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From Flashcardlet > Haematology > Flashcards

Haematology Flashcards

1
Q

Is whole blood commonly transfused?

A

No - only in major trauma

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2
Q

What is leucodepletion?

A

The removal of white cells during filtration of whole blood (ready for transfusion)

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3
Q

Do Fe deficient patients need RBC transfusion due to having acute anaemia?

A

No - only those with acute anaemia from major blood loss like surgery or trauma need RBC transfusion

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4
Q

What is apheresis?

A

It’s a medical technology in which the blood of a donor or patient is passed through an apparatus that separates out one particular constituent and returns the remainder to the circulation. Used to collect platelets

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5
Q

What component of blood has a shelf life of 5 days after collecting from donor?

A

Platelets due to risk of bacterial infection

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6
Q

What component of blood can be stored for up to 24 months?

A

Frozen fresh plasma - stored at -30 degrees celsius

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7
Q

Why do we transfuse FFP?

A

Treat those with MULTIPLE clotting factor deficiencies - severe infection, major trauma and massive bleeding

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8
Q

What special blood components are needed to transfuse to very immunosupressed recipients?

A

Irradiated blood (be it gamma or x-rays)

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9
Q

When are washed red cells or platelets transfused?

A

To patients who get severe recurrent allergic reactions to blood transfusion

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10
Q

How many RBC blood group systems are there?

A

23

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11
Q

What blood type is a universal donor?

A

O group - no antigens so will not be fought if in contact with A or B Abs

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12
Q

What blood type is a universal recipient?

A

AB group - has both A & B antigens therefore has no Abs so can will not attack anyone else’s blood

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13
Q

Which blood type contains Anti-A Abs?

A

B & O

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14
Q

What blood type contains both Anti-A & Anti-B Abs?

A

O

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15
Q

What blood type contains B antigens?

A

B

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16
Q

What blood type contains both A + B antigens?

A

AB

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17
Q

What blood type is the most common in the UK amongst donors?

A

O

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18
Q

What blood group is the least common in the UK amongst donors?

A

AB

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19
Q

What blood group can you donate to someone who has blood group O?

A

only blood group O as they have both anti-A and anti-B Abs

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20
Q

RhD is rhesus positive or negative?

A

Positive

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21
Q

Wat class of Antibody causes agglutination in the ABO blood group?

A

IgM

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22
Q

Would agglutination occur if Anti-B Abs were given to Blood type B?

A

Yes

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23
Q

What is Coomb’s test?

A

detection of incomplete (IgG) antibodies, as these Abs are too small to cause visible agglutination

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24
Q

What is the best way to ensure safe blood?

A

Avoid all unnecessary transfusions

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25
Q

What does TRALI stand for?

A

Transfusion associated lung injury

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26
Q

Most common reaction of transfusions?

A

febrile non haemolytic transfusion reaction

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27
Q

3 types of myeloproliferative disorders?

A

Polycythemia Vera, essential thrombocytosis, Idiopathic myelofibrosis

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28
Q

Which myeloproliferative disorder will show variable cytopenias and have a large spleen?

A

idiopathic myelofibrosis

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29
Q

What condition will present with a patient being very plethoric?

A

Polycythemia vera

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30
Q

What are the three ‘constitutional’ or ‘B’ symptoms seen in lymphoma?

A

Fever, night sweats, and weight loss.

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31
Q

List the six mature blood cells of myeloid origin.

A

Erythrocytes, platelets, neutrophils, macrophages, basophils and eosinophils.

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32
Q

List the three mature blood cells of lymphoid origin.

A

T lymphocytes, B lymphocytes and NK cells.

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33
Q

What causes megaloblastic macrocytic anaemia?

A

B12/folate deficiency.

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34
Q

What is the most common cause of microcytic hypochromic anaemia?

A

Iron deficiency.

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35
Q

JAK2 mutation is diagnostic of which myeloproliferative disorder to a high level of certainty?

A

Polycythemia vera (97%) although is elevated in ET & IMF but only around 50% of cases

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36
Q

What is reactive thrombocytosis caused from?

A

Bleeding, haemolysis, trauma, malignancy, IRON DEFICIENCY, chronic inflam, infection

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37
Q

Drug used to treat all three myeloproliferative disorders?

A

Hydroxycarbamide

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38
Q

Survival for Myelofibrosis?

A

3-5 years

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39
Q

Why do patients who have CML get very fatigued?

A

Due to anaemia

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40
Q

Polycythemia vera has a 5% chance of transforming into what?

A

Acute leukaemia

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41
Q

Which leukaemia is also classed as a myeloproliferative disorder?

A

Chronic myeloid leukaemia

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42
Q

Age affected in CML?

A

40-60

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43
Q

CML gender preference?

A

Males

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44
Q

Characteristics of CML?

