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week 11 Flashcards

1
Q

what are all the leukocytes

A

macrophages,monocytes and dendritic cells
granulocytes
B+T lymphocytes

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2
Q

ontogeny

A

maturation of t and be cells where they develop unique cell receptors

if cell receptors recognise self cells they are eliminated

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3
Q

morphology of neutrophils, eosinophils and basophils

A

neutrophils = trilobed
basophils and eosinphils = biolbed

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4
Q

life span of neutrophils, eosinophils and basophils

A

neutrophils = shortest life span 5days max
eosinphils = 12 days max
basophils = 15days max

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5
Q

function of neutrophils 3 + 2 more facts

A

neutrophils = phagocytosis degranuloation and netosis

rapidly deployed from bone marrow when needed

most common leukocyte

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6
Q

function of eosinophils 2

A

allergic reaction
parasitic infection

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7
Q

function of basophils 3 + 1 additional

A

inflammation
paristic infection
allergic reactions

contain granules which include immune mediators

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8
Q

chemotaxis

A

biological process whereby cells respond to chemical signals

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9
Q

morphology of t cells vs b cells

A

t cells: limited cytoplasm and irregular shape
b cells: large cytoplasm and round shape

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10
Q

primary lymphoid organs

A

where lymphocytes undergo development and otogeny

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11
Q

secondary lymphoid organs

A

where mature lymphocytes encounter antigens and differentiate

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12
Q

chemokines

A

bind to endothelial cells triggering strong homing receptor production which binds to circulating neutrophils

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13
Q

cytokines

A

signalling proteins which mediate immune responses

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14
Q

colony stimulating factors

A

subset of cytokines which stimulate differentiation and production of leukocytes

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15
Q

natural killer cell function

A

circulates in blood acting as early defence against viruses, infected cells and tumour cells

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16
Q

netosis

A

nuclear material forms neutrophil extracellular traps (NETs) which immobilise and kill pathogens

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17
Q

opsinins

A

tag microbes for phagocytosis

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18
Q

process of pathogen recognition (use PRRs and PAMPs) 5

A

PAMP binds to PRR
Activates molecule and transcription of cytokines allowing immune response
phagocytosis of substance
antigen presentation
t cell recognition
further cytokine release
b cell activation
antibodies

