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Lymphoreticular and haematopoeitic > Abnormalities of the leukon 1&2 > Flashcards

Abnormalities of the leukon 1&2 Flashcards

1
Q

How can WBCs be measured?

A
  • machine: impedance and optical
  • RBC lysed, nucleated cells stream through channel where electrical impedance or optical deflection noted
  • accurate for total numbers
  • machine: quantitative buffy coat (QBC)
  • machine scans a spun down large PCV tube and relates fractions to where cell types settle
  • problems with abnormal cells/ platelet enumeration
  • differentials poorly performed
  • manual methods: chamber counts/ unopette systems; not commonly used except for exotic /avian spp
  • blood smear estimates: from monolayer, assuming no clots/ clumping, count number of leukocytes in a monolayer x100 field, divide by four, correlates roughly to WBC*10e9/L. Should average at least 10 fields to minimise variation across smear
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2
Q

What is included in the total WBC concentration?

A
  • neutrophils
  • lymphocytes
  • monocytes
  • eosinophils
  • basophils
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3
Q

What is the leukocytes differential?

A
  • typically 100 consecutive cells
  • ideally 100 cells/ 10*10^9/L
  • e.g. 87% neutrophils
  • neutrophil conc = [WBC] * %
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4
Q

Influences on total leukocyte numbers

A
  • dynamic equilibrium
  • centred on balance b/w peripheral demand and ability of BM to supply adequate replacements
  • other factors include position of leukocyte within BV (marginated or circulating) and availability for sampling
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5
Q

What is CFU-G?

A

colony-forming-unit-granulocyte: a self-renewal stem cell

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6
Q

What in ProNP?

A

proliferation neutrophil pool

  • contains myeloblast (Mb), progranulocyte (Pg) and myelocyte (Mc)’
  • mitotic pool
  • simlated by various factors
  • apoptosis at myelocyte stage to limit production in health
  • timeframe: about 3d
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7
Q

What is MatNP?

A

= Maturation Neutrophil pool

  • metamyelocyte (Mmc), band neutrophil (B) adn segmented neutrophil (S)
  • post-mitotic pool
  • time: 2-3d (dogs)
  • MatNP: ProNP ration = 4-6
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8
Q

What is CNP?

A

Circulating Neutrophil pool: what is sampled during blood collection

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9
Q

What is MNP?

A

Marginated Neutrophil Pool: ready to exit the circulation and migrate into the tissues (TNP - tissue neutrophil pool)

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10
Q

What is the CNP: MNP ratio?

A

near 1 (cats: 3)

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11
Q

What is the neutrophil half-life in blood?

A

5-10 hours

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12
Q

What is neutrophil left shift?

A

if demand high, more immature neutrophils are released (bands or earlier)

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13
Q

What is neutrophil toxic change?

A
  • cytoplasmic foaminess and basophilia
  • Dohle bodies
  • giant neutrophils
  • vacuolation
  • toxic granules
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14
Q

Describe toxic neutrophils

A
  • in peripheral blood
  • accelerated production
  • no need for toxins
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15
Q

Describe degenerate/ lytic neutrophils

A
  • in tissues (fluids)
  • fighting with bacteria
  • bacterial toxins
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16
Q

Classifications of left shift

A
  • REGENERATIVE LEFT SHIFT: neutrophilia, segmented > bands
  • DENEGERATIVE LEFT SHIFT: neutropenia, bands > segmented
  • in between?
  • large vs. small animals
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17
Q

Causes - neutropenia (increased demand)

A
  • peracute bacterial infections (e.g. peritonitis, pyothorax)
  • endotoxaemia
  • immune-mediated: alongside decreased neutrophil survival time
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18
Q

Causes - neutropenia (redistribution)

A
  • in response to endotoxaemia, anaphylactic shock

- neutrophils undergo increased margination to vessel walls (fewer free to sample)

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19
Q

Outline neutropenia (decreased production)

A
  • usually BM disorders
  • INFECTION; parvo, FIV, FeLV, Ehrlichia
  • TOXICITIES: commonly iatrogenic e.g. azathioprine, cyclophosphamide, idiosyncratic drug reactions
  • INEFFECTIVE PRODUCTION: myelodysplasia (often FeLV related)
  • CHANGE IN MARROW ENVIRONMENT: myelofibrosis, myelophthisis (crowding out by neoplasia)
  • CONGENITAL ABNORMALITIES: cyclic neutropenia of grey collies, Chediak-Higashi syndrome (neutropenia in cats)
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20
Q

What is important to know about neutropenia?