A

Leucocytosis +++, anaemia, splenomegaly

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45
Q

What type of translocation is seen in CML?

A

reciprocal

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46
Q

BCR-ABL is a fusion gene formed on what chromosome?

A

Philadelphia - CML

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47
Q

Commercial name for imatinib? Used in treatment for what?

A

Glivec. CML (chronic myeloid leukaemia)

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48
Q

Drug used to treat CML in imatinib resistance?

A

Dasatinib

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49
Q

4 clinical features of acute leukaemia?

A

anaemia, infection, bruising/haemorrhage & organ infiltration into spleen/liver/meninges/testes/skin

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50
Q

Is t(9;22) a good or bad abnormality to have with regards to prognosis in ALL?

A

Bad - whereas in CML those without the Philadelphia Chr have a worse prognosis

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51
Q

List 4 poor prognostic factors for ALL?

A

elderly, high WCC, male, Ph Chr

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52
Q

Who does myelodysplastic syndromes affect?

A

elderly patients >70

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53
Q

What are myelodysplastic syndromes?

A

group of disorders that present with bone marrow failure and dysplasia of one or more of the myeloid lineages

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54
Q

Petechiae, fatigue, pallor, abnormal bleeding, infection are the signs and symptoms of what condition/syndrome/disease?

A

Myelodysplasia

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55
Q

What are reticulotytes?

A

immature RBCs

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56
Q

Cause of MDS?

A

De novo - benzene exposure, fanconi’s anaemia, viruses, cig smoking. Therapy related - radiation or chemo

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57
Q

In MDS, is refractory anaemia with ringed sideroblasts a good or bad prognostically?

A

Good

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58
Q

What are the two bad prognostic subtypes in MDS?

A

refractory cytopenia with multilineage dysplasia & refractory anaemia with excess blasts

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59
Q

What cancer are Auer rods diagnostic of?

A

Acute myeloid leukaemia & of MDS (refractory anaemia with excess blasts)

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60
Q

2 diseases that cause thrombocytopenia?

A

Immune thrombocytopenic purpura & thrombotic thrombocytopenia purpura

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61
Q

How is iron transported?

A

Transferrin

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62
Q

Where is iron stored?

A

In ferritin & haemosiderin

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63
Q

Where is iron mainly absorbed?

A

Duodenum

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64
Q

Is iron excreted

A

No

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65
Q

Lab test which is hallmark of Iron deficiency?

A

Low levels of Ferritin

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66
Q

3 categories for causes of Fe def?

A

blood loss, inc demand (preggo) and reduced intake

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67
Q

3 ways to administer iron?

A

Orally, intramuscularly and intravenously

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68
Q

Where is B12 absorbed?

A

terminal ileum

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69
Q

What cells secrete intrinsic factor?

A

gastric parietal cells

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70
Q

3 main causes of megaloblastic anaemia?

A

B12 def, folate def & alcohol

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71
Q

What is B12 needed for?

A

synthesis of thymidine and hence DNA production, without which RBC production is reduced

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72
Q

What can folic acid deficiency lead to in pregnancy?

A

fetal neural tube defects

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73
Q

Stores for folate last for how long?

A

4 months

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74
Q

Where is folate absorbed?

A

Duodenum & prox jejunum

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75
Q

What type of anaemia is B12 anaemia?

A

Macrocytic megaloblastic anaemia

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76
Q

Achlorhydria is associated with what haematological condition?

A

Pernicious anaemia

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77
Q

What does SACDC stand for?

A

Subacute combined degeneration of spinal cord - severe B12 def

78
Q

What happens in SACDC?

A

demyelination of dorsal and lateral columns and results in peripheral neuropathy, numbness and distal weakness

79
Q

How to treat B12 or folic acid def?

A

treat with both B12 and folate supplements as not to precipitate a neuropathy if you don’t know which def it is straight away

80
Q

Causes of haemolysis within the cell?

A

Haemoglobinopathy or enzyme defects (G6PD)

81
Q

What is raised bilirubin and LDH a marker of?

A

Breakdown products

82
Q

What gives rise to a normocytic anaemia?

A

Anaemia of chronic disease

83
Q

What hormone regulates iron absorption and release from macrophages?

A

Hepcidin

84
Q

What do the drugs used to treat ITP contain?

A

Thrombopoetin which inc platelet production

85
Q

Which one is more common, ITP or TTP?

A

ITP

86
Q

Which one is more severe, ITP or TTP?

A

TTP

87
Q

In TTP, what would be life saving treatment?

A

Plasma exchange with FFP

88
Q

2 types of VTE?

A

DVT & PE

89
Q

arterial thrombosis consists of more of fibrin or platelets?

A

Platelets

90
Q

Venous thrombosis consists more of platelets or fibrin?

