Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Haematology > abnormal white cell count > Flashcards

abnormal white cell count Flashcards

1
Q

what is haemopoeisis *

A

production of mature blood cells in marrow

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

what are the different types of haemopoeisis *

A

normal (polyclonal) - can be reactive or healthy

malignant (abnormal/clonal) - leaukaemia (lymphoid/myeloid), myelodysplasia, myeloproliferative

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

why does malignant haemopoesis cause clonal cells *

A

cancer cells are derived from 1 mother cell

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

what are the precursers for white cells

A

pre t = t cell

pre B = b cell

BFU-E = RBCs

MEG-CFC = mgakaryocytes/platelets

GM-CFC = monocytes and granulocytes

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

why would earlier stages of neutrophils be found in the peripheral blood *

A

in sepsis- marrow compensate because of the stress = myeloid precurser and nucleated red cells present in peripheral blood - this is a leukerythroblastic picture

when pt recieves G-CSF to recover neutrophils after cancer - see myeloid precursers in blood film - this is an expected reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what controls the production of red cells

A

erythropoeitin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what controls the production of lymphoid cells

A

IL2

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

what controls the production of myeloid cells

A

G-CSF

M-CSF - make monocytes

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

how does cancer affect white cells *

A

DNA damage to the DNA controlling proliferation and differentiation

this is likely to lead to cancer - leukaemia, lymphoma, myeloma

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

what cells are found in the marrow

A

matuyre lymphocytes and neutrophils

myeloblasts

promyeloblasts

myelocytes

metamyelocytes

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

what cells are found in the peripheral blood

A

T and B lymphocytes

natural killer cells

granulocytes

monocytes

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

why would you have an increased WBC

A

increased cell production: reactive to infection/inflammation (physiological), or malignant eg leukaemia, myeloproliferative (proliferate without control)

cell survival: failure of apoptosis eg acquireed cancer causing mutations in some lymphomas - mutation of onchosuppressive genes `

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

how can you have a low wite cell count *

A

cell production reduced - imbared marrow function, folate or B12 deficiency (vegan), marrow failure - apoplastic anaemia, post chemo, met cancer or haem cancer

cell survival - immune break down by autoAb - connective tissue disorder - autoimmune

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

describe 2 causes of eosinophilia *

A

normal haemopoesis (morphology normal) - stimulated by infection, inflammation (have increase in monocytes and neutrophils), increased cytokine production - distant tumour, haematopoetic or not

abnormal haemopoeisis - cancers of haemopoetic cells eg hodgekin’s lymphoma, leukaemia (myeloid or lympoid, chronic or acute), myeloproliferative disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

describe what is seen in chronic myeloid leukaemia *

A

mutation early in haematopoesis = increased proliferation of megakaryoytes/platelets, granulocytes, monocytes = high WBC count

see every stage of white cell on film

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how do you investigate a raised white cell count *

A

history and examination - symptomatic or not, might be a coincidence finding, travel history, look for lymphadenopathy and hepatosplenomegaly - suggest underlying lymphomyeloproliferative disorder

Hg and platelet count - isolated neutrophilia = reactive, but high neutrophil, anaemia and low platelets is a sign of leukaemia

look at automated differential - if machine cant recognise cells might be a precurser because of G-CSF injection or malignant cells

examine blood film

is abnormality in white cell only or in all lineages - red/platelets/white - raised all = myeloproliferative disorder

is it 1 type of WBC or all - cancer is clonal so abnormality will be of 1 type of cell, if raised all it would be reactive

mature cells only/mature and immature - chronic lymphocytic anaemian - is mature, CML - mature and immature, AML - immature

17
Q

what is seen in chronic lymphocytic leukaemia *

A

raised lymphocytes but otehr things rarely raised

18
Q

what is seen in chronic myeloid leukaemia *

A

increased all white cell types

eosinophils, basophils

increased number of myeloid precursers

19
Q

causes of neutrophilia *

A

normally 50% neutrophils are margniated - ie adhere to endothelial cell then migrate to tissue - balance of marginateed and circulating neutrophil changes in minutes when stressed - the pool of marginated switches to circulating

early release from marrow increases neutrophils - hours

increased production (eg from infection) - days

tissue inflammation - colitis, pancreatitis, autoimmune tissue necrosis, appendicitis, myocardial infarct

underlying neoplasia - isolated neoplasm eg carcinoma/lymphoma may produce reactive neutrophilia due to aberrent production of stimulatory cytokines

malignant neutropilia - myeloproliferative disorders and CML (myelocytes and rarely myeloblasts, usually basophilia)

corticosteroids

infection - systemic and localised - acute bacterial, fungal, certain viral, but brucella, typhoid and many virals dont produce neutrophilia

acute bacterial - chest/urinary tract, toxic granulation, increased numbers of cytoplasmic granules and vacuoles

