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3b specialties > Haematology > Flashcards

Haematology Flashcards

1
Q

findings in iron studies for iron deficiency anaemia?

A

microcytic
hypochromic
low ferritin
high TIBC

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2
Q

what are haemoglobinopathies?

A

Affect either:
1. quality and structure of Hb-HbS, HbO, HbE

  1. quantity of Hb- thalassaemia
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3
Q

what is normal adult hb?

A

HbA

2 alpha chains and 2 beta chains

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4
Q

what is foetal Hb?

A

HbF

2 alpha chains and 2 gamma

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5
Q

causes of iron deficiency anaemia?

A

blood or GI loss
insufficient dietary intake
malabsorption e.g. coeliac

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6
Q

blood film for iron deficiency anaemia?

A

target cells

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7
Q

signs of iron deficiency anaemia?

A

koilonychia (spoon-shaped nails)
atrophic glossitis
angular stomatitis
post-cricoid webs

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8
Q

tx of iron deficiency anaemia?

A

ferrous sulphate
continue for at least 3 months after Hb is normal

GI investigation

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9
Q

causes of anaemia of chronic disease?

A 
chronic infection
vasculitis
RA
malignancy
renal failure
etc
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10
Q

Ix of all anaemia?

A

FBC, TFTs, U&Es
haematinics- B12 and folate, ferritin, serum iron, TIBC
scoping
CT

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11
Q

causes of normocytic anaemia?

A 
bleeding
aplastic anaemia
haemolytic anaemia
sickle cell disease
pregnancy
chronic disease
hypothyroidism
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12
Q

what is aplastic anaemia?

A

failure of bone marrow development that causes pancytopenia and hypoplastic bone marrow

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13
Q

what is haemolytic anaemia?

A

breakdown of RBCs before their normal life-span

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14
Q

hereditary causes of haemolytic anaemia?

A

hereditary spherocytosis
G6PD deficiency
sickle-cell
thalassaemia

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15
Q

acquired causes of haemolytic anaemia?

A

immune- warm/cold antibody type, transfusion reaction, rhesus disease

non-immune- malaria, dapsone (drug to treat dermatitis herpetiformis), malignancy, DIC, pre-eclampsia

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16
Q

signs of haemolytic anaemia?

A

bilirubin and LDH raised due to breakdown of cells

MCV high because reticulocytes so big

urinary urobilinogen

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17
Q

what is G6PD deficiency?

A

red blood cell enzyme defect

X linked, males, Mediterranean

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18
Q

precipitants of G6PD deficiency?

A

drugs- antimalarials, ciprofloxacin, sulphonamides
infections
fava beans

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19
Q

features of G6PD deficiency?

A

neonatal jaundice
intravascular haemorrhage
gallstones
splenomegaly

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20
Q

blood film of G6PD deficiency?

A

Heinz bodies

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21
Q

what is hereditary spherocytosis?

A

normal biconcave disc shape of RBC is replaced by a sphere- shaped one
AD inheritance

cells are destroyed by the spleen

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22
Q

Ix of hereditary spherocytosis??

A

blood film-spherocytes

EMA binding test

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23
Q

features of hereditary spherocytosis?

A

failure to thrive
jaundice, gallstones
splenomegaly
aplastic crisis- precipitated by parvovirus

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24
Q

Tx of hereditary spherocytosis?

A

folate replacement

splenomegaly

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25
Q

what is sickle-cell anaemia?

A

recessive disorder causing production of abnormal beta globin chains
HbS rather than HbA

the sickled cells are fragine and easily destroyed therefore cause haemolytic anaemia

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26
Q

are reticulocytes increased or decreased in sickle cell disease?

A

increased due to bone marrow trying to keep up with increased destruction of red cells

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27
Q

what is sickle cell trait?

A

60% HbA 40% HbS
Normally asymptomatic with normal FBC and no haemolysis

provides some protection against malaria

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28
Q

how does sick cell present?

A 
at age 6-12 months
anaemia
splenomegaly
overwhelming infection
crises
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29
Q

what are sickle cell crises?

A
  • vaso- occlusive crisis (includes acute chest syndrome)
  • aplastic crisis
  • sequestration crisis
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30
Q

pathology of vaso-occlusive crisis?

A 
lots of Hb become deoxygenated at once
cold-dehydrated, hypoxia
lots of sickling
occlusion of small vessels
sometimes of larger vessels
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31
Q

features of vaso-occlusive crisis?