A

Fibrin

91
Q

Percentage of VTE attributed to hospital acquired?

A

66%

92
Q

List 7 risk factors for VTE?

A

cancer treatment, >60yrs old, dehydration, known thrombophilias, obesity, major trauma, surgery, immobility, preggo, varicose veins, HRT, OCP, personal history

93
Q

Is protein C an anticoagulant or pro-coagulant?

A

Anti coagulant

94
Q

Name a direct thrombin inhibitor?

A

Dabigatran

95
Q

Prophylaxis of VTE?

A

Low molecular weight heparin

96
Q

What is Wells score used to diagnose?

A

DVT

97
Q

Name 4 heritable thrombophilias

A 
antithrombin deficiency, 
protein C def, 
protein S def, 
Activated protein C resistance/FV Leiden, Prothrombin 20210A, 
dysfibrinogaemia
98
Q

What type of haematological conditions is antiphospholipid syndrome?

A

Acquired thrombophilia - Antiphospholipid Abs on at least 2 occasions 8 wks apart associated with venous thrombosis, arterial thrombosis or recurrent foetal loss.

99
Q

Coumarin induced skin necrosis occurs in what conditions?

A

Thrombophilias - protein C and S deficiency

100
Q

Factor V Leiden results from what mutation?

A

Arg replaced by Gln which renders FV resistant to cleavage by APC

101
Q

Heterozygotes or homozygotes increase risk of venous thrombosis in FV Leiden?

A

Homozygotes = 30-50 fold increase

102
Q

Lupus anticoagulant and anticardiolipin antibodies are associated with what syndrome?

A

Antiphospholipid syndrome (acquired thrombophilia)

103
Q

At birth how much HbF is present?

A

60%

104
Q

HbF consists of what chains?

A

2 alpha and 2 gamma

105
Q

HbA consists of what chains?

A

2 alpha and 2 beta

106
Q

What type of immunity does breast milk give?

A

Passive immunity

107
Q

In neonatal haemostasis, are procoagulant proteins raised?

A

no they are reduced

108
Q

2 haemoglobinopathies?

A

thalassaemia & sickle cell disease

109
Q

2 enzyme defects with regards to peripheral destruction as a congenital cause of anaemia in neonates?

A

Pyruvate kinase def and G6PD def

110
Q

Define haemopoesis?

A

Physiological developmental process that gives rise to cellular components of blood.

111
Q

Life span of RBCs?

A

About 120 days

112
Q

Components of myeloid and lymphoid lineages?

A 
Myeloid = granulocytes, erythrocytes, platelets
Lymphoid = B/T-lymphocytes
113
Q

Name for low neutrophils?

A

Neutropenia

114
Q

Name for high monocytes?

A

Monocytosis

115
Q

What are platelets derived from?

A

Megakaryocytes

116
Q

Features of microcytic anaemia? And possible causes?

A

MCV <27 pg

Iron deficiency, thalassemia, anaemia of chronic disease, lead poisoning, sideroblastic anaemia.

117
Q

Features of normocytic normochromic anaemia? And possible causes?

A

MCV 80-95 fl and MCH > 27 pg

Mainly haemolytic anaemia, anaemia of Crohn’s disease, after acute blood loss, renal disease, mixed deficiencies, bone marrow failure.

118
Q

Features and possible causes of macrocytic anaemia?

A

MCV > 95 fl

Megaloblastic - vit B12 or folate deficiency
Non-megaloblastic - alcohol, liver disease, myelodysplasia, aplastic anaemia

119
Q

Adhesion molecule for fibrinogen?

A

GP-iib-iiia

120
Q

Adhesion molecule for vWF?

A

GP-ib-ix

121
Q

Action of aspirin?

A

Inhibits cycloxygenase, produces thromboxane. Stops platelet activation

122
Q

Action of clopidogrel?

A

Acts on ADP receptor - blocks GP-iib-iiia

123
Q

Difference between extrinsic and intrinsic pathways?

A

Extrinsic needs something external to blood (I.e. Tissue factor). Intrinsic doesn’t (auto activation of FXii)

124
Q

Intrinsic or extrinsic pathway - which is faster?

A

Extrinsic because it has less steps

125
Q

What are the pathways in the coagulation cascade measured by?

A 
Extrinsic/common = prothrombin time 
Intrinsic = APTT (advanced p.. thromboplastin time or something)
126
Q

What do primary bleeding disorders affect and cause?

A

Platelets/vessel wall - affect mucosa and skin. Petechial and superficial bruises, skin and mucous membrane bleeding, spontaneous bleeds - bleeding immediate, prolonged and non-recurrent

127
Q

Why do secondary bleeding disorders affect and cause?

A

Coagulation.
Affects deep muscular and joint bleeds. Deep spreading haematomas, harmarthrosis, retroperitoneal bleeding, bleeding prolonged and often recurrent.

