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M1 > week 11 > Flashcards

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
Q

the direct and indirect way of triggering phagocytsosis

A

direct way: recognise microbes via PRRs
indirect way: recognises microbes via opsonins

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26
Q

what do mhc calss 1 proteins display and what do they react w

A

endogenous antigens

present on all cells and viral,tumour cells

react w CD8

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27
Q

what do mhc calss 2 proteins display and what do they react w

A

display exogenous antigens from an endosome or phagosome

present in antigen presenting cells

react with CD4 cells

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28
Q

what is the human leukocyte antigen

A

the molecules which corresponds with either a MHC1 or MHC2 receptor

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29
Q

two ways a b cell can get activated

A

T dependent antigen pathway
T independent antigen pathway

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30
Q

t dependent antigen pathway for b cell activation 4

A

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

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31
Q

t independent antigen pathway for b cell activation 3

A

b cell binds to antigen
activates b cell
only igM cells can be produced

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32
Q

isotype switching in b cells

A

a process by whcih b cells can change the type of antibody produced

requires t follicular cells to cause this change

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33
Q

idiotype of an immunoglobulin

A

the variable region

34
Q

epitote

A

the region where the antigen and antibody bind

35
Q

role of igM (function+structure)

A

produced upon initial response
pentameric structure

36
Q

igG 2

A

provides long term protection
most abundant antibody

37
Q

Ignore

A
38
Q

igD

A

found in mucosal seretions protecting the mucosa from pathogens

39
Q

igE 2

A

induce allergic reactions and hypersensnitivity
triggers mast cell degranulation

40
Q

igA

A

found on b cells and act as a receptor to initate cell activation and maturation

41
Q

key functions of antibodies 4

A

neutralisation
agglutination
opsonisation
complement activation

42
Q

multiple myeloma

A

malignancy in the final stage of b lymphocyte development whereby plasma cells become malignant and produce monoclonal immunoglobulins

43
Q

lymphoma

A

malignancy that occurs in the lymph nodes predominantly involving b cells

there are two classifications: hodgikins and non hodkins lymphoma

44
Q

hodgkins lymphoma

A

presence of Reed sternberg cells

45
Q

what key gene mutation is chronic myeloid leakaemia associated with

A

the Philadelphia chromosome

46
Q

differences between acute and chronic leakaemia

A

acute: invlves immature lymphocytes
chronic: involves dysfunctional mature cells

47
Q

difference between lymphoma and leukaemia

A

lymphoma localised to lymph nodes
leukaemia in blood

48
Q

common complications of haematological malignancies 6

A

organomegaly
bleeding
infection
anaemia
renal failure
bone pain

49
Q

why does organomegaly occur

A

uncontrolled growth and accumulation of cancerous cells

disrupts structure and function

50
Q

bleeding

A

malignant cells invade blood vessels impairing their integrity and disrupting normal clotting processes

51
Q

infection

A

underproduction of immune cells due to bone marrow failure

52
Q

renal failure

A

due to accumulation of abnormal proteins produced by the cancerous cells which clog and damage the renal tubules

53
Q

anaemia

A

due to a dysruption in erythroppoeiss as a result of bone marrow failure and crowding

54
Q

bone pain

A

results from the infiltration of abnormal cells into the bone marrow disrupting normal bone structure

55
Q

what is the most common paedeatric luekaemia

A

acute lymphoblastic leukaemia

56
Q

blood findings in acute myeloid leukaemia

A

excessive immature WBCs

57
Q

blood findings in chronicmyeloid leukaemia

A

excessive mature WBCs with features of granulocytes

58
Q

blood findings in chronic lymphocytic leukeamia 2

A

excessive mature lymphocytes
smudge cells

59
Q

blood findings in multiple myeloma

A

excess clonal plasma cells

60
Q

flow cytometry

A

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
Q

binet staging system in CLL

A

extent of leukocyte involvement
presence of anemia or thrombocytopenia

62
Q

stage a of binnet system

A

less than 3 enlarged lymph node groups and no anaemia/thrombocytopenia

63
Q

stage b of binnet system

A

greater than 3 enlarged lymph node groups with no anaemia or thrombocytopenia

64
Q

stage c of binnet staging system

A

patients have anaemia and thrombocytopenia

65
Q

three phases of treatment in haematological malignancy management

A

induction
consolidation
Maintenance

66
Q

induction (haematological malignancies treatment)

A

upon diagnosis of acute leukaemia it is intense chemotherapy

67
Q

consolidation (haematological malignancies treatment)

A

when patient is in remission
continual high level of chemotherapy

68
Q

maintenance (haematological malignancies treatment)

A

decreased rate of chemotherapy

69
Q

mechanism of monoclonal antibodies in the treatment of haematological malignacies

A

they bind to surface antigens on cancer cells
exert therapeutic effects including:
- inteference of cell signalling pathways
-direct cytotoxiicty

70
Q

how is the philadelphia chromosome

A

translocation of chromosome 9 to 22 resulting in translocation of ABL1 gene to BCR forming a BCR-ABL1

71
Q

what is the result of this translocation

A

causes increased proliferation, increased survival and increased adherance

72
Q

targeted treatment method in chronic myeloid leaukaemia

A

use of a tyrosine kinase inhibitor

73
Q

what does a tyrosine kinase inhibitor do 2

A

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
Q

what is aplastic anaemia

A

bone marrow failure resulting in a lack of all blood cell production

it is characterised by bone marrow hypoplaisia

75
Q

what are myeloproliferative neoplasms

A

these are a group of chronic blood cancers that result in excessive production of near-mature blood cells

76
Q

examples of myeloproliferative neoplasms

A

chronic myeloid leukaemia
polycythemia vera
essential thrombocytosis
primary myelofibrosis

77
Q

polycythemia vera 3

A

most comon MPN

malignant increased RBC levels independent of EPO levels

caused by JAK 2 mutation

78
Q

essential thrombocytosis

A

malignant excess in platelets

high risk of thrombotic complications

JAK 2 mutation

79
Q

JAK 2 mutations 4

A

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
Q

myelodysplastic snydromes

A

group of syndromes whereby the bone marrow fails to produce healthy cells

81
Q

whats a key characteristic of myeloproliferatiove neoplasmic disorders

A

JAK mutations

M1 (13 decks)

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