Leukocytes Flashcards
neutrophil kinetics
left-shift = younger neutrophils (band, hyposegmented and bigger in size)
right-shift = older neutrophils (hypersegmented)
Pelger-Huet anomaly
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.
causes of mature neutrophilia
catecholamines
glucocorticoids
mild/chronicc inflammation
acute inflammation without left-shift
catecholamines
(exercise, fear, excitement) e.g. adrenaline
Immediate effects but short half-life and so short DOA
glucocorticoid response
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
mild or chronic inflammation
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
neutrophilia with left shift
- Indicated by presence of banded neutrophils (hyposegmented)
- Causes by acute inflammation with either regenerative or degenerative left shift
enerative vs degenerative left-shift neutrophilia
regenerative = mature neutrophils more numerous than band neutrophils
degenerative = band neutrophils more numerous than mature neutrophils (demand for neutrophils is massive - indicates severe infection)
toxic changes in neutrophils
foamy vacuolation
dohle bodies
increased basophilia
neutropenia
one of the most severe signs of life-threatening bacterial infection
- massive consumption of neutrophils
leukaemia
presence of neoplastic cells of haematopoietic origin in blood and/or bone marrow
it can be of any haematopoietic cell lineage
maturative stages of leukaemia
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.
classification of leukaemia by origin of cells
myeloid = megakaryocytes, granulocytes, monocytes and erythrocytes
lymphoid = lymphocytes
distinguishing between myeloid and lymphoid leukaemia cells based on morphology
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).
distinguishing between myeloid and lymphoid leukaemia cells based on clinical testing
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.
thrombopoietin
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
platelet kinetics
- 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
why are errors in platelet enumeration common?
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
thrombocytopaenia
decrease in circulating platelets
the most common acquired haemostatic disorder in veterinary medicine
clinical signs of thrombocytopaenia
petechiation/ecchymosis in tissues or mucosal membranes, epistaxis, melena, hematochezia, haematuria, prolonged bleeding after venipuncture, retinal haemorrhage or hyphema.
what can cause decreased production of platelets?
Acquired megakaryocyte hypoplasia or aplasia
Bi- or pan-cytopenia
Infectious agents, chemical/physical agents, drugs, toxins, immune-mediated.
differentials for thrombocytopaenia
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
Acquired coagulation disorders
DIC
Thromboembolism
liver disease
vit K deficiency
snake envenomation
Hereditary coagulation disorders
Scott syndrome
Haemophilia A & B
DIC
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.
non-overt vs overt DIC
Non-overt = early stage, contained or compensated by inhibitors (antithrombin 3 and protein C)
Overt = all anticoagulant molecules used, uncompensated.
thromboembolism
virchows triad = endothelial injury, abnormal blood flow, hyper-coagulability
causes: neoplasia, sepsis, IMHA, heart diseases, protein-losing nephropathy, hyperthyroidism (cats)
liver disease
liver = primary site for the synthesis of coagulation factors
liver disease = lack of coagulation factors = excessive bleeding
vitamin K deficiency
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
snake envenomation
Venom contains procoagulant molecules -> venom-induced consumption coagulopathy due to pro-thrombin activators -> DIC
scott syndrome
Rare disorder in German Shepherds
Platelets do not express phosphatidylserine on their surface = no intrinsic pathway
Clinical signs: intramuscular haemorrhage, epistaxis, hyphema
haemophilia A & B
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.
thrombocytopenia with normal APTT, PT and FDP
= lack of production or enhanced platelet destruction
thrombocytopenia with prolonged APTT, PT and positive FDP
consumption of platelets and coagulation factors = DIC
normal platelet count, prolonged PT and aPTT, negative FDP test
multiple coagulation defects = rodenticide toxicity
normal platelet count and PT, prolonged aPTT, negative FDP
early anti-coagulant rodenticide toxicity
normal platelet count, aPTT and PT, negative FDP test in the presence of a bleeding diathesis
platelet function defect (vW disease, Scott syndrome etc.)
differentials for thrombocytosis
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
what are the features of a stress leukogram?
neutrophilia, monocytosis, lymphopenia, eosinopenia
