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Y3 immunology and haematology > intro to haematology > Flashcards

intro to haematology Flashcards

1
Q

what is haematology

A

investigation and management of disorders of blood and bone marrow

interactions w/ other organs also

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2
Q

blood components and products

A
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3
Q

functions of blood

A

transport

maintenance of vascular integrity

protection from pathogens

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4
Q

functions of blood - transport

what is transported and where

A

gases (O2, CO2) - red cells

nutrients, waste, messages - plasma

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5
Q

functions of blood - maintenance of vascular integrity

what does it prevent and how

A

prevention of leaks - platelets and clotting factors

prevention of blockages - anticoagulants and fibrinolytics

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6
Q

functions of blood - protection from pathogens

what and how

A

phagocytosis and killing - granulocytes/monocytes

antigen recognition and antibody formation - lymphocytes

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7
Q

pathogenesis of haematological abnormalities

A

high levels

  • increased rate of production
  • decreased rate of loss - very occasionally

low levels

  • decreased rate of production
  • increased rate of loss

altered function

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8
Q

what is haematopoiesis

A

production of all of the cellular components of blood and blood plasma

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9
Q

haematopoiesis in the bone marrow

A
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10
Q

properties of stem cells

A

totipotent - capable of giving rise to any cell type

self-renewal

amplify number by binary fission and flux through differentiation pathways

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11
Q

stem cells and bone marrow

A

home to marrow niche - CXCR4 (antagonist plerixafor)

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12
Q

what regulates the flux of stem cells through differentiation pathways

A

regulated by hormones/growth factors

- some used therapeutically (erythropoietin, G-CSF, thrombopoietin agonists)

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13
Q

what are induced pluripotent stem cells

A

stem cell properties can now be induced in more differentiated cells by getting certain proteins to be expressed

potential for therapeutic value

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14
Q

where is bone marrow located

A

bones - most in children, axial in elderly

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15
Q

appearance of bone marrow

A

stroma - made up of fibroblasts, collagen

sinusoids - blood vessels, as cells differentiate they make their way into the sinusoids

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16
Q

erythroid differentiation

A

erythroblast - reticulocyte - erythrocyte

governed by erythropoietin

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17
Q

what cells are these

A

reticulocytes

still contain RNA

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18
Q

what does reticulocyte count indicate

A

measure of red cell production

usual value = 1%

when red cells are released from marrow they have a reticulocyte appearance for ~24hrs, so if reticulocyte count increases you know blood volume is being replaced for some reason

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19
Q

what is erythropoietin

A

hormone made in kidney in response to hypoxia

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20
Q

what is polycythaemia

A

too many red cells

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21
Q

consequences of anaemia

A

poor gas transfer: SOB, fatigue

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22
Q

what causes anaemia

A

decreased production
- haematinics deficiency (iron, folate, B12)

increased loss
- bleeding, haemolysis

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23
Q

what can be seen here

what causes it

A

microcytic, hypochromic red cells

iron deficiency

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24
Q

what can be seen here

what causes it

A

macrocytic red cells

e.g. folate deficiency

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25
Q

what can be seen here

what causes it

A

schistocytes (fragmented cells)

haemolytic uraemic syndrome

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26
Q

what can be seen here

what causes it

A

sickle cells and target cells

sickle cell disease

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27
Q

how many red cells can we produce daily

A

~10g/L/day

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28
Q

what can be seen here

A

L: platelets, beginning to clump

R: megakaryocyte

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29
Q

function of platelets

A

haemostasis

also some immune function

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30
Q

what regulates platelet production

A

thrombopoietin

  • produced in liver
  • regulation by platelet mass feedback
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31
Q

lifespan of platelets

A

7 days

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32
Q

what is thrombocytosis

A

too many platelets

33
Q

what is thrombocytopaenia

A

marrow failure

immune destruction (immune thrombocytopaenia purpura)

34
Q

what is the commonest cause of altered platelet function

A

drugs

e.g. aspirin, clopidogrel, abciximab etc

35
Q

neutrophil function

A

ingest and destroy pathogens esp. bacteria and fungi

36
Q

communication between WBC

A

interleukins - between WBC

CSFs - colony stimulating factors
- G-CSF - granulocyte colony stimulating factor

37
Q

what regulates neutrophil production

A

immune responses and macrophages

produced in response to mainly bacterial infections

IL-17 stimulates production when bacterial infection is detected

38
Q

neutrophil differentiation

A
  1. blast in bone marrow (many granules of big open nu) - too many in AML
  2. promyelocyte - granules begin to form
  3. myelocyte
  4. metamyelocyte
  5. neutrophil
39
Q

when is neutrophilia seen

A

infection - left shift, toxic granulation

inflammation - MI, post-op, RA

40
Q

therapeutic use of G-CSF

A

neutropenia

mobilisation of stem cells

41
Q

what is neutrophilia

A

increased neutrophil numbers

42
Q

causes of neutrophilia

A

production regulated by G-CSF

43
Q

what is neutropenia

A

decreased neutrophil numbers

44
Q

causes of neutropenia

A

decreased production - drugs, marrow failure

increased consumption - sepsis, AI

altered function - e.g. chronic granulomatous disease

45
Q

functions of monocytes

A

ingest and destroy pathogens esp bacteria and fungi

subset of monocytes migrate into tissues and become macrophages or dendritic cells
- some populations of macrophages self-maintaining

