Haematology Flashcards

1
Q

B symptoms are a sign of…
what cancer? (1)
what prognosis? (1)

A

Hodgkins lymphoma
poor prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

B symptoms in Hodgkins lymphoma

A

weight loss > 10% in last 6 months
fever > 38ºC
night sweats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Afro-carribeans have worse prognosis of what haematological cancer

A

ALL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Hodgkins lymhpoma:
what cells

A

malignant proliferation of lymphocytes characterised by the presence of the Reed-Sternberg cell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Vitamin B12 and folate deficiency together - what is important to do in treatment?

A

treat B12 first otherwise –> subacute combined degeneration of spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

where is B12 absorbed

A

terminal ileum (impacted in Crohns/ following resection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

most common inherited thrombophilia

A

factor 5 leiden (–> clotting!/ VTE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

most common acquired thrombophilia

A

antiphospholipid syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Antiphospholipid syndrome in pregnancy

A

aspirin + LMWH

low-dose aspirin should be commenced once the pregnancy is confirmed on urine testing
low molecular weight heparin once a fetal heart is seen on ultrasound. This is usually discontinued at 34 weeks gestation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

a reversal agent for dabigatran

A

idarucizumab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

vWD:
management (3)

A

tranexamic acid for mild bleeding
desmopressin (DDAVP): raises levels of vWF by inducing release of vWF from Weibel-Palade bodies in endothelial cells
factor VIII concentrate (F8 can be low)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

vWD:
types (3)

A

type 1: partial reduction in vWF (80% of patients)
type 2*: abnormal form of vWF
type 3**: total lack of vWF (autosomal recessive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ITP (Immune (or idiopathic) thrombocytopenic purpura (ITP)):
trigger (1)
investigations (2)
management (2)

A

immune reaction –> low platelets post infection/ vaccination

FBC
blood film (bone marrow no longer needed)

1st line= prednisolone
2nd= pooled normal human immunoglobulin (IVIF) to raise count if urgent or active bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Evan’s syndrome

A

ITP in association with autoimmune haemolytic anaemia (AIHA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

major criteria determining the use of cryoprecipitate in bleeding

A

fibrinogen level - Cryoprecipitate is a blood product that contains concentrated amounts of fibrinogen, factor VIII, and von Willebrand factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

when to give Fresh frozen plasma (FFP)

A

prothrombin time (PT) ratio or activated partial thromboplastin time (APTT) ratio > 1.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

When to use prothrombin complex concentrate

A

used for the emergency reversal of anticoagulation in patients with either severe bleeding or a head injury with suspected intracerebral haemorrhage
can be used prophylactically in patients undergoing emergency surgery depending on the particular circumstance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Fever, abdominal pain, hypotension during a blood transfusion →

A

acute haemolytic reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Blood transfusion complications

A

immunological: acute haemolytic, non-haemolytic febrile, allergic/anaphylaxis
infective
transfusion-related acute lung injury (TRALI)
transfusion-associated circulatory overload (TACO)
other: hyperkalaemia, iron overload, clotting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Non-haemolytic febrile reaction:
main features (2)
what to do (1)

A

fever+ chills
stop/ slow transfusion and paracetamol

Thought to be caused by antibodies reacting with white cell fragments in the blood product and cytokines that have leaked from the blood cell during storage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Minor allergic reaction
features
management

A

itch urticaria
stop+ histamine + monitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Anaphylaxis:
features (4)
management (1)

A

hypotension, SOB, wheeze, angioedeam
stop+ adrenaline+ABC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Acute haemolytic reaction
what is it? (1)

A

ABO incompatable
abdo pain+ hypotension+ fever
STOP + confirm with Coombs test
fluid resuscitation (supportive care)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Transfusion-associated circulatory overload (TACO)

A

PO due to overload
diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Transfusion-related acute lung injury (TRALI)

A

Non-cardiogenic pulmonary oedema thought to be secondary to increased vascular permeability caused by host neutrophils that become activated by substances in donated blood

Hypoxia, pulmonary infiltrates on chest x-ray, fever, hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

complications acute haemolytic reaction

A

renal failure and DIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Post thrombotic syndrome:
what is it? (1)
management (1)

A

venous problems post DVT
However, once post-thrombotic syndrome has developed compression stockings are a recommended treatment. Other recommendations including keeping the leg elevated.