A
  • severe pain from oxygen deprivation of tissues and avascular necrosis of the bone marrow
  • swollen joints
  • dactylitis
  • acute abdomen
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32
Q

mx of vaso-occlusive crisis?

A

strong analgesia
high flow O2
hydration
blood transfusion

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33
Q

specific types of vaso-occlusive crisis?

A

thrombotic stroke
acute chest syndrome
priapism

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34
Q

features of acute chest syndrome?

A

new pulmonary infiltrate on XR and dyspnoea, pain, cough and fever

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35
Q

mx of acute chest syndrome?

A 
oxygen 
chest physio
may require NIV or I&v
antibiotics
transfusion/exchange transfusion
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36
Q

what causes an aplastic crisis?

A

parvovirus b19 infection

massive drop in Hb over 1 week

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37
Q

what is a sequestration crisis?

A

splenomegaly
drop in Hb, elevated reticulocytes
circulatory collapse, shock

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38
Q

mx of sickle cell disease?

A
  • avoid cold, dehydration, hypoxia, exhaustion, alcohol and smoking
  • folic acid supplementation
  • oral penicillin V
  • full vaccinations plus pneumococcal, flu and hep B
  • iron chelation to prevent fe overload with repeated tx e.g. deferoxamine
  • hydroxycarbamide- increases HbF
  • annual transcranial USS
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39
Q

complications of sickle cell disease?

A 
chronic pain
pulmonary hypertension
stroke
infection
gallstones
retinopathy
avascular necrosis of femoral or humeral head
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40
Q

what is beta thalassaemia trait?

A

BB,__

mildly anaemic, asymptomatic

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41
Q

what is beta thalassaemia major?

A

__,__
severe anaemia
chronic transfusion dependent
bony deformities

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42
Q

what are the different types of alpha thalassaemia?

A

4 deletions- in utero death
3 deletions- very anaemic, hypochromic, microcytic, splenomegaly, variable bone changes
2 deletions= slightly anaemic
1 deletion- asymptomatic, borderline Hb

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43
Q

what is pernicious anaemia?

A

autoimmune condition with antibodies against parietal cells and intrinsic factor

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44
Q

what is normal b12 absorption?

A

B12 is bound by salivary R protein then bound to intrinsic factor which is produced by the parietal cells

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45
Q

features of pernicious anaemia?

A

macrocytic anaemia
megaloblasts (big fragile immature red cells)
paraesthesia, glossitis fatigue

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46
Q

mx of pernicious anaemia?

A

B12 injections (hydroxycobalamin) 1mg IM every other day for 2 weeks

maintenance- 1mg every 3 months for life

can take orally if dietary cause

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47
Q

what can maternal folate deficiency cause?

A

neural tube defects (spina bifida)

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48
Q

causes of folate deficiency?

A 
poor diet
increased demand- pregnancy, malignancy, IBD
malabsorption-coeliac
drugs- anti-epileptics
alcohol
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49
Q

tx of folate deficiency?

A

oral folic acid

prophylaxis in pregnancy- 400mcg from conception until 12 weeks

50
Q

what is intracapsular vs extracapsular haemolytic anaemia?

A

intravascular- complement fixation, trauma, DIC, enzymes

extravascular (more common)- removed from circulation because of defective or antibodies on them

51
Q

what is seen on blood film post-splenectomy?

A

Howell-jolly bodies
increased risk from encapsulated bacteria e.g. strep pneumonia, HIB

need regular vaccines and lifelong penicillin

52
Q

what are the myeloproliferative disorders?

A

RBC- polycythaemia rubra vera
WBC- CML
Platelets- essential thrombocytopenia
Fibroblasts- myelofibrosis

53
Q

what are primary and secondary polycythaemia?

A 
primary= polycythaemia vera
secondary= hypoxia, renal carcinoma, smoking, COPD
54
Q

what is polycythaemia rubra vera?

A

neoplastic proliferation of haemopoietic cells in the bone marrow

55
Q

mutation causing polycythaemia rubra vera?

A

JAK2 mutation

56
Q

risk of polycythaemia rubra vera?

A 
hyperviscosity -> thrombosis
prutitis after hot bath
splenomegaly
haemorrhage
plethoric appearance
57
Q

tx of polycythaemia rubra vera?

