Leukocytes Flashcards

1
Q

neutrophil kinetics

A

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

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2
Q

Pelger-Huet anomaly

A

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.

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3
Q

causes of mature neutrophilia

A

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

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4
Q

catecholamines

A

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

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5
Q

glucocorticoid response

A

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

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6
Q

mild or chronic inflammation

A

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

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7
Q

neutrophilia with left shift

A
  • Indicated by presence of banded neutrophils (hyposegmented)
  • Causes by acute inflammation with either regenerative or degenerative left shift
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8
Q

enerative vs degenerative left-shift neutrophilia

A

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

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9
Q

toxic changes in neutrophils

A

foamy vacuolation
dohle bodies
increased basophilia

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10
Q

neutropenia

A

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

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11
Q

leukaemia

A

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

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12
Q

maturative stages of leukaemia

A

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.

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13
Q

classification of leukaemia by origin of cells

A

myeloid = megakaryocytes, granulocytes, monocytes and erythrocytes

lymphoid = lymphocytes

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14
Q

distinguishing between myeloid and lymphoid leukaemia cells based on morphology

A

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).

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15
Q

distinguishing between myeloid and lymphoid leukaemia cells based on clinical testing

A

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.

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16
Q

thrombopoietin

A

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

17
Q

platelet kinetics

A
  • 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
18
Q

why are errors in platelet enumeration common?

A

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

19
Q

thrombocytopaenia

A

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

20
Q

clinical signs of thrombocytopaenia

A

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

21
Q

what can cause decreased production of platelets?

A

Acquired megakaryocyte hypoplasia or aplasia

Bi- or pan-cytopenia

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

22
Q

differentials for thrombocytopaenia

A

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

23
Q

Acquired coagulation disorders

A

DIC
Thromboembolism
liver disease
vit K deficiency
snake envenomation

24
Q

Hereditary coagulation disorders

A

Scott syndrome
Haemophilia A & B

25
Q

DIC

A

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.

26
Q

non-overt vs overt DIC

A

Non-overt = early stage, contained or compensated by inhibitors (antithrombin 3 and protein C)

Overt = all anticoagulant molecules used, uncompensated.

27
Q

thromboembolism

A

virchows triad = endothelial injury, abnormal blood flow, hyper-coagulability

causes: neoplasia, sepsis, IMHA, heart diseases, protein-losing nephropathy, hyperthyroidism (cats)

28
Q

liver disease

A

liver = primary site for the synthesis of coagulation factors

liver disease = lack of coagulation factors = excessive bleeding

29
Q

vitamin K deficiency

A

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

30
Q

snake envenomation

A

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

31
Q

scott syndrome

A

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

32
Q

haemophilia A & B

A

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.

33
Q

thrombocytopenia with normal APTT, PT and FDP

A

= lack of production or enhanced platelet destruction

34
Q

thrombocytopenia with prolonged APTT, PT and positive FDP

A

consumption of platelets and coagulation factors = DIC

35
Q

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

A

multiple coagulation defects = rodenticide toxicity

36
Q

normal platelet count and PT, prolonged aPTT, negative FDP

A

early anti-coagulant rodenticide toxicity

37
Q

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

A

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

38
Q

differentials for thrombocytosis

A

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

39
Q

what are the features of a stress leukogram?

A

neutrophilia, monocytosis, lymphopenia, eosinopenia