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Lymphoreticular > Abnormal Leukon: Neutrophilia (Balasz) > Flashcards

Abnormal Leukon: Neutrophilia (Balasz) Flashcards

1
Q

What may cause hypersegmented neutrophilia? What effect may this have on counts?

A

Steroids prevent adhesion of neutrophils to wall
- less cells enter tissues and marginate
- neutrophilia results
“steroid neutrophilia”

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2
Q

What is a physiological casue of neutrophilia?

A

Being scared ^ BP washes marginaed neutrophils off

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3
Q

What causes neutrophilia?

A
  • infections (bacterial, viral, protozoal)
  • immune mediated dz (IMHA, polyarthritis)
  • 2* to neoplasia
  • haemolysis, haemorrhage, necorsis, thrombosis
    > acute/chronic inflam leukogram, steroid, physiological shift, chronic myeloid leukaemia
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4
Q

What is the most common type of leukaemia?

A
  • lymphoid
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5
Q

What is the difference ebetween chronic and acute leukaemia?

A

> chronic =
- well differentiated neutrophils transformed: chronic granulocytic leukaemia
- numbers can be v high, r/o other casues of increase
acute =
- poorly differentiated (early precursor) transformed: acute myeloid leukaemia
- porg v poor

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6
Q

eg. Neutrophilia d/t increased persistence in the circulation?

A

> stress/steroid response(neutrophils remain in circulation longer)

  • may be hypersegmeneted
  • accompanied by monocytosis and lymphopenia (other steroid effects)
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7
Q

Egs. Neutrophilia d/t Redistribution. Other changes seen concurrently?

A
  • stress/excitement ^ BP
  • marginated neutrophils not normally sampled swept into circulation
  • may ^ WBC >200% cats
  • lymphocytes prevented from leaving circulation and mobilised from thoracic duct so numbers also increase
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8
Q

Tx of neutrophilia?

A

Tx the patient!

- tx underlying cause

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9
Q

Px chronic granulocytic leukaemia?

A
  • good short term
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10
Q

Px acute myeloid leukaemia?

A
  • no successful tx
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11
Q

Normal description of a mature lymphocyte?

A

Small, round ,very small amount blue cytoplasma, nucleus massive and about the same size as RBC

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12
Q

How do B and T lymphocytes differ? Where are they formed and where do they circulate?

A
  • look the same
  • formed in BM but production and clonal proliferation in thymus, spleen LNs
  • travel blood - tissues - lymphatics - in and out of lymphoid tissue - blood
    > B cells
  • short lived (d/weeks) except memory cells
    > T cells
  • long lived months/years
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13
Q

Are lymphoctes commonly looked at when assessing BM function?

A

No!

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14
Q

Reactive changes of lymphocytres seen micrscopically?

A
  • ^ cytoplasm, dark blue
  • indentation of nucleus
  • vauloated/dotty cytoplasma (constipated plasma cell)
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15
Q

Causes of lymphopenia?

A
  1. acute inflammatory
    - stay in tissues
    - stay in LNs
  2. steroid lymphopenia
    - egression into LNs and BM
    - destroys LNs
  3. depletion lymphopenia
    - chylous effusion
  4. lymphoid hypoplasia or aplasia
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16
Q

Causes of lymphopenia d/t ^ demand

A
  • PLE (loss of lymphocyte rich chyle)
  • chylothorax/peritoneum if drained
  • recruitment and emigration into tissue with some antigens
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17
Q

Causes of lymphopenia d/t redistribution?

A
  • steroids (exo/endo) stress
    > redistribution into BM, tissues and trapping in LN
  • trapping in lymph rich fluid (chylothorax etc.)
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18
Q

Causes of lymphopenia d/t v production?

A

> infectious
- virsuese (canine distemper, parvo, panleucopenia, FeLV, FIV)
lympholytic drugs
- chemo (eg. cyclophosphamide, azathioprine, long term steroids)
congential immunodeficiency
- eg. Bassett hound B and T cells affected

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19
Q

Causes of lymphocytosis?

A
  1. chonic inflammatory
  2. physiological (Shift)
    = neutrophils ,will ^ circulating no.
  3. lymphoproliferative
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20
Q

Which animals will have high unmbers of reactive lymphocytes?

A

young animals esp puppies

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21
Q

^ no. to ^ demand LOOK

A
  • puppies can be higher than range of adult (normal!)
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22
Q

^ no indepednent of demand

A 
> chronic lymphocytic leukaemia
> acute lymphoiblastic leukaemia
- v poor px, no tx
- poorly differentiated
- v. quick progressive aggressive dz 
> Stage V lymphoma (spleen, liver etc. involved aswell)
- w/ BM involvement 
- release of neoplastic lymphocytes into circulation
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23
Q

Redistribution

A 
> phyisological
- inhibition of recirculation
- release from thoracic duct
> Hypoadrenocorticism
- lymphocytosis even when stressed (which should cause lymphopenia) 
- d/t cortisol
24
Q

How can a monocyte be identified

A
  • larger than neutrophil
  • blue grey cytoplasm
  • +- cytoplasm can contain vacuoles (neutrophils dont)
  • nucleus can look like anything!! lymphoid/nuetrophilic but is lighter than neutrophil nucleus
  • can look like toxic neutrophils (bluer cytoplasm, vacuolated, giant neutrophils etc.)
25
Q

Where are monocytes produced? How long do they take?

A
  • BM

- 6d

26
Q

How do pools of monocytes differ to neutrophils?