A

aspirin
venesection
bone marrow suppression- hydroxycarbamide

58
Q

complications ofpolycythaemia rubra vera?

A

2-8% transform to myelofibrosis and 1-3% transform to AML

59
Q

causes of massive splenomegaly?

A

CML
myelofibrosis
malaria

60
Q

what is ITP?

A

immune thrombocytopenic purpura

61
Q

causes of ITP in adults vs children?

A

children- follows viral infection, benign, self-limiting

adults- insidious and chronic

usually self-limiting and as easy bruising/ mucosal bleeding

62
Q

tx of ITP?

A 
stop any NSAIDS or aspirin and observe any platelet count
prednisolone
IVIG
anti-D
avoid contact sports
63
Q

what is TTP?

A

thrombotic thrombocytopenic purpura

MEDICAL EMERGENCY

64
Q

pathology of TTP?

A

MICROANGIOPATHIC THROMBOSES -> HAEMOLYSIS AND PLATELET COMSUMPTION

congenital deficiency or autoimmune attack

65
Q

features of TTP?

A 
anaemia and haemolysis
thrombocytopenia
fever
purpura
cerebral dysfunction
66
Q

mx of TTP?

A

plasma exchange

67
Q

indications for platelet transfusion?

A

platelet count <30 with clinically sigf bleeding

or <100 and bleeding and critical sites e.g. CNS

68
Q

what is haemophilia?

A

X linked disorder of coagulation

69
Q

types of haemophilia?

A

A- factor VIII deficiency

B- (Christmas disease)- factor IX deficiency

70
Q

features of haemophilia?

A

haemoarthroses
haematomas
prolonged bleeding after surgery or trauma (long APTT)

71
Q

tx of haemophilia?

A

A- factor VIII replacement

B- factor IX replacement

72
Q

which anticoagulants work at which pathways?

A

intrinsic pathway- heparin (affects APTT)

extrinsic pathway- warfarin (PT- measured by INR)

73
Q

how is warfarin reversed?

A

immediately- beriplex (4 factor concentrate- 2,7,9,10)

over 12 hours- vitamin K

74
Q

how does warfarin work?

A

inhibits production of the vitamin K dependent clotting factors

75
Q

how does heparin work?

A

activates antithrombin-> which inactivates thrombin and Xa

76
Q

what is the difference between unfractionated heparin and LMWH?

A

unfractionated heparin- IV, short half life, monitored by APTT

LMWH- sub cut, longer half life, monitor with anti Xa level

77
Q

how is heparin reduced?

78
Q 
how do the DOACs
- rivaroxaban
- apixaban 
-dabigatran
work?
A

rivaroXAban and apiXAban are anti XA

dabigatron is a direct thrombin inhibitor

79
Q

what is a clotting profile of DIC?

A

low platelets, prolonged PT/APTT, prolonged bleeding time

80
Q

what is the most common inherited bleeding disorder?

A

von Willebrand’s disease

AD

81
Q

feature of VWD?

A

mucosal bleeding- epistaxis, menorrhagia

82
Q

mx of VWD?

A

tranexamic acid for mild bleeding
desmopressin-raises levels of vWF
factor VIII concentrate

83
Q

name some transfusion reactions?

A

GOT A BAD UNIT
Graft vs host disease
Overload
Thrombocytopenia

Alloimmunisation

Blood pressure unstable
Acute haemolytic reaction
Delayed haemolytic reaction

Urticaria
Neutrophilia
Infection
TRALI

84
Q

What is hyper viscosity syndrome?

A

an increase in whole body viscosity due to raised immunoglobulins produced by malignant clonus of plasma cells (myeloma) or WBCs

85
Q

what is raised ESR and osteoporosis until proven otherwise?

86
Q

what is myeloma?

A

malignancy of plasma cells

produce a monoclonal paraprotein (IgA or IgG- abnormal serum electrophoresis and urinary bence jones protein)

87
Q

features of myeloma?

A 
CRABI
Hypercalcaemia
Renal impairment
Anaemia
Bone pain
Infection
88
Q

Ix of myeloma

A 
serum protein electrophoresis- monoclonal antibodies IgA or IgG
Urine- bence jones protein 
Bone marrow biopsy- high plasma cells
FBC- anaemia, thrombocytopenia
XR-pepper pot skull
CT/MRI
89
Q

what can be seen on blood film in myeloma?

