vit K deficiency
snake envenomation

Question 24

Hereditary coagulation disorders

Answer 24

Scott syndrome
Haemophilia A & B

Question 25

DIC

Answer 25

Widespread small and medium vessel thrombosis not necessarily where there is any endothelial damage (coagulation gone crazy!) -> platelets and coagulation factors all get consumed. Always secondary to an underlying disease process e.g. septicaemia, viremia, protozoal parasites.

Question 26

non-overt vs overt DIC

Answer 26

Non-overt = early stage, contained or compensated by inhibitors (antithrombin 3 and protein C) Overt = all anticoagulant molecules used, uncompensated.

Question 27

thromboembolism

Answer 27

virchows triad = endothelial injury, abnormal blood flow, hyper-coagulability causes: neoplasia, sepsis, IMHA, heart diseases, protein-losing nephropathy, hyperthyroidism (cats)

Question 28

liver disease

Answer 28

liver = primary site for the synthesis of coagulation factors liver disease = lack of coagulation factors = excessive bleeding

Question 29

vitamin K deficiency

Answer 29

Vitamin K is essential in the synthesis of factors 2, 7, 9 and 10, as well as protein C. These factors are important in intrinsic and extrinsic pathways. Causes of vit K deficiency: - Rodenticide toxicity (dogs, cats) - Sweet clover and sweet vernal grass (cattle) - Decreased absorption e.g. severe inflammatory bowel disease

Question 30

snake envenomation

Answer 30

Venom contains procoagulant molecules -> venom-induced consumption coagulopathy due to pro-thrombin activators -> DIC

Question 31

scott syndrome

Answer 31

Rare disorder in German Shepherds Platelets do not express phosphatidylserine on their surface = no intrinsic pathway Clinical signs: intramuscular haemorrhage, epistaxis, hyphema

Question 32

haemophilia A & B

Answer 32

Transmitted as X chromosome-linked recessive traits = usually in male Haemophilia A: factor VIII deficiency. Much more common than haemophilia B. many breeds of dogs, cats, horses, Hereford cattle. Haemophilia B: factor IX deficiency. Many breeds of dogs and British shorthair, and Siamese-cross cats. Clinically severe coagulopathies with bleeding.

Question 33

thrombocytopenia with normal APTT, PT and FDP

Answer 33

= lack of production or enhanced platelet destruction

Question 34

thrombocytopenia with prolonged APTT, PT and positive FDP

Answer 34

consumption of platelets and coagulation factors = DIC

Question 35

normal platelet count, prolonged PT and aPTT, negative FDP test

Answer 35

multiple coagulation defects = rodenticide toxicity

Question 36

normal platelet count and PT, prolonged aPTT, negative FDP

Answer 36

early anti-coagulant rodenticide toxicity

Question 37

normal platelet count, aPTT and PT, negative FDP test in the presence of a bleeding diathesis

Answer 37

platelet function defect (vW disease, Scott syndrome etc.)

Question 38

differentials for thrombocytosis

Answer 38

Physiologic - Splenic contraction – due to adrenaline, intense exercise - Epinephrine Drug-induced - Epinephrine – temporary - Vinchristine – used for cancer treatment Reactive - Inflammation, infection, neoplasia, trauma, rebound from thrombocytopenia - Iron deficiency-related Essential thrombocythemia

Question 39

what are the features of a stress leukogram?

Answer 39

neutrophilia, monocytosis, lymphopenia, eosinopenia