DO NOT offer compression stockings for DVT routinely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

do you rescan patients post DVT

A

no!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

DIC typical picture
plaetles
fibrinogen
APTT and PT
D Dimer

A

↓ platelets
↓ fibrinogen
↑ PT & APTT
↑ fibrinogen degradation products
schistocytes due to microangiopathic haemolytic anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

causes of DIC

A

sepsis
trauma
obstetric complications e.g. aminiotic fluid embolism or hemolysis, elevated liver function tests, and low platelets (HELLP syndrome)
malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Prothromibin time, APTT, bleeding time and platelet count of:
warfarin
aspirin
heparin
DIC

A

Warfarin- prolonged PT but rest normal
Aspirin- prolonged bleeding time but rest normal
Hepatin prolonged APTT but rest normal
DIC: prolonged everything and low platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Tonsilitis and neutropenia

A

Epstein-Barr virus may result in neutropaenia
(infectious mononucleosis)
An increase in the number of circulating activated T and B lymphocytes seen in the virus causes lymphocytosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Neutropenia:
what classes mild/ moderate/severe? (3)

A

mild= 1-1.5
moderate= 0.5-1
severe= <0.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

neutropenia causes:
viral (3)
drugs (3)
ethnic (1)
haematological (1)
other (4)

A

viral
HIV
Epstein-Barr virus
hepatitis
drugs
cytotoxics
carbimazole
clozapine
benign ethnic neutropaenia
common in people of black African and Afro-Caribbean ethnicity
requires no treatment
haematological malignancy
myelodysplastic malignancies
aplastic anemia
rheumatological conditions
systemic lupus erythematosus: mechanisms include circulating antineutrophil antibodies
rheumatoid arthritis: e.g. hypersplenism as in Felty’s syndrome
severe sepsis
haemodialysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Hodgkins: High potassium, high phosphate, and low calcium - what causes this (1)
prophylaxis for this? (1)
who to suspect in? (1)

A

timor lysis syndrome (post chemo) due to the cancer cells breaking down
ALLOPURINOL
suspect in any patient with AKI and high phopshate/ uric acid level

36
Q

Tumor lysis syndrome:
how to treat

A

IVF
rasburicase (higher risk)
alluring (lower risk)
rasburicase and allopurinol should not be given together in the management of tumour lysis syndrome as this reduces the effect of rasburicase

37
Q

Definition tutor lysis syndrome

A

laboratory tumour lysis syndrome plus one or more of the following:
increased serum creatinine (1.5 times upper limit of normal)
cardiac arrhythmia or sudden death
seizure

38
Q

‘tear drop’ poikilocytes on blood film causes (3)

A

thalassaemia, megaloblastic anaemia and myelofibrosis.
(the bone is all fibrosed so the blood cells have to squeeze out - making them tear drop shaped)

39
Q

tear drop’ poikilocytes + weight loss/ fatigue + large spleen

A

myelofibrosis
reduces the ability of the bone marrow to produce normal cells, thus causing thrombocytopenia, anaemia and extramedullary haematopoiesis in the spleen.

40
Q

Cryoprecipitation contains

A

factor VIII, fibrinogen, von Willebrand factor and factor XIII

Indications include massive haemorrhage and uncontrolled bleeding due to haemophilia

41
Q

When to do exchange transfusion in sickle cell

A

if neurological complications

42
Q

Long term management sickle cell (2)

A

Hydroxyurea (prophylaxis)
Pneumococcal polysaccharide vaccine every 5 years

43
Q

A grossly elevated APTT (3)

A

may be caused by heparin therapy, haemophilia (bleeding) or antiphospholipid syndrome (clotting)

44
Q

Haemophilia A and B factors

A

A= Factor VIII
B= Factor IX

45
Q

blood tests haemophilia

A

prolonged APTT, rest normal

46
Q

Lymphoma: why special irradiated blood products?

A

Irradiated blood products are often treated with gamma or x-ray radiation to deplete T-lymphocytes in order to prevent transfusion-associated graft versus host disease

47
Q

Blood film in hyposplenism

A

target cells
Howell-Jolly bodies
Pappenheimer bodies
siderotic granules
acanthocytes

48
Q

common cause of hyposplenism

A

Coeliac disease

49
Q

Iron def anaemia

A

target cells
‘pencil’ poikilocytes
if combined with B12/folate deficiency a ‘dimorphic’ film occurs with mixed microcytic and macrocytic cells

50
Q

Sickle cell crisis:
Thrombotic crisis what is it?