A
  • beware breed differences (greyhounds) and individual variation (if mild, track)
  • CS are indirect
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21
Q

Therapeutic intervention - neutropenia

A

most give BS ABs if neutrophils

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22
Q

Causes - neutrophilia (increased production to increased demand)

A
  • INFECTIONS: bacterial, viral, protozoal
  • IM diseases: IMHA, PA etc
  • secondary to neoplasia
  • haemolysis, haemorrhage, necrosis, thrombosis
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23
Q

Causes - neutrophilia (increased production independent of demand)

A
  • well differentiated neutrophils transformed: chronic granulocyte leukemia, numbers can be v high, rule out appropriate causes for increase
  • poorly differentiated (early precursors) transformed: acute myeloid leukaemia, prognosis v poor
24
Q

Outline neutrophilia d/t increased persistence in circulation

A
  • stress/steroid response: neutrophils remain in circulation longer, more available to sample
  • may be hypersegmented (been around long enough for extra segmentation to occur)
  • accompanied by monocytosis and lymphopaenia (other steroid effects)
25
Q

Outline neutrophilia d/t redistribution

A
  • stress/ excitement increases BP
  • marginated neutrophils not normally sampled swept of BV wall into circulation
  • may increase WBC numbers up to 200% in cats
  • lymphocytes prevented from leaving circulation/ mobilised from thoracic duct - numbers increase
26
Q

Tx - neutrophil abnormalities

A
  • tx underlying cause
  • chronic granulocytic leukaemias: good short term prognosis
  • acute myeloid leukemias: no successful tx
27
Q

Outline differences in lymphocytes

A
  • BC and TC look same
  • BC mostly short-lived, days to wks, memory BCs and a few others longer lived
  • TCs long lived (months to years)
  • formed in BM but production and clonal proliferation in thymus, spleen, LNs
  • can recirculate from blood into tissues, back via lymphatics, in and out of lymphoid tissue and back into blood
28
Q

Location - leukocyte production

A
  • BM (all cell lines)
  • spleen and liver maintain potential to produce all WBC lines
  • thymus, spleen, LNs, bursa of fabricius (birds): mostly differentiation of lymphoid
  • complex interplay of growth factors
29
Q

Causes - lymphopaenia d/t increased demand

A
  • some PLE (loss of lymphocyte rich chyle)
  • chylo-thorax/ peritoneum with drainage
  • recruitment and emigration into tissue with some antigens
30
Q

Causes - lymphopaenia d/t redistribution

A
  • STEROIDS: endogenous (stress) or exogenous: redistribution to BM, tissues, trapping in LNs
  • Trapping in lymph rich fluid (chylothorax)
31
Q

Causes - lymphopaenia d/t decreased production

A
  • INFECTION: virus (canine distemper, parvo, panleukopaenia, FeLV, FIV)
  • LYMPHOLYTIC DRUGS: chemotherapeutics (e.g. cyclophosphamide, azathioprine, long-term corticosteroids)
  • CONGENITAL IMMUNODEFICIENCIES(e.g. Bassett Hounds) where BC and TC affected
32
Q

Causes - lymphocytosis d/t increased demand

A
  • persistent Ag stimulaton (fungal, protozoal, FeLV, leishmania, brucellosis)
  • post-vaccination
  • young animals
33
Q

Causes - lymphocytosis independent of demand

A
  • chronic lymphocytic leukaemia (well-differentiated)
  • acute lymphoblastic leukaemia (more poorly differentiated)
  • Stage 5 lymphoma: BM involvement and release of neoplastic lymphocytes into circulation
34
Q

Causes - lymphocytosis d/t redistribution

A
  • physiological leukocytosis, inhibition of recirculation, release from TD
  • hypoadrenocorticism (11-20%)
35
Q

What are monocytes?

