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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is included in the total WBC concentration?

A
  • neutrophils
  • lymphocytes
  • monocytes
  • eosinophils
  • basophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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] * %
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is CFU-G?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is CNP?

A

Circulating Neutrophil pool: what is sampled during blood collection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is MNP?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the CNP: MNP ratio?

A

near 1 (cats: 3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the neutrophil half-life in blood?

A

5-10 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is neutrophil left shift?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is neutrophil toxic change?

A
  • cytoplasmic foaminess and basophilia
  • Dohle bodies
  • giant neutrophils
  • vacuolation
  • toxic granules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe toxic neutrophils

A
  • in peripheral blood
  • accelerated production
  • no need for toxins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe degenerate/ lytic neutrophils

A
  • in tissues (fluids)
  • fighting with bacteria
  • bacterial toxins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Causes - neutropenia (increased demand)

A
  • peracute bacterial infections (e.g. peritonitis, pyothorax)
  • endotoxaemia
  • immune-mediated: alongside decreased neutrophil survival time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Causes - neutropenia (redistribution)

A
  • in response to endotoxaemia, anaphylactic shock

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is important to know about neutropenia?

A
  • beware breed differences (greyhounds) and individual variation (if mild, track)
  • CS are indirect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Therapeutic intervention - neutropenia

A

most give BS ABs if neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Outline neutrophilia d/t redistribution
- 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
Tx - neutrophil abnormalities
- tx underlying cause - chronic granulocytic leukaemias: good short term prognosis - acute myeloid leukemias: no successful tx
27
Outline differences in lymphocytes
- 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
Location - leukocyte production
- 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
Causes - lymphopaenia d/t increased demand
- some PLE (loss of lymphocyte rich chyle) - chylo-thorax/ peritoneum with drainage - recruitment and emigration into tissue with some antigens
30
Causes - lymphopaenia d/t redistribution
- STEROIDS: endogenous (stress) or exogenous: redistribution to BM, tissues, trapping in LNs - Trapping in lymph rich fluid (chylothorax)
31
Causes - lymphopaenia d/t decreased production
- 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
Causes - lymphocytosis d/t increased demand
- persistent Ag stimulaton (fungal, protozoal, FeLV, leishmania, brucellosis) - post-vaccination - young animals
33
Causes - lymphocytosis independent of demand
- chronic lymphocytic leukaemia (well-differentiated) - acute lymphoblastic leukaemia (more poorly differentiated) - Stage 5 lymphoma: BM involvement and release of neoplastic lymphocytes into circulation
34
Causes - lymphocytosis d/t redistribution
- physiological leukocytosis, inhibition of recirculation, release from TD - hypoadrenocorticism (11-20%)
35
What are monocytes?
- 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
Describe decreased monocyte cell numbers
Not recognised as a clinically separate entitiy
37
Causes - monocytosis d/t increased demand
- INFECTION: bacteria, fungal, protozoal - IMMUNE-MEDIATED DISEASE: IMHA, meningitis, PA - NECROSIS, trauma, burns - Neoplasia
38
Causes - monocytosis independent of demand
- secondary to immune neutropaenia - common precurosis (CFU-GM) - myelomonocytic leukaemia: acute or chronic - acute mnocytic leukaemia: with or without maturation
39
What may cause monocytosis d/t redistribution?
Steroids may move monocytes out of the marginated pool
40
Tx - monocytosis
- tx underlying cuase - chronic myelomonocytic much the same as chronic granulocytic - no really successful tx for acute myelomonocytic leukemias in SA
41
Describe eosinophil lifecycle
- differentiate and mature in 2-6d (spp dependent) | - variable persistence in circulation (
42
Cause - eosinopaenia
- mechanism unclear: - corticosteroids (endogenous or exogenous) via apoptosism possible neutralisation of histamine/ mast cell degranulation and other mechanisms - catecholamines
43
Cause - eosinophillia d/t increased demand
- 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
Causes -eosinophilia independent of demand
- PARANEOPLASTIC (lymphoma, MCT, others where IL-5 elaborated) - HYPEREOSINOPHILIC SYNDROME -numbers increase in circulation, tissue w/o clear cause - EOSINOPHILIC LEUKAEMIA - rare
45
Describe basophil lifecycle and role
- 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
Causes - decreased numbers of basophils
possible with anaphylactic, inflammatory and steroid responses
47
How to detect decreased numbers of basophils
impossible to detect on normal blood screens - reference interval begins at 10 for most
48
Causes - basophilia d/t increased demand
- IMMEDIATE OR DELAYED HYPERSENSITIVITIES: drugs, food, insect bites/stings - PARASITISM: especially dirofilaria, also GIT parasites, fleas and ticks - OTHER INFLAMMATORY RESPONSES
49
Causes - basophilia independent of demand -2
- PARANEOPLASITC: especially MCT | - BASOPHILIC LEUKEMIA - rare
50
What is a stress leukogram?
= response to CORTICOSTEROID (endogoenous or exogenous) - mild to moderate mature neutrophilia - lymphopaenia - monocytosis - eosinophilia
51
What leukocyte response may be seen with Addison's?
may get reverse stress leukogram: - neutrophils and monocytes usually WNL - lymphocytosis - eosinophilia - changes usually mild
52
Describe an acute inflammatory leukogram
- neutrophilia +/- left shift - lymphopaenia - monocytosis +/- eosinopenia
53
Describe a chronic inflammatory leukogram
- neutrophilia +/- left shift - lymphocytosis - monocytosis
54
What is the leukocyte adrenaline response? 2
- neutrophilia | - lymphocytosis
55
Describe normal haemogram of young animals
- increased WBC #s - lower Hct - changes are mild and generally normalised by 3mo