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haematology Flashcards

1
Q

features of myeloma

A

OLD age
Ca elevated
Renal failure
Anaemia (+neuropenia + thrombocytopenia)
Bone lytic lesions

Usually afro-caribbean, 70 yrs, M

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2
Q

what is myeloma

A

a haematological cancer characterised by proliferation of plasma cells in the bone marrow

Plasma cells produe excess of 1 type of immunoglobulin (IgG) + levels of others are low

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3
Q

myeloma ix

A

serum protein electrophoreses = monoclonal protein bands (excess of M protein)
-> GS

Bence-Jones protein in urine

Blood film = Rouleaux formations

X-ray = lytic lesions (pepper-pot skull), osteoporosis, fractures

Bone marrow biopsy = excess plasma cells

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4
Q

what is immune thrombocytopenic purpura

A

a condition where antibodies are created against platelets. An immune response against platelets leads to their destruction and a low platelet count (thrombocytopenia)

Usually IgG antiplatelet autoantibodies

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5
Q

presentation immune thrombocytopenic purpura

A

Usually an isolated thrombocytopenia found as an incidental finding or w features of pupura/other minor bleeding
may follow infection/vaccination espesh in kids (adults it is more chronic)

PURPURA are non-blanching lesions caused by bleeding under the skin

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6
Q

mx immune thrombocytopenic purpura

A

monitor platelet count
control BP
suppressing menstrual periods

<30x10^9/L platelet count / >+ features/high risk = ORAL PREDNISOLONE

IV immunoglobulin if active bleeding as works faster

Splenectomy if this doesn’t work

Rituximab (a monoclonal antibody that targets B cells - B cells produce antibodies)

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7
Q

indication for blood transfusion

A

Hb < 70g/L

or <80 if they have acute coronary syndrome

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8
Q

most common inherited thrombophilia

A

factor V leiden

increases risk of VTE

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9
Q

Any of the following features in a person aged 0-24 years should prompt a very urgent full blood count (within 48 hours) to investigate for leukaemia:

A

Pallor
Persistent fatigue
Unexplained fever
Unexplained persistent infections
Generalised lymphadenopathy
Persistent or unexplained bone pain
Unexplained bruising
Unexplained bleeding

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10
Q

young px w hepatosplenomegaly or unexplained petichiae

A

referred for immediate assessment

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11
Q

what is essential thrombocythaemia

A

proliferation of megakaryocytes (responsible for production of platelets)
a type of blood cancer

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12
Q

what is primary myelofibrosis

A

proliferation of hematopoietic stem cells
- normal bone marrow tissue is gradually replaced with a fibrous scar-like material
-> extramedullary haematopoiesis

rare chronic disorder

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13
Q

features of Buerger’s disease (a small and medium vessel vasculitis)

A

strongly assoc w smoking

extremity ischaemia (as blood vessels become blocked)
- intermittent claudication
- ischaemic ulcers
superficial thrombophlebitis
Raynaud’s phenomenon

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14
Q

what is neutropenic sepsis

A

overwhelming infection that can affect people who have a low neutrophil count
an emergency

usually comp of chemo 7-14 days after

may be defined as a neutrophil count of < 0.5 * 109 in a patient who is having anticancer treatment and has one of the following:
a temperature higher than 38ºC or
other signs or symptoms consistent with clinically significant sepsis

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15
Q

most common cause of neutropenic sepsis
(a bacteria)

A

coagulase-negative, Gram-positive bacteria - particularly Staphylococcus epidermidis

probs due to indwelling lines

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16
Q

neutropenic sepsis prophylaxis

A

a fluoroquinolone
e.g. ciprofloxacin

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17
Q

tx for neutropenic sepsis

A

empirical antibiotic therapy with piperacillin with tazobactam (Tazocin) immediately

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18
Q

what inheritance pattern is hereditary spherocytosis

A

autosomal dominant

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19
Q

what is the presentation of Hereditary spherocytosis

A
  • jaundice
  • anaemia
  • gallstones
  • splenomegaly

can have episodes of haemolytic crisis / aplastic crisis

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20
Q

what is aplastic crisis

A

increased anaemia, haemolysis and jaundice, without the normal response from the bone marrow of creating new RBCs (demonstrated by extra reticulocytes).