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19
Q

effects of complement activation 3

A

opsonisation
inflammatory response
membrane attack complex formation

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20
Q

3 pathways through which complement can be activated

A

classical
alternative
lectin

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21
Q

three substances are associated with each complement activation pathway

A

classical = C1
alternative C3 and C3b
lectin = mannose binding lectin

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22
Q

classical complement activation pathway

A

complement C1 recognises immune complexes formed by binding antibodies

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23
Q

alternative complement activation pathway

A

complement C3 breaks down C3b depositing it on microbes

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24
Q

lectin complement pathway

A

mannose binding lectin attaches to mannose sugars on bacteria surfaces

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25
the direct and indirect way of triggering phagocytsosis
direct way: recognise microbes via PRRs indirect way: recognises microbes via opsonins
26
what do mhc calss 1 proteins display and what do they react w
endogenous antigens present on all cells and viral,tumour cells react w CD8
27
what do mhc calss 2 proteins display and what do they react w
display exogenous antigens from an endosome or phagosome present in antigen presenting cells react with CD4 cells
28
what is the human leukocyte antigen
the molecules which corresponds with either a MHC1 or MHC2 receptor
29
two ways a b cell can get activated
T dependent antigen pathway T independent antigen pathway
30
t dependent antigen pathway for b cell activation 4
B cell binds to pathogen Antigens internalised and presented to T follicular cell T follicular cell binds and releases cytokines which activate b cell B cell can produce both igG and igM
31
t independent antigen pathway for b cell activation 3
b cell binds to antigen activates b cell only igM cells can be produced
32
isotype switching in b cells
a process by whcih b cells can change the type of antibody produced requires t follicular cells to cause this change
33
idiotype of an immunoglobulin
the variable region
34
epitote
the region where the antigen and antibody bind
35
role of igM (function+structure)
produced upon initial response pentameric structure
36
igG 2
provides long term protection most abundant antibody
37
Ignore
38
igD
found in mucosal seretions protecting the mucosa from pathogens
39
igE 2
induce allergic reactions and hypersensnitivity triggers mast cell degranulation
40
igA
found on b cells and act as a receptor to initate cell activation and maturation
41
key functions of antibodies 4
neutralisation agglutination opsonisation complement activation
42
multiple myeloma
malignancy in the final stage of b lymphocyte development whereby plasma cells become malignant and produce monoclonal immunoglobulins
43
lymphoma
malignancy that occurs in the lymph nodes predominantly involving b cells there are two classifications: hodgikins and non hodkins lymphoma
44
hodgkins lymphoma
presence of Reed sternberg cells
45
what key gene mutation is chronic myeloid leakaemia associated with
the Philadelphia chromosome
46
differences between acute and chronic leakaemia
acute: invlves immature lymphocytes chronic: involves dysfunctional mature cells
47
difference between lymphoma and leukaemia
lymphoma localised to lymph nodes leukaemia in blood
48
common complications of haematological malignancies 6
organomegaly bleeding infection anaemia renal failure bone pain
49
why does organomegaly occur
uncontrolled growth and accumulation of cancerous cells disrupts structure and function
50
bleeding
malignant cells invade blood vessels impairing their integrity and disrupting normal clotting processes
51
infection
underproduction of immune cells due to bone marrow failure
52
renal failure
due to accumulation of abnormal proteins produced by the cancerous cells which clog and damage the renal tubules
53
anaemia
due to a dysruption in erythroppoeiss as a result of bone marrow failure and crowding
54
bone pain
results from the infiltration of abnormal cells into the bone marrow disrupting normal bone structure
55
what is the most common paedeatric luekaemia
acute lymphoblastic leukaemia
56
blood findings in acute myeloid leukaemia
excessive immature WBCs
57
blood findings in chronicmyeloid leukaemia
excessive mature WBCs with features of granulocytes
58
blood findings in chronic lymphocytic leukeamia 2
excessive mature lymphocytes smudge cells
59
blood findings in multiple myeloma
excess clonal plasma cells
60
flow cytometry
uses antibodies which are fluorescently labelled which bind to cell surface markers the presence/absence of surface markers indicates the level of cell maturation in leukaemias, there will be an absence of the correct surface marker
61
binet staging system in CLL
extent of leukocyte involvement presence of anemia or thrombocytopenia
62
stage a of binnet system
less than 3 enlarged lymph node groups and no anaemia/thrombocytopenia
63
stage b of binnet system
greater than 3 enlarged lymph node groups with no anaemia or thrombocytopenia
64
stage c of binnet staging system
patients have anaemia and thrombocytopenia
65
three phases of treatment in haematological malignancy management
induction consolidation Maintenance
66
induction (haematological malignancies treatment)
upon diagnosis of acute leukaemia it is intense chemotherapy
67
consolidation (haematological malignancies treatment)
when patient is in remission continual high level of chemotherapy
68
maintenance (haematological malignancies treatment)
decreased rate of chemotherapy
69
mechanism of monoclonal antibodies in the treatment of haematological malignacies
they bind to surface antigens on cancer cells exert therapeutic effects including: - inteference of cell signalling pathways -direct cytotoxiicty
70
how is the philadelphia chromosome
translocation of chromosome 9 to 22 resulting in translocation of ABL1 gene to BCR forming a BCR-ABL1
71
what is the result of this translocation
causes increased proliferation, increased survival and increased adherance
72
targeted treatment method in chronic myeloid leaukaemia
use of a tyrosine kinase inhibitor
73
what does a tyrosine kinase inhibitor do 2
binds to the ATP site of the BCR-ABL1 preventing ATP to bind prevents substrate from forming as this requires ATP prevents downstream effects
74
what is aplastic anaemia
bone marrow failure resulting in a lack of all blood cell production it is characterised by bone marrow hypoplaisia
75
what are myeloproliferative neoplasms
these are a group of chronic blood cancers that result in excessive production of near-mature blood cells
76
examples of myeloproliferative neoplasms
chronic myeloid leukaemia polycythemia vera essential thrombocytosis primary myelofibrosis
77
polycythemia vera 3
most comon MPN malignant increased RBC levels independent of EPO levels caused by JAK 2 mutation
78
essential thrombocytosis
malignant excess in platelets high risk of thrombotic complications JAK 2 mutation
79
JAK 2 mutations 4
encodes for tyrosine kinase resulting in the increased proliferation as seen in CML also induces EPO indepedent erythrocytosis hypersensitivity to cytokines and growth factors (this is why in CML treatment we use a tyrosine kinase inhibitor)
80
myelodysplastic snydromes
group of syndromes whereby the bone marrow fails to produce healthy cells
81
whats a key characteristic of myeloproliferatiove neoplasmic disorders
JAK mutations

M1 (13 decks)

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