A

also known as painful crises or vaso-occlusive crises
precipitated by infection, dehydration, deoxygenation (e.g. high altitude)
painful vaso-occlusive crises should be diagnosed clinically - there isn’t one test that can confirm them although tests may be done to exclude other complications
infarcts occur in various organs including the bones (e.g. avascular necrosis of hip, hand-foot syndrome in children, lungs, spleen and brain

51
Q

Sickle cell:
what is acute chest syndrome

A

vaso-occlusion within the pulmonary microvasculature → infarction in the lung parenchyma
dyspnoea, chest pain, pulmonary infiltrates on chest x-ray, low pO2
management
pain relief
respiratory support e.g. oxygen therapy
antibiotics: infection may precipitate acute chest syndrome and the clinical findings (respiratory symptoms with pulmonary infiltrates) can be difficult to distinguish from pneumonia
transfusion: improves oxygenation
the most common cause of death after childhood

52
Q

Sickle cell:
what is aplastic crisis

A

infection with parvovirus
sudden Hb cfall
bone marrow supprossion–> reduced reticule count

53
Q

Sequestriation crisis

A

Spleen or lungs
increased reticulocyte count

54
Q

What blood film associated with DIC?

A

schistocytes

55
Q

splenomegaly:
causes (5)

A

myelofibrosis
chronic myeloid leukaemia
visceral leishmaniasis (kala-azar)
malaria
Gaucher’s syndrome

56
Q

Myeloid leukaemia vs lymphoid leukaemia

A

Myeloid: neutrophils

Lymphoid: lymphocytes

ALL –> CML –> AML –> CLL
acute= immature blast cells
chronic= mature cells
ALL (Tdt)–> CML (Philadelphia chromosome, splenomegaly) –> AML (Auer rods)–> CLL

57
Q

AML cells

A

Auer rods (large uncles with rods)

(A)uer rods and (M)yeloperoxidase positive

58
Q

Why is CML a problem

A

if it progresses to AML
(AML in 80%, ALL in 20%)

59
Q

Age ranges ALL–>CML–>AML–>CLL

A

10, 40, 50, 80

60
Q

CML treatment

A
  1. imatinib is now considered first-line treatment
    inhibitor of the tyrosine kinase associated with the BCR-ABL defect
    very high response rate in chronic phase CML
  2. hydroxyurea
  3. inferno alpha
  4. allogenic bone marrow transplant
61
Q

Raised haemoglobin, plethoric appearance, pruritus, splenomegaly, hypertension

A

polycythaemia vera

62
Q

Polycythaemia vera mutation

A

JAK2

63
Q

Iron studies in iron deficiency anaemia

A

↓ Ferritin, ↑ total iron-binding capacity, ↓ serum iron, ↓ transferrin saturation

The total iron-binding capacity (TIBC) increases as the body produces more transferrin (the iron transport protein) to maximise iron uptake. Serum iron levels fall due to depleted stores. Transferrin saturation, which is calculated as (serum iron ÷ TIBC) × 100, will be low due to the combination of low serum iron and high TIBC.

Transferrin is like a delivery truck that carries iron around your body. When you need more iron, there are more delivery trucks on the road. If you have too much iron, there are fewer trucks driving around. TIBC (Total Iron Binding Capacity) is like the number of seats on the delivery trucks. If you need more iron, you add more seats to the trucks. If you have too much iron, the seats on the trucks are mostly empty.

64
Q

How is myeloma diagnosed

A

urine protein electrophoresis and serum-free light-chain assay

Rouleaux formation blood film

65
Q

3-month history of tiredness, back pain and both increased urination and thirst. The GP requests a urine protein electrophoresis and a serum-free light-chain assay, which confirm the diagnosis.

A

myeloma (rouleaux formation)

66
Q

Multiple myeloma CRAB features

A

‘CRAB’ features of multiple myeloma = hyperCalcaemia, Renal failure, Anaemia (and thrombocytopenia) and Bone fractures/lytic lesions

67
Q

The transfusion threshold for patients with ACS

A

80
(without ACS= 70)

68
Q

most aggressive hodgkin lymphoma

A

Lymphocyte-depleted Hodgkin lymphoma

69
Q

what type of anaemia is sickle cell disease?