In aplastic crisis there is no reticulocyte response

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21
Q

what infection usually causes aplastic crisis

A

parvovirus B19

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22
Q

lymph node biopsy for Burkitt’s lymphoma

A

starry sky appearance

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23
Q

infection assoc w Burkett lymphoma

A

EBV

(HIV, malaria)

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24
Q

infection assoc w diffuse large B-cell lymphoma

A

hep C virus

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25
Q

infection assoc w T cell lymphoma

A

Human T cell lymphotropic virus type 1

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26
Q

what is polycythaemia rubra vera

A

blood cancer that causes bone marrow to make too many RBCs

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27
Q

inheritance of haemophilia A + B

A

X-linked recessive
- so mostly affects males

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28
Q

more common haemophilia

A

A

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29
Q

what is haemophilia A caused by

A

deficiency in factor VIII (8)

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30
Q

what is haemophilia B caused by

A

deficiency in factor IX (9)

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31
Q

presentation of haemophilia

A

Most cases present in neonates or early childhood
- intracranial haemorrhage, haematomas and cord bleeding in neonates.

Severe
- spontan bleeding into joints (haemoarthrosis) + muscles

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32
Q

how is haemophilia dx

A

Diagnosis is based on bleeding scores, coagulation factor assays and genetic testing.

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33
Q

mx of haemophilia

A
  • Infusions of the affected factor (VIII or IX)
  • Desmopressin to stimulate the release of von Willebrand Factor
  • Antifibrinolytics such as tranexamic acid
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34
Q

what is von willebrand disease (VWD)

A

most common inherited cause of abnormal bleeding

most AD

deficiency, absence or malfunctioning of a glycoprotein called von Willebrand factor (VWF)

type 1-3 (3 most severe)

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35
Q

presentation of VWD

A

unusually easy, prolonged or heavy bleeding:
Bleeding gums with brushing
Nose bleeds (epistaxis)
Heavy menstrual bleeding (menorrhagia)
Heavy bleeding during surgical operations

FHx

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36
Q

mx of VWD

A
  • tranexamic acid for mild bleeding
  • Desmopressin can be used to stimulates the release of VWF
  • VWF can be infused
  • Factor VIII is often infused along with plasma-derived VWF
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37
Q

what is Richter’s transformation

A

occurs when leukaemia cells enter the lymph node and change into a high-grade, fast-growing non-Hodgkin’s lymphoma

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38
Q

sx in Richter’s transformation

A

px get unwell suddenly

lymph node swelling
fever without infection
weight loss
night sweats
nausea
abdominal pain

suspect when you get new B sx in CLL

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39
Q

what is ALL

A

malignancy of immature lymphoid cells - B + T cells

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40
Q

who gets ALL

A

2-4 yrs
assoc w Down’s

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41
Q

what is the most common childhood cancer

A

ALL

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42
Q

ix in ALL

A

blood film = blast cells
bone marrow biopsy = >20% blast cells

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43
Q

what is AML

A

uncontrolled proliferation of myeloid blast cells (myeloblasts)

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44
Q

who gets AML

A

commonest acute leukaemia in adults
65+
can be a result of transformation from myeloproliferative disorder

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45
Q

characteristics of AML

A

neutropenia and thrombocytopenia
more acute presentation

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46
Q

how does leukaemia normally present

A

fatigue
fever
bone marrow failure - anaemia -> pallor, decreased WCC -> infection, decreased platelets -> bleeding + bruising (petechiae)
infiltration -> bone pain
hepatosplenomegaly
lymphadenopathy

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47
Q

what do the blast cells have in AML

A

Auer rods

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48
Q

what is CML

A

uncontrolled proliferation of myeloid (mature) cells

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49
Q

CML presentation

A

anaemia

weight loss and sweating are common
splenomegaly may be marked → abdo discomfort, fullness

an increase in GRANULOCYTES AT DIFFERENT STAGES IN MATURATION
+/- thrombocytosis

decreased leukocyte ALP

slow + steady decline

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50
Q

who gets CML

A

65+
philadelphia chromosome (t(9;22)) present in > 80%

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51
Q

phases of CML

A

chronic phase - long + asx (raised WCC)
accelerated phase - abnormal blast cells take up a high prop of cells, dev anaemia + thrombocytopenia, immunocomp
blast phase - higher prop, severe sx, pancytopenia

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52
Q

CML tx

A

IMATINIB is first-line treatment
- inhibitor of the tyrosine kinase

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53
Q

what is CLL

A

accumulation of mature B lymphocytes in peripheral blood

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54
Q

who gets CLL

A

most common leukaemia
M
Elderly - 72 yrs
1/3 never progress, 1/3 progress slowly, 1/3 progress actively

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55
Q

ix for CLL

A

blood film = smudge cells

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56
Q

what is CLL assoc w

A

warm AI haemolytic anaemia
Richters transformation

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57
Q

electrolyte disturbances in tumour lysis syndrome

A

hyperkalaemia
hyperuricaemia
hyperphosphataemia
hypocalcaemia

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58
Q

G6PD deficiency inheritance

A

X-linked recessive

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59
Q

features G6PD deficiency

A

neonatal jaundice is often seen
intravascular haemolysis
gallstones are common
splenomegaly may be present

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60
Q

G6PD deficiency blood film

A

Heinz bodies on blood films. Bite and blister cells may also be seen

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61
Q

what can precipitate G6PD deficiency crisis

A

anti-malarials: primaquine
ciprofloxacin
sulph- group drugs: sulphonamides,
sulphasalazine, sulfonylureas

broad (fava) beans

infection

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62
Q

what is G6PD deficiency

A

reduced ability of the red cells to respond to oxidative stress -> red cells have a shorter life span + are more susceptible to haemolysis, particularly in response to drugs (e.g. nitrofurantoin), infection, acidosis and certain dietary agents (e.g. fava beans)

63
Q

reversal for rivaroxaban and apixaban

A

andexanet alfa

64
Q

reversal for heparin

A

protamine sulfate

65
Q

what is thrombotic thrombocytopenic purpura (TTP)

A

a condition where tiny thrombi develop throughout the small vessels (microangiopathy), using up platelets

66
Q

what does thrombotic thrombocytopenic purpura (TTP) cause

A

Thrombocytopenia
Purpura
Tissue ischaemia and end-organ damage

67
Q

why do thrombi develop in thrombotic thrombocytopenic purpura (TTP)

A

problem with a specific protein called ADAMTS13

This protein normally:
- Inactivates von Willebrand factor
- Reduces platelet adhesion to vessel walls
- Reduces clot formation

Deficiency can be due to:
- An inherited genetic mutation
- Autoimmune disease

68
Q

tx for thrombotic thrombocytopenic purpura (TTP)

A

guided by a haematologist and may involve plasma exchange, steroids and rituximab

69
Q

what is heparin-induced thrombocytopenia (HIT)

A

the development of antibodies against platelets in response to heparin (usually unfractionated heparin, but it can occur with low-molecular-weight heparin)

70
Q

what do heparin induced antibodies target

A

platelet factor 4 (PF4).

71
Q

presentation of heparin-induced thrombocytopenia (HIT)

A

typically presents around 5-10 days after starting treatment with heparin

HIT antibodies bind to platelets and activate the clotting system, causing a hypercoagulable state and thrombosis. They also break down platelets and cause thrombocytopenia
-> there is a counterintuitive situation where a patient is on heparin, has a low platelet count, and develops abnormal blood clots.