20
Q

describe film in infection *

A

neutrophilia >7.5x10(power 9)/L

toxic granulation - distribution of granules is abnormal

vacuoles - white spots in cytoplasm

21
Q

describe film in leukaemia *

A

basophils

band cells - no segmentation of nucleus

myelocytes

22
Q

causes of eosinophilia *

A

reactive - drugs, parasitic (schistosomiasis, filariasis), allergic diseases (asthma, reumatoid arthritis, polyarthritis, pul eosinophilia, eczema), neoplasms (Hodgkin’s, T cell NHL), hypereosinophilic syndrome if >1.5 count = organ damage

malignant chronic eosinophilic leukaemia - mutation in a or B gene of PDGFR fusion gene

23
Q

describe hodgkin’s

A

eosinophilia because of production of IL 5

24
Q

describe the difference in the blood film for eosinophila - reactive and malignant *

A

reactive - no change in shape - they look normal

malignant clonal - look abnormal - toxic agranulation`

25
Q

describe monocytosis *

A

in chronic infections and primary haematological disorders

as part of inflammatory process

TB, brucella, typhoid

viral, CMV, varicella zoster

sarcoidosis

chronic myelomonocytic leukaemia

26
Q

cause of basophilia *

A

POX virus

27
Q

describe lymphocytosis *

A

if mature - reactive to infection (polyclonal) or primary disorder (chronic lymphocytic leukaemia - have monomorphic population of cells) , autoimmune or inflammatory disease.

if immature - priamry disorder (leukaemia/lymphoma, eg acute lympoblastic leukaemia)

28
Q

describe blood film for immature or mature lymphocytosis *

A

mature - they are small, increased nuleocytoplasmic ratio, no nucleolus, hard to see cytoplasm, chromatin dense

immature - large, nucleolus

29
Q

hwo can you tell if mature lymphocytosis is primary or reactive *

A

reactive - polyclonal response to infection/chronic inflammation/underlying malignancy

primary - monoclonal lympoid prolif

30
Q

describe causes of reactive lymphocytosis *

A

smoking

infection - EBV, CMV, toxoplasma, infectious hep, rubella, herpes, adenovirus, varicellazoster, infectious hepatitis, pertussis, Tb, brucellosis

autoimmune disorders

neoplasma, sarcoidosis - reactive to thee underlying cancer

31
Q

describe mononucleosis syndrome *

A

because of infection - sweat and fatigue

large lymphocytes, plastic appearance

RBC and platelets have no sig change

32
Q

describe glandular fever *

A

EBV infection of B lymphocytes via CD21 receptor

infected B cell proliferates and expresses EDV associated antigens

lead to cytotoxic T cell response - prodduce cytokines responsible for symptoms

acute infection resolved resulting in lifelong sub-clinical glandular fever for wks/months

33
Q

how can you distinguish between reactive or malignant lymphocytosis *

A

consider age, clinical features and labatory investigation

abnormal forms eg smear cells (lymphocytes damaged by film preparation) or blast cells - suggestive of lymphproliferative disorder eg leukaemia/lymphoma

look at blood film - polyclonal in normal or monoclonal if malignant

look at light chain restriction - expect similar amounts of kappa and lambda in polyclonal, in monoclonal there will be K/L only - meaning not equal proportion in entire blood smaple

gene rearrangement - Ig and TCR genes undergo recombination in antigen stimulated B or T cells - in monoclonal prolif all daughter cells have identical Ig or TCR - detected by southern blot analysis

34
Q

what is suggested by an elevated total white cell count due to blasts *

A

underlying leukaemia

35
Q

define neutrophilia *

A

an absolute neutrophil count of >7.5x10(power 9)/L

36
Q

describe the response to pyogenic bacterial infection *

A

tissue damage = release of inflamm cytokines eg G-CSF and GM-CSF = stimulated granulocyte and monocyte production in the bone marrow and early release of immature cells = increase in circ granulocyte count and a L shifted appearance in the blood

chemotaxis - phagocytes circ in periphery - at site of infection they will move out of circulation and into tissues (response to chemotactic factors)

phag - phagocytes use Fc and C3b receptors to recognise and phagocytose opsinated material

killing and digestion - ingested material killed in phagocytic vacuoles by oxidative and non-oxidative mechanisms

37
Q

what is lymphocytosis *

A

lymphocyte count >4x10(power 9)/l

38
Q

what do you check a blood film for after observing lymphocytosis *

A

typical/reactive lymphocytesseenin mononucleosis syndromes

immediate response to acute stress - heart attack/other severe pain

small lymphocytes and smudge cells seen in chronic lymphocytic leukaemia

primitive blasts seen in acute lymphoblastic leukaemia

Haematology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions