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haem Flashcards

1
Q

von willebrand tx for bleeding

A

mild = transexamic acid

desmopression (DDAVP): increased levels of vWF by causing its release from weibel palade bodies in endothelial cells

factor VIII concentrate

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2
Q

pernicious anaemia path

A

antibodies against intrinsic factor and gastric parietal cells = cant absorb b12 at terminal ileum

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3
Q

causes of b12 defiiciency

A

pernicious anaemia
post gastrectomy
vegan or poor diet
terminal iluem disorders ie crohns or ileocecal resection

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4
Q

b12 features

A

macrocytic anaemia
glossitis
neuro - proporception and vib lost first then distal parathesia
mood disturbances

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5
Q

b12 def tx

A

IM hydroxocobalamin

no neuro sx = 3x a week for 2 weeks
neuro = alternate days until sx resolve

TREAT B12 BEFORE FOLATE to avoid subacute degene of spinal cord

maintenence
pernicious = 2-3mhtly injecttions forveer
diet related = 2x yearly inhections or oral

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6
Q

hereditory spherocytosis

A

autosomal dominant

spherical shape RBCs = get stuck in spleen = haemolytic anaemia

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7
Q

g6pd avoid what

A

fava beans cipro sulfonurea
trimethoprim
nitrofurantoin
anti malarials

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8
Q

henz bodies

A

blobs of denatured hb inside RBCs

g6pd and alpha thalassemia

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9
Q

autoimune haemolytic anaemia

A

Warm – common, idiopathic, CLL
Cold – secondary to lymphoma, leukaemia, SLE, etc.

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10
Q

Alloimmune haemolytic anaemia

A

Transfusions
New-born – rhesus disease

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11
Q

thalassaemia gene and path

A

autosomal recessive

= either defective alpha chains or beta chains
= fragile rbc breakdown and collected by spleen = splenomegaly

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12
Q

risk of iron with thalasaaemia (esp in B major)

A

iron overload

bc regular transfusion and
increased iron absorb at GI tract

iron chelation ie desferrioxamine

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13
Q

B thalassaemia major presentation

A

first year of life failure to thrive and hepatosplenomegaly
microcyitic anaemia

face changes:
Frontal bossing (prominent forehead)
Enlarged maxilla (prominent cheekbones)
Depressed nasal bridge (flat nose)
Protruding upper teeth

bc bone marrow under so much strain to produce extra red blood cells to compensate for the chronic anaemia that it expands enough to increase the risk of fractures and change the patient’s appearance

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14
Q

CLL

age
path
sx
ix

complications

A

over 60
too many B cells
often Asx
blood film = sludge cells
immunophenotyping

Richters transformation (b cell lymophoma)
warm haemolytic anaemia
hypogammaglobulinaemia
anaemia

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15
Q

what is richters transformation

A

CLL cells go into lymph node and change into high grade fast growing non hodgkins lymphoma

pt become v unwell suddenly

of of following sx
lymph node swelling
fever w/o infection
wt loss
night sweats
nausea
abdo pain

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16
Q

CML

phases

A

philadephia chromosome
(= excess acitivity of tyrosine kinase)

increase in granulocytes at different stages of maturation (neutro,baso,eosin) +/- thrombocytosis
decreased leukocyte alkaline phospatase

3 phases
chronic, accelerated, blast

accelerated = 10-20% of bone marrow is blast cell
blast =>20%

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17
Q

cml mx

A

imatinib
hydroxyurea
interferon alpha
bone marrow transplant

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18
Q

AML

A

adults anytime but usually middle age onwards
can be from myeloproliferative disorder ie polycythemia rubra vera or myelofibrosis
blast cells with AUER RODS

features of bone marrow failure; anaemia, neutropenia, thrombocytopenia, bonepain, splenomegaly

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19
Q

acute promyelocytic leukemia

A

type of AML (m3 subtype)

translocation of chromosome 15&17

presents young ie average age 25
DIC or thrombocytopenia at presentation
good prognosis

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20
Q

acute promyelocytic anaemia tx

A

all trans retinoic acid (ATRA)
chemo

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21
Q

CLL tx

A

tyrosine kinase inhibitors (e.g., ibrutinib)
Monoclonal antibodies (e.g., rituximab, which targets B-cells)

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22
Q

tumor lysis syndrome

A

high uric acid (deposit in tubule = AKi)
high potass (arthyth)
high phosphate
high creatinine

low calcium
arythmia
seizure

make sure good hydration and urine output b4 chemo –> allopurinol and rasburicase to supress uric if at risk

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23
Q

myeloproliferative disorders/ myelofibrosis what is it and what causes it

associated w which gene

A

proliferation of a single type of stem cell = bone marrow fibrosis = extramedullary haematopoeisis ie in liver and spleen

primary myelofibrosis
polycythaemia vera
essential thrombocytopenia

JAK2

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24
Q

blood film in myelofibrosis and ix

A

teardrop shaped rbcs
Anisocytosis (varying sizes of red blood cells)
Blasts (immature red and white cells)

bone marrow biopsy (dry) –> trephine biopsy

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25
Q

polycythaemia vera proliferating cell line and blood finding

A

erthroid cells

high hb (&neutrophilia &inc plts)
low esr
high leukocyte alkaline phos

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26
Q

Primary myelofibrosis proliferating cell line and blood finding

A

Haematopoietic stem cells

low hb
(high or low red/white cells)

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27
Q

essential thrombocythemia proliferating cell line and blood finding

A

Megakaryocyte

high plts

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28
Q

myeloproliferative risk

A

potential to transform to AML

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29
Q

myeloproliferative disorders chemo tx

A

hydroxyurea ( hydroxycarbamide

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30
Q

polycythaemia tz

A

aspirin (bc thrombo events)
venesection 1st line
hydrocycarbamide
phosphorus 32

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31
Q

myelodyspastic syndrome

A

mutation of myeloid cells = inadequate production of blood cells (either red white plts or 3)

can transform in AML

bone marrow biopsy

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32
Q

Antiplatelets
- COX inhibitors

A

aspirin

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33
Q

antiplatlets P2Y12 inhibitors

A

clopidogrel, ticagrelor, prasugrel

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34
Q

antiplatelets Phosphodiesterase inhibitors

A

– dipyridamole

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35
Q

anticoags Indirect thrombin inhibitors

A

heparins fondaparinux

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35
Q

Anticoagulants
- Direct thrombin inhibitors

A

dabigatran

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36
Q

anticoags
direct Xa inhib

A

DOACS

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37
Q

what is FFP when is it given

A

part of blood that contains clotting factors – liver disease,
massive transfusion, bleeding disorders

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38
Q

factor 7 deficiency =

A

prolonged PT and prolonged APTT

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39
Q

Factor 8, 9, 11, 12 (intrinsic pathway) deficiency

A

normal platelets, normal PT, prolonged APTT

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40
Q

factor 10 deficiency

A

PT prolonged and APTT prolonged

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41
Q

Budd-chiari syndrome

A

thrombosis in hepatic vein/IVC (outflow of liver)
caused by hypercoaguable states (ie myeloprolif disroders)

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42
Q

budd chiari triad

A

abdo pain
hepatomegaly
ascites

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43
Q

Thrombotic thrombocytopenic purpura (TTP)

A

deficiency of ADAMTS-13 protein

= tiny thrombi in micro vessels

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44
Q

pernicious anaemia risk of ca

A

inc risk gastric cancer

45
Q

lemon tinge skin

A

pernicious anaemia

bc pallor (anaemia) + jaundice (haemolysis) = lemon tinge

46
Q

CML sx

A

anaemia: lethargy
wt loss n sweating
SPLENOMEGALY

granulocytyes at diff stages +/- thrombocytosis (too many plts)

47
Q

myelodysplasia anaemia type

A

normocytic

48
Q

haemolytic anaemia bloods

A

normocytic anaemia
inc reticulocyte count
increased lactate dehydrongenase
high billirubin

49
Q

antiphosphlipid syndrome PE tx

A

LMWH then vit k anatg ie warfarin

50
Q

what are bands cell

A

intermediate neutrophil

ie half mature neutrophils

51
Q

steps to differentiate between leukemias

A
  1. Look at lymphocytes
  2. Look at WBC
  3. Others hint (blast cell/ bands)

ie
1.Low Lymphocytes -> the answer should be AML or CML
2. WBC > 100 -> Chronic causes so Consider CML (rule out AML)
3. Presence of bands cell -> confirm CML

blast= acute
bands = chronic

52
Q

why low lymphocytes in aml/cml

A

overprolif of myeloid cells (ie rbc plts granulocytes and monocytes)

this crowds out bone marrow cells ie lymphocytes

53
Q

INR 5-8 on warfarin no bleed, bleed and major bleed

when restart

A

oral vit k

IV

Iv vit k and Prothrombin complex concentration

restart when INR<5

54
Q

ALL cause of haemorrhagi or thrombotic complications

A

DIC

55
Q

pt stable with CVD but has AF

A

stop anti platelet ie clopidrgel
start anticoagulant monotherapy

56
Q

Post ACS/PCI and has af w stroke risk what meds

A

triple therapy (2antiplt 1 anticoag) 4wks to 6mths post event
dual (1 of each) to complete 12 mths

57
Q

p450 inhibitors

A

ie Increase INR

SICKFACES.COM-Group

Sodium valp
Isonizid
Cimetidine
Ketoconazole
Fluconazole
Alcohol(binge)
Chloramphenicol
Erythromycin
Sulfonamides (I fir inhibit)
Ciprofloxacin
OMEPRAZOLE
METRONIDAZOLE
Grapefruit juice

58
Q

ALL poor prognostic factors

A

<2yo >10yo
WBC>20 at diagnosis
T or B cell surface markers
non caucasion
male

59
Q

UFH monitoring

A

APTT

60
Q

lMWH monitering

A

no regular monitoring needed

but if needed ie renal imapirment, obesity, preg

moniter anti factor Xa

61
Q

why do you feeling of fullness/ constant satiety with cml

A

enlarged spleen compressing other organs

62
Q

PE CXR

A

usually normal
may see wedge shaped opacification

63
Q

Howell jolly bodies what is it and seen in

A

blobs of DNA material inside RBCs - spleen usually supposed to remove them

post splenectomy
sickle cell
severe anaemia

64
Q

schistocytes what are they when seen

A

fragments of RBCs - being damaged

microangiopathic haemolytic anaemia (MAHA) eg: TTP,DIC, haemolytic uremic syndrome ( HUS)

65
Q

sideroblasts

A

immature RBCs w nucleus surrounded by iron blobs - ie iron cant be incorporated in

myelodydysplatic syndrome

66
Q

smudge cells

A

ruptured wbcs

CLL

67
Q

spherocytes

A

sphere shaped RBCs

hereditary spherocytosis
autoimmune haemolytic anaemia

68
Q

difference and why dont you moniter lwmh compared to UFH

A

LMWH has shorter longer half life = longer durations of action

more predictable pharmacokinetics

69
Q

epistaxis failed all emergency tx

A

sphenopalatine ligation in theatre

70
Q

beta thallassemia bloods

A

mild hypochromic microcytic anaemia

microcytosis disprop to anaemia ie

crazy small size even compared to hb which isnt asss low

71
Q

beta thalassaemia hb electropharesis

A

HbA2

HbA2 only in trait

HbA2 and HbF in major

72
Q

emergency surgery but on warfarin

A

stop warfarin (emergency or elective)

if surg can wait (6-8hrs) = vit K 5mg IV

emergency = 25-50 units/kg four factor prothrombin complex

73
Q

hypersegmented polymorphs

A

pernicious anaemia

74
Q

heparin induced thrombocytopenia (HIT)

A

antibodies against platelet factor 4

5-10 days post heparin tx

75
Q

syphhilis how to tell if reinfection and tx

A

RPR if increases by more than 4 fold = no tx response or reinfection

tx = benzathine penicillin G IM STAT dose

76
Q

causes of false positive non treponemal tests
(Cardiolipin ) (in syphyliis)