A
  • monoblasts to monocytes in 6d
  • no storage pool, don;t have marginated and circulating pools
  • persistence in circulation varies (20h in cattle), shortens with inflammation
  • leave circulation to tissues, differentiate into macrophages with inflammatory cytokines
36
Q

Describe decreased monocyte cell numbers

A

Not recognised as a clinically separate entitiy

37
Q

Causes - monocytosis d/t increased demand

A
  • INFECTION: bacteria, fungal, protozoal
  • IMMUNE-MEDIATED DISEASE: IMHA, meningitis, PA
  • NECROSIS, trauma, burns
  • Neoplasia
38
Q

Causes - monocytosis independent of demand

A
  • secondary to immune neutropaenia - common precurosis (CFU-GM)
  • myelomonocytic leukaemia: acute or chronic
  • acute mnocytic leukaemia: with or without maturation
39
Q

What may cause monocytosis d/t redistribution?

A

Steroids may move monocytes out of the marginated pool

40
Q

Tx - monocytosis

A
  • tx underlying cuase
  • chronic myelomonocytic much the same as chronic granulocytic
  • no really successful tx for acute myelomonocytic leukemias in SA
41
Q

Describe eosinophil lifecycle

A
  • differentiate and mature in 2-6d (spp dependent)

- variable persistence in circulation (

42
Q

Cause - eosinopaenia

A
  • mechanism unclear:
  • corticosteroids (endogenous or exogenous) via apoptosism possible neutralisation of histamine/ mast cell degranulation and other mechanisms
  • catecholamines
43
Q

Cause - eosinophillia d/t increased demand

A
  • via sensitised TCs, mast cells: IL-5 release
  • parasite Ag
  • ‘allergic dz’: atopy, drug allergy, asthma, pulmonary infiltrate with eosinophils
  • inflammation of MC rich tissue (gut, skin, lungs, uterus)
44
Q

Causes -eosinophilia independent of demand

A
  • PARANEOPLASTIC (lymphoma, MCT, others where IL-5 elaborated)
  • HYPEREOSINOPHILIC SYNDROME -numbers increase in circulation, tissue w/o clear cause
  • EOSINOPHILIC LEUKAEMIA - rare
45
Q

Describe basophil lifecycle and role

A
  • maturation and release from BM over 2.5d
  • persist in circulation for 6h
  • role in type 1 hypersensitivities: anaphylaxis, rhinitis, asthma, GI sensitivities, parasites
  • ? role in delayed hypersensitivities
  • poorly understood in most domestic spp
46
Q

Causes - decreased numbers of basophils

A

possible with anaphylactic, inflammatory and steroid responses

47
Q

How to detect decreased numbers of basophils

A

impossible to detect on normal blood screens - reference interval begins at 10 for most

48
Q

Causes - basophilia d/t increased demand

A
  • IMMEDIATE OR DELAYED HYPERSENSITIVITIES: drugs, food, insect bites/stings
  • PARASITISM: especially dirofilaria, also GIT parasites, fleas and ticks
  • OTHER INFLAMMATORY RESPONSES
49
Q

Causes - basophilia independent of demand -2

A
  • PARANEOPLASITC: especially MCT

- BASOPHILIC LEUKEMIA - rare

50
Q

What is a stress leukogram?

A

= response to CORTICOSTEROID (endogoenous or exogenous)

  • mild to moderate mature neutrophilia
  • lymphopaenia
  • monocytosis
  • eosinophilia
51
Q

What leukocyte response may be seen with Addison’s?

A

may get reverse stress leukogram:

  • neutrophils and monocytes usually WNL
  • lymphocytosis
  • eosinophilia
  • changes usually mild
52
Q

Describe an acute inflammatory leukogram

A
  • neutrophilia +/- left shift
  • lymphopaenia
  • monocytosis
    +/- eosinopenia
53
Q

Describe a chronic inflammatory leukogram

A
  • neutrophilia +/- left shift
  • lymphocytosis
  • monocytosis
54
Q

What is the leukocyte adrenaline response? 2

A
  • neutrophilia

- lymphocytosis

55
Q

Describe normal haemogram of young animals

A
  • increased WBC #s
  • lower Hct
  • changes are mild and generally normalised by 3mo

Lymphoreticular and haematopoeitic (21 decks)

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