A
  • no storage pool
  • marginatd and circulating pool present
  • persistence in circulation varies (20hrs cattle)
    > shorter with inflammation
  • leave circulation to tissues, differentiate into macrophages with inflammatory cytokines
27
Q

Causes of monocytopenia ?

A

Does not occour

- normal levels very low/zero

28
Q

Causes of monoytosis?

A

= neutrophils
> infectious (bacterial, fungal, protozoal)
>immune mediated dz (IMHA, meningitis, poly arthritis)
> necrosis, trauma, burns
> neoplasia

29
Q

When do monocyte and neutrophil numbers not change in parallel?

A

Immune mediated destruction of neutrophils

  • > GM-CSF release that stimulates neutrophil and monocyte production
  • neutrophils destroyed but monocytosis d/t consant stimulation with GM-CSF
30
Q

Causes of monocytosis?

A 
> 2* to immune neutropenia
- common precursor CFU-GM 
> myelomonocytic leukaemia 
- acute and chronic forms
> acute monocytic leukaemia
- with/without maturation 
- AML M5a/M5b
31
Q

Redsitribution causes of monocytosis?

A
  • steroids may move them fom the marginated pool
32
Q

Tx monocytosis?

A
  • Tx underlying cause!!
  • chronic myelomonocytic = chronic granulocytic
  • no really successful tx for acute myelomonocytic leakaemias in SA
33
Q

How do eosinophils look like?

A
  • granulocyte
  • segemneted nucleus like neutrophils
  • lots of eosinophilic (orange) granules
  • lots of vacuoles in dogs (granules that dont stain, not true vacuoles)
  • species differences
    > dogs
  • variable granule size
    > greyhounds
  • none of the granules stain at all!
  • looks like a very toxic neutrophil
    > cats
  • speckled full granulated
    > horses
  • huge granules liek a raspberry
    > cows
  • smaller round granules
34
Q

How long do eosinophils take to differentate and mature/

A
  • 2-6d species dependent
35
Q

How long do eosinophils persist in circulation?

A
  • variable (
36
Q

Causes of eosinopenia?

A

> eosinopenia erference range starts at zro

  • theoretically corticosteroids (endo/exo) via apoptosis
  • possible neutraliation of histamine/MC degranulation and other mechanisms
  • catecholamines
37
Q

Casues of eosinophilia?

A
  • Via sensitised T cells, mast cells: IL-5 release
  • parasite antigen
  • allergic dz - atopy, drug allergy, asthma, pulmonary infiltrate with eosinophils
  • inflammatoion of MC rich tissue (gut, skin, lungs, uterus)
38
Q

How do eosinophils attack destroy things?

A

Kill big things outside the cell (cg. neutorphils phagocytosing)

39
Q

Eosinophilia ^ independent of demand?

A 
> paranoplastic
- lymphoma
- mast cell tumour
- IL5
> hyperoesinic syndrome in cats
- numbers ^  in circulation with no cause
- looks like leukaemia
> eosinophilic leukaemia
- rare
40
Q

How commonly are basophils seen?

A

not!

41
Q

Appearance of basophila?

A

> dog
- Ribbon like nucleus
- granules around and on top of nucleus (look like pores)
cat
- oval lavender/lilac/pale coloured granules

42
Q

How long do basophils take to mature and release from BM? Persist in circulation?

A
  • .5d

- persist for 6hrs

43
Q

Persisence in cicrulcation

A
  • 6hrs
44
Q

ROle of basophils

A
  • Type 1 hypersensistivity : analphylaxis, rhinitis, asthma, GI snesitivity, parasites
  • ? role in delayed hypersensitivity
  • poorly understood most domestic spp
45
Q

Causes of decresed no. basophils

A
  • impossibel to detect on normal blood screens (reference interval begins at 0)
  • possible with anaphylactic, inflammatory and steroid responses
46
Q

Causes of basophilia d/t ^ demand?

A
  • immediate/delayed hypersensitivity (drugs, food, insects)
  • parasitism (especially Dirofilaria, also GI paasites, fleas and ticks)
  • other inflam
47
Q

Causes of basophilia independent on demand?

A
  • paraneoplastic (esp with MCTs)

- basophilic leukaemia (rare)

48
Q

What is the stress leukogram

A

response to endogenous/exogenous steroid (stress/drugs prednisolone)

  • neutrophilia
  • lymphopenia
  • monocytosis
  • eosinopenia
49
Q

Addisons leukogram?

A
  • REVERSE stress leukogram (lack of cortisol)
  • neutrophils and monocytes normal
  • lymphocytosis
  • eosinophilia
  • changes mild
50
Q

Acute inflammatory leukogram?

A
  • neutrophilia +- left shift
  • lymphopenia
  • monocytosis
    +- eosinopenia
51
Q

Chronic inflammatory leukogram?

A
  • neutrophilia +- left shift
  • lymphocytosis
  • monocytosis
52
Q

Adrenaline response?

A

neutrophilia
lymphocytosis
(d/t ^ BP)

53
Q

How does the blood of young animals differ to older?

A

> normal haemogram
- ^ WBC
- v HCT
changes mild and normalise ~3m

54
Q

How would an acute and chronic inflammatory neutrophilia differ?

A 
> acute
- no storage pool 
- band neutrophils
> chronic
- storag pool re-established
- fewer band neutrophils
55
Q

What is a Mott cell?

A

Reactice B lymphocyte plasma cell full of vaculole like things

Lymphoreticular (31 decks)

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