72
Q

mx of heparin-induced thrombocytopenia (HIT)

A

testing for HIT antibodies on a blood sample.

Stopping heparin and using an alternative anticoagulant guided by a specialist (e.g., fondaparinux or argatroban).

73
Q

RFs Hodgkin’s lymphoma

A

HIV
Epstein-Barr virus
Autoimmune conditions, such as RA and sarcoidosis
Family history

74
Q

ages who get Hodgkin’s lymphoma

A

bimodal age distribution with peaks around 20-25 and 80 years.

75
Q

types of non-Hodgkin’s lymphoma

A

Diffuse large B cell lymphoma - typically presents as a rapidly growing painless mass in older patients
Burkitt lymphoma - particularly associated with Epstein-Barr virus and HIV
MALT lymphoma - affects the mucosa-associated lymphoid tissue, usually around the stomach

76
Q

RFs for non-Hodgkin’s lymphoma

A

HIV
Epstein-Barr virus
Helicobacter pylori (H. pylori) infection is associated with MALT lymphoma
Hepatitis B or C infection
Exposure to pesticides
Exposure to trichloroethylene (a chemical with a variety of industrial uses)
Family history

77
Q

lymphoma presentation

A

Lymphadenopathy - neck, axilla or inguinal region, non-tender, firm/rubbery

HODGKINS - lymph node pain after drinking alcohol

B sx - Fever
Weight loss
Night sweats

additional no specific sx

78
Q

ix lymphoma

A

Lymph node biopsy
CT, MRI, PET to help dx + stage

79
Q

characteristic finding Hodgkin’s lymphoma

A

Reed-Sternberg cells - large cancerous B lymphocytes with two nuclei and prominent nucleoli, giving them a cartoonish appearance of an owl face with large eyes.

80
Q

classification of lymphoma

A

Lugano Classification
Stage 1: Confined to one node or group of nodes
Stage 2: In more than one group of nodes but on the same side of the diaphragm (either above or below)
Stage 3: Affects lymph nodes both above and below the diaphragm
Stage 4: Widespread involvement, including non-lymphatic organs, such as the lungs or liver

a / b ? (b has systemic sx)

81
Q

blood film in myelofibrosis

A

Teardrop-shaped red blood cells

Anisocytosis (varying sizes of red blood cells)

Blasts (immature red and white cells)

82
Q

blood finding in polycythaemia vera

A

High haemoglobin

83
Q

blood finding in essential thrombocythaemia

A

High platelet count

84
Q

what gene mutation are the myeloproliferative disorders assoc w

A

JAK2

85
Q

myelofibrosis presentation

A

non-specific symptoms: Fatigue
Weight loss
Night sweats
Fever

underlying comps: Anaemia (tiredness, SOB and dizziness)
Splenomegaly (abdominal pain)
Portal hypertension (ascites, varices and abdominal pain)
Low platelets (bleeding and petechiae)
Raised haemoglobin (itching, headaches and a red face)
Low white blood cells (infections)
Gout is a complication of polycythaemia

Thrombosis

86
Q

Clinical signs of polycythaemia

A

Ruddy complexion (red face)
Conjunctival plethora (the opposite of conjunctival pallor)
Splenomegaly
Hypertension

87
Q

dx myelofibrosis

A

Bone marrow biopsy to confirm dx
the aspiration may be dry as it has turned to scar tissue
Testing for the JAK2, MPL and CALR genes

88
Q

mx primary myelofibrosis

A

no active tx if mild
supp mx comps e.g. anaemia, splenomegaly, portal HTN
chemo - hydroxycarbamide
targeted therapies, such as JAK2 inhibitors (ruxolitinib)

89
Q

mx polycythaemia vera

A

venesection
aspirin to reduce the risk of thrombus formation
Chemotherapy - hydroxycarbamide

90
Q

mx essential thrombocythaemia

A

aspirin to reduce the risk of thrombus formation
Chemotherapy - hydroxycarbamide
Anagrelide is a specialist platelet-lowering agent

91
Q

what is sickle cell anaemia

A

genetic condition that causes sickle (crescent) shaped RBCs
- more fragile + easily destroyed -> haemolytic anaemia.
prone to various sickle cell crises.

