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THIRD YEAR > Haem 3 > Flashcards

Haem 3 Flashcards

1
Q

malignant haemopiesis is what

A

increased number of dysfunctional cells that have lost the normal haemopoiteic reserve

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2
Q

one or more of what is in malignant haemopoiesis

A

increased proliferation
lack of differentiation
lack of maturation
loss of apoptosis

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3
Q

acute leukaemia

A

abnormal proliferation and lack of maturation

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4
Q

ix for acute leukaemia

A

excess of blasts >20% in either peripheral blood or bone marrow
decreased/ loss of normal haemopoietic reserve

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5
Q

ALL is a malig disease of what
most common what
symptoms

A

malig disease of lymphocytes
most common childhood cancer
very severe bone pain, BM failure : infections, bleeding, anaemia
increased WCC, venous obstruction, CNS involvement

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6
Q 
AML in who 
may be what of two 
similar to what 
subgroups 
occurs after treatment of what 
ix
A 
>60s
may be denovo or decondary 
similar to ALL
DIC or gum infiltration 
alkylating agents 
auer rods
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7
Q

what can be done as ALL and AML look the same sometimes

A

BM aspirate immunophenytyping

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8
Q

myeloproliferative disorders is what

A

clonal haemopoietic stem cell disorders with an increase production of one or more haemopoitetic cells - in contrast to acute leukaemia maturation is relatively preserved

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9
Q

common features of myeloproliferative disorders

A 
asymp
gout
weight loss
fatigue
sweats 
splenomegaly
thrombus in unusual place - no reactive explanation
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10
Q

CML is what

A

over production of grnaulocutes

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11
Q

pattern of CML

A

prolif of myeloid cells, chronic phase with intact maturation 3-5y, accelerated phase, blast crisis (acute leukaemia)

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12
Q

when is fatal of CML

A

fatal without stem cell/BM transplant in chronic phase

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13
Q

ix for CML

A

normal or low Hb
leucocytes/neurtrophilia
myeldoi precursors
eosinophilia, basophilia, thrombocytosis

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14
Q

philapdelphia

A

9+22 -> tyrosine kinase which causes abnormal phosphorylation - signalling leading to haematological changes in CML

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15
Q

treatment of CML

A

imatinib

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16
Q

PRV is overproduction of what

A

overproduction of RBCs

high Hb/hc accompanied by erythrocytes

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17
Q

ddx of secondary polycythaemia

A

chronic hypoxia, smoking, erytho secreting tumour

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18
Q

ddx of pseudopolycythaemia

A

dehydration, diuretics, obesity

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19
Q

aquagenic pruritus

A

polycythaemia ruba vera

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20
Q

ix for PRV

A

FBC
film
JAK2 mutation
px with secondary won’t have splenomegaly

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21
Q

JAK2

A

kinase

activation of erythropoiesis in absence of ligand

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22
Q

treatment of PRV

A

venesection to haemocrit <0.45
aspirin to reduce thromb risk
hydroxycarbomide - oral chemo

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23
Q

essential thrombocytopenia

high can lead to what

A

uncontrolled production of abnormal platelets

at high levels can lead to VW dx

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24
Q

symp of ET

A

MPD symp and bleeding (unpredictable risk of surgery)

microvascular occlusion

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25
Q

ix for ET

A

exclude reactive thrombosis
JAK2 in 50% CALR in rest MPL mutation
characteristic bone marrow appearance

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26
Q

treatment for ET

A

aspirin
hydoxycarbamide
anagrelide
interferon alpha last line

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27
Q

myelofibrous idiopathic

A

marrow failure, marrow fibrosis, extra medullary haemopoesis, leukthrombin film

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28
Q

tear dropped shaped RBC

A

myelofibrosis

29
Q

when else can you get myelofibrosis

A

post polycythaemia or ET

30
Q

BF in ET

A

tear dropped shaped RBC and leucoerythroblastic
dry aspirate
fibrate on trophine biopsy
JAK2 or CALR mutation