A

roleaux formation (stacking of RBCs)

90
Q

mx of myeloma?

A 
stem cell transplants
chemo
zoledronic acid for pathological fracture prevention
Annual influenza vaccine
VTE prophylaxis
Analgesia
91
Q

features of Hodgkin’s lymphoma?

A

young adults
rubbery, painless lymphadenopathy
B symptoms
alcohol-induced lymph node pain

92
Q

causes of Hodgkin’s lymphoma?

A

unknown
infections- EBV, helicobacter pylori
immunodeficiency- HIV, transplant patients
autoimmune disorders

93
Q

findings on lymph node biopsy for Hodgkin’s lymphoma?

A

Reid sternberg cells

94
Q

staging for Hodgkin’s lymphoma?

A

Ann Arbor staging

95
Q

4 types of Hodgkin’s lymphoma?

A

Nodular sclerosing- most common
mixed cellularity
lymphocyte depleted- worst prognosis
lymphocyte rich- best prognosis

96
Q

features of non-Hodgkin’s lymphoma?

A

commonest are follicular and diffuse large B cell (latter has worst prognosis)
Present with painless lymphadenopathy with or without B symptoms
hepatosplenomegaly

97
Q

extra-nodal disease of NHL?

A

gastric MALT
small bowel lymphomas
non-MALT gastric lymphoma

98
Q

what is Burkitt’s lymphoma?

A

associated with EBV, rapid proliferation

99
Q

what cancer does myelofibrosis increase the risk of?

A

myelofibrosis

100
Q

what cells are seen on blood film of myelofibrosis?

A

tear drop cells

101
Q

features of AML?

A

ADULTS

presents with pancytopenia (bruising, infection, mouth sores, anaemia)

102
Q

what is a variant of AML?

A

acute promyelocytic myeloid leukaemia

103
Q

what is the prognosis of AML?

A

POOR- 20% 3 year survival with chemotherapy

104
Q

causes of CML?

A

adults, sometimes incidental finding
Philadelphia chromosome t9,22
forms BCR ABL fusion gene, makes tyrosine kinase pathway always on

105
Q

features of CML?

A

B symptoms

chronic -> accelerated phase -> blast transformation (transformation to acute leukaemia)

106
Q

Ix of CML?

A

high WCC, low Hb, variable platelets, high urate, high B12
bone marrow biopsy
Ph Chr

107
Q

tx of CML?

A

Tyrosine kinase inhibitor e.g. dasatinib, imatinib

108
Q

who does ALL affect?

A

children

Down’s syndrome, ionising radiation

109
Q

features of ALL?

A 
Anaemia
bruising
infection
hepatosplenomegaly
lymphadenopathy
bone pain
joint pain
110
Q

blood film of ALL?

A

blast cells

111
Q

tx of ALL?

A 
Blood/platelet transfusion
IV fluids
Allopurinol (prevents tumour lysis syndrome)
infection management
chemo
112
Q

features of CLL?

A

COMMONEST
older adults
asymptomatic or non-specific systemic symptoms or B symptoms

113
Q

blood film of CLL?

A

smudge cells

114
Q

staging for CLL?

A

binet staging

115
Q

prognosis for CLL?

A

1/3 never progress
1/3 progress slowly
1/3 progress actively

116
Q

what is the level for anaemia in men and women?

A

men <135g/L

women <115g/L

117
Q

what can CLL transform to and what is it called?

A

Richter’s transformation

high grade lymphoma

118
Q

what is seen on blood film of AML?

119
Q

what does TIBC measure?

A

the amount of transferrin in the blood (binds to iron)

Both TIBC and transferrin levels increase in iron deficiency and decrease in iron overload.

120
Q

what is ferritin?

A

Ferritin is the form that iron takes when it is deposited and stored in cells. Extra ferritin is released from cells in inflammation, such as with infection or cancer. If ferritin in the blood is low it is highly suggestive of iron deficiency. If ferritin is high then this is difficult to interpret and is likely to be related to inflammation rather than iron overload. A patient with a normal ferritin can still have iron deficiency anaemia, particularly if they have reasons to have a raised ferritin such as infection.

121
Q

why is it important to treat B12 deficiency before folate deficiency?

A

Treating patients with folic acid when they have a B12 deficiency can lead to subacute combined degeneration of the cord.

3b specialties (7 decks)

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