92
Q

inheritance sickle cell

A

AR

  • affecting the gene for beta-globin on chromosome 11
93
Q

sickle cell + malaria

A

sickle cell is more common in patients from areas traditionally affected by malaria, such as Africa, India, the Middle East and the Caribbean

Having sickle cell trait reduces the severity of malaria so these px are more likely to survive malaria and pass on their genes.

ie there is a selective adv to having the sickle cell gene

94
Q

complications of sickle cell

A

Anaemia
Increased risk of infection
Chronic kidney disease
Sickle cell crises
Acute chest syndrome
Stroke
Avascular necrosis in large joints such as the hip
Pulmonary hypertension
Gallstones
Priapism (painful and persistent penile erections)

95
Q

what is sickle cell crisis triggered by

A

dehydration, infection, stress or cold weather.

96
Q

tx sickle cell crisis

A

Low threshold for admission to hospital
Treating infections that may have triggered the crisis
Keep warm
Good hydration (IV fluids may be required)
Analgesia (NSAIDs should be avoided where there is renal impairment)

97
Q

what is vaso-occlusive Crisis

A

most common crisis
also called painful crisis
sickle-shaped red blood cells clog capillaries -> distal ischaemia

98
Q

Vaso-occlusive Crisis presentation

A

pain and swelling in the hands or feet but can affect the chest, back, or other body areas. It can be associated with fever.

can cause priapism in men by trapping blood in the penis, causing a painful and persistent erection (uro emergency and needs blood to be aspirated from the penis)

99
Q

what is splenic sequestration crisis

A

emergency caused by sickled RBCs blocking BF within the spleen
-> acutely enlarged and painful spleen. Blood pooling in the spleen can lead to severe anaemia and hypovolaemic shock.

100
Q

mx aplastic crisis

A

supportive - may need blood transfusions

usually resolves spontaneously within around a week

101
Q

what is acute chest syndrome

A

occurs when the vessels supplying the lungs become clogged with RBCs
med emergency w high mortality

102
Q

what can trigger acute chest syndrome

A

A vaso-occlusive crisis, fat embolism or infection

103
Q

presentation acute chest syndrome

A

fever
SOB
chest pain
cough
hypoxia

104
Q

CXR acute chest syndrome

A

pulmonary infiltrates

105
Q

mx sickle cell disease

A

Avoid triggers for crises, such as dehydration, smoking, alcohol, cold, exhaustion

Up-to-date vaccinations

Antibiotic prophylaxis (3 MTHS - 5 YRS) to protect against infection, typically with penicillin V
(phenoxymethylpenicillin)

Hydroxycarbamide (/HYDROXYUREA) (stimulates HbF)
- reduces the frequency of painful episodes and the risk of life-threatening illness or death

1 mg of folic acid orally every day

Crizanlizumab

Blood transfusions for severe anaemia

Bone marrow transplant can be curative

106
Q

what is myelodysplastic syndrome

A

cancer caused by mutation in the myeloid cells in the bone marrow -> inadequate production blood cells (ineffective haematopoiesis)

various types

had potential to dev into AML

107
Q

bloods in myelodysplastic syndrome

A

causes low levels of blood components that originate from the myeloid cell line:

Anaemia (low haemoglobin)
Neutropenia (low neutrophil count)
Thrombocytopenia (low platelets)

-> PANCOCYTOPENIA

108
Q

Dx myelodysplastic syndrome

A

Full blood count will be abnormal. There may be blasts on the blood film.

Bone marrow biopsy is required to confirm the diagnosis.