A

pregnancy
SLE, anti-phospholipid syndrome
tuberculosis
leprosy
malaria
HIV

77
Q

two types of tets for syphyliis and eg

A

non treponemal (non specific)
- RPR
- (venereal disease research lab) VDRL
(become -ve after tx)

Treponemal specific
- TP EIA ( T.palladium enzyme immunoassay)
- TPHA (t.p . HaemAgglutination )
(stay after disease)

78
Q

ITP blood and tx

A

isolated thrombocytopenia

1st = pred
IVIG if active bleeding or urgent prodecure required

79
Q

hodgkins lymphoma sx associated w poor prognosis

A

B sx

wt loss>10%in 6mths
fever >38C
night sweats

80
Q

hodgkins lymphoma RF and sx

A

HIV, EBV

B sx
pruritis
lympadenopathy
painful w alcohol
hepatosplenomegaly

81
Q

hodgkins bloods and ix

A

bloods

normocytic anaemia
eosinophillia
inc LDH

LN biopsy - reed sternberg
Imaging

82
Q

hodgkins staging

A

ann arbour

83
Q

complication of hodgkins

A

mediastinal LN enlargment =SVC obstruction

84
Q

iron def anaemia signs

and specific signs

A

conjuctival pallor
tachyardia
tachypneoa
ejection systolic murmur

angular cheilosis
atrophic glossitis
koilionychia

85
Q

iron def iron studies

A

low transferrin sat
low ferritin

high TIBC

86
Q

side effects ferrous sulphate

A

constipation
diarohea
nausea
black stools

87
Q

sickle cell pt what dx will be in hx

A

hydroxyurea
folic acid

penicillin ( bc autoinfarct of spleen - hyposplen = suseptible infections)

88
Q

causes of sickle cell crisis

A

cold
dehydration
hypoxia
acidosis
infection

89
Q

principles of tx w sickle crisis

A

oxygen
analgesia
iv fluids
empirical abx

90
Q

if pt as sickle cell and partner completelty normal likelehood of child having SICKLE TRAIT

A

100%

91
Q

Sickle cell protective against what

A

malaria

92
Q

why doesnt sickle show until 6 mths

A

High levels of foetal haemoglobin (HbF) which mask the effect of the disease until levels of HbF begin to fall at 6 months old.

93
Q

what is multiple myeloma

A

malignant clonal prolif of B lymphocytic plasma cells

= bare igG

94
Q

MM sx

A

fatigue
bruise easy
recurrent infxn
polydipsia
bone pain

95
Q

MM ix

A

blood - fbc ue ca2 igG + film
urine electropharesis
serum electropharesis
Bm sampling
XR

96
Q

causes of splenomeg

A

Leukemia
malaria
liver cirrhosis w port htn
mono
haemolytic anameia

97
Q

hoe to diff cml and aml on film

A

aml = immature blast cells

cml = white cells in full spectrum of lineage band cells

98
Q

cml breathru tx

A

imatinib
tyrosine kinase inhib
oral

99
Q

immediate transfusion if hb

A

<7

100
Q

signs of super low hb

A

pallor
tachycardia
tachypnoe
flow murmur

101
Q

early blood transfusion reactions

A

acute haemolytic reaction
bacterial contamination
allergic/anaphylaxis

TRALI
Fluid overload

febrile non haemolytic
massive transfusion

102
Q

delayed tranfusion reactions

A

delayed haemolytic 1-7d

post trans purpura 7-10d

GvHD 4-30d

fe overload chronic

103
Q

pt transfuse instant reaction n temp

A

haemolytic anaemia –> DIC
bact contam

allergic wouldnt have fever

104
Q

macrocytic anemia

A

megaloblastic
b12 folate cytotox dx

non
alcohol, liver dz
preg, hypothyroid

105
Q

beta thal major name

A

cooleys anameia

106
Q

confim mm

A

serum electopharesis

107
Q

confirm thalasema

A

serum electopharesis

108
Q

haemophillia a n b factor

A

a = factor viii
b = 9

109
Q

haemophilia mx

A

avoid nsaids n IM injections

minor bleed =desmopression and tranxemic acid

major = Purifies factor vii, FFP w VII,

110
Q
A

finals (28 decks)

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