46
Q

macrophages in tissues

A
47
Q

what types of cells are these

A

monocytes

slight granulation and grey cytoplasm

48
Q

what are eosinophils important for

A

fighting parasites

allergy

49
Q

what type of cells are these

A

eosinophils

50
Q

what type of cells are these

A

basophils

dark granules

51
Q

what parts of the immune system are lymphocytes involved in

A

adaptive immune system

- immunological memory

52
Q

surface antigens of lymphocytes

A

CD markers (cluster of differentiation)

53
Q

what type of cells are these

A

lymphocytes

nucleus and thin rim of cytoplasm

54
Q

what can cause lymphocytosis

A

infectious mononucleosis

pertussis

  • too many lymphocytes in the blood
55
Q

what causes lymphopaenia

A

usually post-viral

lymphoma

56
Q

subtypes of lymphocytes

A

B - antibody production
T - helper, cytotoxic, regulatory
natural killer cells - fight viral infection

57
Q

where are lymphocytes produced and where do they mature

A

bone marrow

B cells - bone marrow

T cells - thymus

circulate in blood, lymph and LNs

58
Q

what into and where do lymphocytes differentiation

A

effector cells in 2y lymphoid organs (lymph nodes or mucosal associated lymphoid tissue)

59
Q

adaptive receptor diversity

A

each naïve T and B cell has a unique surface receptor

  • T cell - in plasma membrane
  • B cell - either in plasma membrane or secreted as antibody

each receptor has a constant region and a variable region

60
Q

what are antibodies

A

adaptors between pathogens and clearance systems

61
Q

creation of a receptor chain gene

A

shuffling of genes that form receptors and recombination within developing lymphocyte

variability in this process causes variability of T and B cell receptors

combinatorial diversity, junctional diversity

62
Q

where does combinatorial diversity occur

A

within each chain: V-region combined w/ J- or D- then C-region

between chains: each alpha chain pairs with a beta chain, each light chain pairs with a heavy chain

63
Q

where does junctional diversity occur

A

at join

additional nucleotides added

64
Q

mistakes in diversity of T and B cell receptor variability lead to…

A

cause lymphoid malignancies

early B cell maturation, chromosome segments joining and rejoining - acute lymphoblastic leukaemias

exit bone marrow, naïve B cells met by macrophages and expand and form immune response - lymphomas

become plasma cells, make antibodies, more mistakes in the process - myelomas

65
Q

positive and negative selection in the bone marrow

A

+ve: if gene rearrangement results in a functional receptor the cell is selected to survive

-ve (tolerance): if the receptor recognises ‘self’ antigens the cell is triggered to die

B cells that survive this selection are exported to the periphery

66
Q

classes of HLA

A

I: internal antigens on all nucleated cells

II: displays antigens eaten by professional antigen presenting cells

constant within, variation between individuals

67
Q

immune responses against HLA

A

immune cells read HLA ‘barcode’ on cells to help identify self vs non-self cells or infected vs non-infected cells

immune response is triggered if infected cell is identified

68
Q

RA and impacts on blood

A

anaemia of chronic disease

iron, folate deficiency

immune haemolysis - 5% of pts

neutrophilia

immune thrombocytopaenia

cytopenias 2y to medication

felty syndrome - splenomegaly and 2y cytopenia

69
Q

systemic diseases and impact on blood

A

hepatic - anaemia, deficient clotting factors

renal - anaemia, HUS

CV - anaemia

resp - polycythaemia

GI - anaemia

70
Q

problems with plasma

A

too much - paraproteins (early marker of myeloma)

too little - clotting factors: haemophilia

abnormal function - clotting factors: haemophilia

71
Q

normal FBC

A

underlined ones are important to know

72
Q

diagnostic tools for blood problems

A

FBC

clotting time for clotting factors and platelets

chemical assays

marrow aspirate and trephine biopsy

LN biopsy or other organ

imaging

73
Q

diagnostic tools for blood problems - clotting time

A

platelet and leucocyte function tests

74
Q

diagnostic tools for blood problems - chemical assays

A

iron (ferritin - storage molecule for iron)
B12
folate

75
Q

haematology treatments

A

replacement

transplantation

drugs

76
Q

haematology treatments - replacement

A

blood
haematinics
coagulation factors
plasma exchange

77
Q

haematology treatments - drugs

A 
cytotoxics
monoclonal antibodies
inhibitors of cellular proliferation
immunosuppressants
inhibitors of coagulation
inhibitors of fibrinolysis
78
Q

haematology treatments

A

Y3 immunology and haematology (20 decks)

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