A

normocytic anaemia with raised reticulocyte count - due to haemolysis

70
Q

Cancer patients with VTE

A
  • 6 months of a DOAC
71
Q

beta-thalassaemia major management (1)
what to give alongside (1)

A

repeated transfusion
this leads to iron overload → organ failure
iron chelation therapy is therefore important (e.g. desferrioxamine)

72
Q

what is behcets syndrome

A

a rare and chronic condition that causes inflammation of the blood vessels (vasculitis) throughout the body. It can lead to numerous symptoms, including painful mouth sores, genital sores, and eye inflammation. it can increase the risk of venous thromboembolism due to the inflammation of the blood vessels. This inflammation can cause damage to the vessel walls leading to activation of the coagulation cascade and the formation of blood clots.

73
Q

Iron studies and infection: what to remember

A

Ferritin HIGH in infection REGARDLESS of iron status

74
Q

microcytic aneamia causes (5)

A

Causes
iron-deficiency anaemia
thalassaemia*
congenital sideroblastic anaemia
anaemia of chronic disease (more commonly a normocytic, normochromic picture)
lead poisoning

A question sometimes seen in exams gives a history of a normal haemoglobin level associated with a microcytosis. In patients not at risk of thalassaemia, this should raise the possibility of polycythaemia rubra vera which may cause an iron-deficiency secondary to bleeding.

75
Q

The antidote for heparin

A

protamine sulfate.

76
Q

sickle cell crisis main management

A

analgesia, oxygen, and IV fluids (+ consider Abx if infection and transfusion if Hb low)

77
Q

Wells score DVT Cut off

A

If a 2-level DVT Wells score is ≥ 2 points then arrange a proximal leg vein ultrasound scan within 4 hours

78
Q

Paraproteinaemia:
benign causes (2)
malignant causes (4)

A

Benign paraproteinaemia:
Monoclonal gammopathy of undetermined significance (MGUS)
Transient paraproteinaemia (e.g., following an infection)

Malignant paraproteinaemia:
Multiple myeloma
Waldenstrom macroglobulinemia
Primary amyloidosis (AL)
B-cell lymphoproliferative disorders (e.g., chronic lymphocytic leukaemia, non-Hodgkin lymphoma)

79
Q

Oaraproteinuriea

A

Clinical features
Hyperviscosity syndrome
Neuropathy (e.g., sensory, motor, or autonomic dysfunction)
Renal dysfunction
Hematologic abnormalities (e.g anaemia, thrombocytopenia, or leukopenia)
Bone pain or pathologic fractures (in the context of multiple myeloma)

80
Q

intense itching which usually occurs after exposure to hot water or hot and humid weather.

A

Polycythaemia vera is a neoplasm of the bone marrow which results in the production of excessive red blood cells. The classic symptom of this condition is intense itching which usually occurs after exposure to hot water or hot and humid weather. It is believed that this is due to abnormal histamine or prostaglandin production.

81
Q

Polycythaemia:
primary (1)
relative (2)
secondary (4)

A

polycythaemia rubera vera
relative: stress/ dehydration
secondary: COPD, altitude, sleep apnoea, excessive erythropoietin

–> look at blood cell mass to tell

82
Q

most common cause of: prolonged APTT (Activated Partial Thromboplastin Time) but normal PT (Prothrombin Time) and platelet count

A

Haemophilia A (factor VIII) MORE common than factor B (IX)

83
Q

inheritance haemophilia A/B

A

X-linked recessive disorder of coagulation

84
Q

AP and APTT

A

PT signifies the extrinsic pathway (Play Tennis Outside=EXtrinsic). Since the extrinsic pathway has only factor VII which is rarely deficient in isolation, PT would be a more generalised test for clotting (liver disease, DIC, warfarin, Vit K deficiency)

APTT signifies the intrinsic pathway (Play Table Tennis Inside= INtrinsic). This consists of factors VIII, IX and XI.
Haemophilia A- Factor VIII (X linked recessive)
Haemophilia B- Factor IX (X linked recessive)
Haemophilia C- Factor XI (autosomal recessive)
Von Willebrand as vWF binds to factor VIII

EXCEPTION- antiphospholipid syndrome can cause increase APTT despite being a clotting disorder

85
Q

Sickle cell crisis + fever = what to do?

A

admit urgently as increased risk overwhelming sepsis by encapsulated organisms

86
Q

When do you do exchange transfusion in sickle cell?

A

indications include: acute vaso-occlusive crisis (stroke, acute chest syndrome, multiorgan failure, splenic sequestration crisis
(rapidly reduce the percentage of Hb S containing cells)

87
Q

Which blood products have the highest risk of bacterial§ contamination?

A

platelets