109
Q

causes of microcytic anaemia

A

T – Thalassaemia
A – Anaemia of chronic disease
I – Iron deficiency anaemia
L – Lead poisoning
S – Sideroblastic anaemia

110
Q

when can you commonly get anaemia of chronic disease + why

A

in CKD
due to reduced production of erythropoietin by the kidneys
tx w erythropoietin

111
Q

causes of normocytic anaemia

A

3 As 2 Hs
A – Acute blood loss
A – Anaemia of chronic disease
A – Aplastic anaemia
H – Haemolytic anaemia
H – Hypothyroidism

112
Q

types of macrocytic anaemia

A

megaloblastic - as a result of impaired DNA synthesis, instead of dividing they grow into large, abnormal cells
normoblastic

113
Q

causes of megaloblastic macrocytic anaemia

A

B12 deficiency
Folate deficiency

114
Q

causes of normoblastic macrocytic anaemia

A

Alcohol
Reticulocytosis (usually from haemolytic anaemia or blood loss)
Hypothyroidism
Liver disease
Drugs, such as azathioprine

115
Q

signs that point to iron deficiency anaemia

A

Koilonychia - spoon-shaped nails
Angular cheilitis
Atrophic glossitis - smooth tongue due to atrophy of papillae
Brittle hair + nails

116
Q

causes of low B12

A

Pernicious anaemia - AI condition
Insufficient dietary B12 (particularly a vegan diet, as B12 is mostly found in animal products)
Medications that reduce B12 absorption (e.g., PPIs and metformin)

117
Q

what is pernicious anaemia

A

autoimmune condition involving antibodies against the parietal cells or intrinsic factor

parietal cells of the stomach produce intrinsic factor protein which is essential for the absorption of vitamin B12 in the distal ileum

-> there is lack of B12

118
Q

sx of B12 deficiency

A

neurological:
Peripheral neuropathy, with numbness or paraesthesia
Loss of vibration sense
Loss of proprioception
Visual changes
Mood and cognitive changes

119
Q

autoantibodies for pernicious anaemia

A

Intrinsic factor antibodies (the first-line investigation)
Gastric parietal cell antibodies (less helpful)

120
Q

mx pernicious anaemia

A

IM hydroxocobalamin (manufactured version of B12)
- if no neuro sx give 3x weekly for 2 weeks
- if neuro sx give pn alt days until there is no further improvement in sx

121
Q

maintenance mx in B12 deficiency

A

Pernicious anaemia – 2-3 monthly injections hydroxocobalamin for life
Diet-related – oral cyanocobalamin or twice-yearly injections

122
Q

what to do when a px has both B12 + folate deficiency

A

treat B12 deficiency 1st
if you give px folic acid when they have B12 deficiency -> subacute combined degeneration of the cord

123
Q

what does normal haemoglobin consist of

A

two alpha-globin and two beta-globin chains

124
Q

inheritance of thalassaemia

A

AR

(both alpha + beta)

125
Q

what happens to RBCs in thalassaemia

A

they are more fragile + break down easily -> haemolytic anaemia
-> splenomegaly

126
Q

what is thalassaemia

A

caused by a genetic defect in the protein chains that make up haemoglobin.
Defects in alpha-globin chains lead to alpha thalassaemia. Defects in the beta-globin chains lead to beta thalassaemia

127
Q

beta thalassaemia minor

A

also called thalassaemia trait,
carriers of an abnormally func beta-globin gene

  • mild microcytic anaemia - microcytosis is characteristically disproportionate to the anaemia
  • HbA2 raised (> 3.5%)

usually asx
just needs monitoring

128
Q

beta thalassaemia intermedia

A

two abnormal copies of the beta-globin gene. This can be either:
Two defective genes
One defective gene and one deletion gene

more signif microcytic anaemia
monitoring, might need occasional blood transfusions, may need iron chelation to prevent iron overload

129
Q

beta thalassaemia major

A

homozygous for the deletion genes. They have no functioning beta-globin genes.

severe anaemia + failure to thrive in early childhood

bone marrow under strain to produce extra RBCs -> expands increasing fracture risk + changing px appearance

mx = regular transfusions, iron chelation and splenectomy. A bone marrow transplant can be curative.