31
Q

what are the causes of a leukoerythroblastic film

A

reactive - sepsis
marrow infiltration - cancer
myelofibrosis

32
Q

treatment of myelofibrosis

A

transfusion, AB, allogenic SC tranplant, splenectomy

JAK2 inhibitors

33
Q

CLL is the commonest what

A

leukaemia

34
Q

CLL who

A

65-75

35
Q

what is CLL

A

clonal expansion os small lymphocytes

36
Q

symp of CLL

A 
asymp
recurrent infection 
anaemia 
splenomegaly 
lymphocytes >5x109/L
37
Q

what is pancytopenia

A

anaemia
thrombocytopenia
neutropenia

38
Q

decreased production

A

inherited bone marrow failure
arise due to to defects in DNA repair/ribosome
falcon;s

39
Q

fanconi’s symp

what happens in it

A

short, skin abnormalities, radial ray abnormalities, hypogenitilia, endocrine, GI, haem, renal

unable to repair inter stand cross links

40
Q

fanconi’s 97%

52%

A

BM failure by 20yo

leukaemia by 40yo

41
Q

acquired primary BMF

A

aplastic anaemia
myelodysplastic dysplasia
acute leukaemia

42
Q

aplastic anaemia

A

AI attack against haemopoetic stem cells

hypocellular

43
Q

myelodysplastic dyaslsoa

A

hypercellular mass
ineffective haemopoiesis
20-30% risk of AML

44
Q

acute leukaemia

A

prevention of normal haemopoiesis

45
Q

secondary BMF

A

drug - chemo, chloramphenicol
alcohol, B12 and folate
infiltrative - malignancy, lymphoma, viral (HIV), storage disease

46
Q

increased destruction

A

hypersplenism

portal htn, CCF, fieltys, splenic lymphoma

47
Q

clinical features of pan

A

anaemia - fatigue, SOB
CDV compromise, neutropenia
infections - bleeding
symp depending on cause

48
Q

ix for for pan

A

FBC, film, B12/folate
LFTs - hyersplenism
HIV/virology
AB tests (SLE)

49
Q

test for fanconis

A

chromosome fragility test

50
Q

hypocellular pan

hypercellular pan

A

aplastic

MDS, B12/folate, hypersplenism

51
Q

rx for pan

A 
malig - chemo
congenital - transplan
idiopathic aplastic anaemia - immunosuppression 
supportive 
transfusions
ABs
52
Q

normla splenic RC mass
RC transit
platelets pool

A

5%
fast
20-40%

53
Q

hyposplenic RC mass
RC transit
platelets pool

A

40%
slow
90%

54
Q

hodgkins symptoms

A 
painless cervical LD
mediastinum spread - cough 
hepatospleno 
B symp
pruritus and alcohol related pain
55
Q

burkitts translocation

A

8 and 14

56
Q

burrkitts lymphoma

A

very high grade

57
Q

mantle cell

A

similar tp low grade hodgkins but very aggressive and incurable with chemo

58
Q

marginal zone NHL

A

low grade

59
Q

other types of B cell NHL

A

follicular
diffuse large b cell - commonest world wide
lymphplasmocytic lymphoma

60
Q

major haemorrhage protocol what does the blood bank send

A

4 units of RBC
4 frozen plasma
1 platelets

61
Q 
ongoing bleeding after transfusion management 
ix
what should be given RBC how
cryprecipitate when
consider further what
A

repeat blood samples
transfuse further RBC:FFP 2:1 (1:1 in trauma)
cryoprecipitate if fibrinogen <1 (<2 in obstetric haem)
consider further platelets

62
Q 
management if bleeding stopped after transfusion 
Hb
ATTP and PT
platelets 
fibrinogen 
use what
A 
Hb>80
AtPP and PT ration <1.5
platelets >50
fibrinogen >1.5 (>2 in obstetrics)
use blood warmer
63
Q

when should you assume neutropenic sepsis

A

if received chemo within past 3 weeks, temp >=38 or clinical evidence of significant sepsis SIRS>=2

64
Q

standard risk px

A

neutropenia and sepsis and SEWS score <6

65
Q

standard risk px treatment

A

piperacillin/tazobactam
PA teioplanin and aztreonam
if anaphylaxis or angiooedema Teicoplanin and ciprofloxacin

66
Q

high risk px

A

neutropenic and severe septic/septic shock or SEWS >=6

67
Q

high risk px treatment

A

pipercillin/tazobactem and gentamicin
PA - teicoplanin and aztreonam and gent
if anaphylaxis or angiooedema teicplanin and ciprofloxacin and gentamicin

68
Q

when should AB be started in neutropenic sepsis

A

within 1hr

don’t wait for blood culture results

THIRD YEAR (27 decks)

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