130
Q

common comp in thalassaemia

A

iron overload due to
Increased iron absorption in the gastrointestinal tract
Blood transfusions

monitor serum ferritin

131
Q

what vaccine should sickle cell px have + how often

A

the pneumococcal polysaccharide vaccine every 5 years

132
Q

phosphate levels in myeloma

A

high as reduced renal excretion

133
Q

indications for exchange transfusion in sickle cell disease

A

acute vaso-occlusive crisis, stroke, acute chest syndrome, multiorgan failure, splenic sequestration crisis
in individuals with a ‘high’ haemoglobin (>90g/L), where a blood transfusion could worsen the outcome by increasing serum viscosity and clogging the vessels more

it rapidly reduces the percentage of Hb S containing cells

134
Q

indications for blood transfusion in sickle cell disease

A

severe or symptomatic anaemia, pregnancy, pre-operative

does not rapidly reduce the percentage of Hb S containing cells

135
Q

what is a non-haemolytic febrile reaction
to blood transfusion

A

due to white blood cell HLA antibodies
often the result of sensitization by previous pregnancies or transfusions
paracetamol may be given
commonly presents with fever, rigors, and general discomfort

136
Q

what is an acute haemolytic transfusion reaction

A

results from a mismatch of blood group (ABO) which causes massive intravascular haemolysis. This is usually the result of red blood cell destruction by IgM-type antibodies.

137
Q

presentation acute haemolytic transfusion reaction

A

Symptoms begin minutes after the transfusion is started and include a fever, abdominal and chest pain, agitation and hypotension.

138
Q

what is transfusion-related acute lung injury (TRALI) + features

A

Rare but potentially fatal complication of blood transfusion.
Characterised by the development of hypoxaemia / acute respiratory distress syndrome within 6 hours of transfusion.

Features include:
hypoxia
pulmonary infiltrates on chest x-ray
fever
hypotension

139
Q

what is transfusion-associated circulatory overload (TACO)

+what is a key thing to differentiate it from TRALI

A

A relatively common reaction due to fluid overload resulting in pulmonary oedema. As well as features of pulmonary oedema the patient may also by HYPERTENSIVE (a key difference from patients with TRALI)

140
Q

blood film in hyposplenism (in coeliac, or post-splenectomy)

A

target cells
Howell-Jolly bodies
Pappenheimer bodies
siderotic granules
acanthocytes

141
Q

what is raised + reduced in beta thalassaemia major

A

HbA2 & HbF raised
HbA absent

142
Q

signs of poor prognosis in hodgkin’s lymphoma

A

lymphopenia
leukocytosis
raised ESR
raised LDH
decrease in albumin

143
Q

features of lead poisoning

A

Abdominal pain, constipation, neuropsychiatric features, basophilic stippling

blue lines on gums (Burton’s line)

144
Q

what type of blood products to give in immunosuppressed + why

A

Irradiated blood products are used to avoid transfusion-associated graft versus host disease

145
Q

2ndary causes of thrombocytosis

A

bleeding
inflammation
cancer

146
Q

types of AI haemolytic anaemia + which is most common

A

warm type - most common
cold type

147
Q

causes of warm AIHA

A

idiopathic
autoimmune disease: e.g. SLE
lymphoma
chronic lymphocytic leukaemia
drugs: e.g. methyldopa

148
Q

tx warm AIHA

A

treatment of any underlying disorder
steroids (+/- rituximab) are generally used first-line

149
Q

potential cure for thalassaemia

A

bone marrow transplant

150
Q

dx test for thalassaemia

A

haemoglobin electrophoresis

151
Q

tx non-hodgkin’s lymphoma

A

Rituximab in combo w conventional chemotherapy regimes

152
Q

cancer likely to cause tumour lysis syndrome

A

burkitt’s lymphoma

153
Q

reversal agent for DAbigatran

A

iDArucizumab

finals (27 decks)

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