128
Q

What is the most common heritable bleeding disorder?

A

Von Wilebrand Disease

129
Q

Define the types of vWD?

A

Type I - Reduced production of vWF
Type II - normal production of LMW vWF, it’s less sticky.
Type III - (severe) vWF absent

130
Q

In type I vWD there are reduced levels of which coagulation factor in the blood?

A

FVIII - vWF is its carrier in blood

131
Q

How is vWD inherited?

A

Type I/II = autosomal dominant

Type III = autosomal recessive

132
Q

Effects of vWD?

A

Post operative and post partum bleeding

133
Q

Which clotting factors do the two haemophilias affect?

A

A = Fviii
B = Fix
(Intrinsic pathway factors - increases APTT)

134
Q

How are the haemophilias inherited?

A

X-linked recessive

135
Q

What is lymphadenopathy?

A

Swollen lymph nodes

136
Q

Causes of lymphadenopathy?

A

LOCALISED - local infection (pyogenic, viral, cat scratch, TB), lymphoma, carcinoma.

GENERALISED - infection (viral, bacterial, fungal, protozoal), non-infectious (inflammation), malignant (leukaemia, lymphoma), miscellaneous (drugs/hyperthyroidism)

137
Q

What is Hodgkin’s lymphoma?

A

Malignant lymphoma of B-lymphoid lineage

138
Q

Clinical features of Hodgkin’s lymphoma?

A

Enlargement of superficial lymph nodes, mild hepatomegaly, mediastinal involvement (pleural effusion, SVC obstruction), constitutional symptoms (fever, pleuritis, weight loss, night sweats, weakness, fatigue, anorexia, cachexia, alcohol induced lymph node pain)

139
Q

Epidemiology of Hodgkin’s lymphoma?

A

More common in males - peaks in 20s and 70s

140
Q

Findings in Hodgkin’s lymphoma?

A

Normocytic normochromic anaemia, neutrophilia, eosinophilia

141
Q

Blood test findings in non-Hodgkin’s lymphoma?

A 
Normocytic, normochromic anaemia. 
Neutropenia, thrombocytopenia.
Circulating lymphoma cells in blood.
Raised LDH (esp in high grade/extensive)
Abnormal LFTs in disseminated disease
Increased uric acid
Para protein - IgM or IgG
142
Q

Can non-Hodgkin’s lymphoma be cured?

A

Aggressive form yes, indolent form no.

143
Q

Most common high and low grade B cell lymphomas? (Non-Hodgkin’s)

A

High grade - diffuse large B cell lymphoma

Low grade - follicular lymphoma

144
Q

What is multiple myeloma?

A

Cancer of most mature B cells (plasma cells)

145
Q

Median age for multiple myeloma?

A

70

146
Q

Symptoms of multiple myeloma?

A
  • Bone pain (back)
  • Lethargy, dyspnoea, pallor prior to anaemia
  • Recurrent infections
  • Leg weakness, loss of sensation, sphincter disturbance due to cord compression
  • Visual disturbance, headaches, confusion, somnolence, bleeding due to hyperviscosity
147
Q

Blood test findings in multiple myeloma?

A
  • Normocytic normochromic/macrocytic anaemia
  • Rouleaux formation (stacking of red cells)
  • High ESR/plasma viscosity
  • High calcium
  • Raised creatinine/urea (reduced renal function)
  • Reduced normal immunoglobulins
  • Lytic lesions in skeletal survey
148
Q

Multiple myeloma prognosis?

A

Poor - not curable

149
Q

What the fucking hell is benign polyclonal hypergammaglobulinaemia?

A

General increase in polyclonal Ab in blood rather than monoclonal. Lots of reasons - not necessarily malignant. 1 most common - chronic liver disease, connective tissue disease.

150
Q

What is monoclonal gammopathy of unknown significance? (MGUS)

A

Para protein in blood - no Evidence that cells producing it are behaving in aggressive fashion or causing damage. no symptoms or treatment. Pre-malignsnt condition. Progress to myeloma 1%/yr

151
Q

What is amyloidosis?

A

Extra cellular deposition of protein in abnormal fibrillar form - very stiff, disrupts normal tissue function. Associated with myeloma, MGUS and lymphoplasmacytic lymphoma.

152
Q

Clinical features of amyloidosis?

A
  • Blood vessels - bleeding/bruising, panda eyes
  • Tongue (macroglossia)
  • Heart - congestive cardiac failure, conduction system dysfunction
  • Kidneys (renal impairment, nephrotic syndrome)
  • Carpal tunnel
  • Peripheral/autonomic nerves - postural hypotension, constipation, diarrhoea (eugh).
153
Q

Levels of leukocytes? Overall WCC & list WBCs in order of their percentage.

A

4-11x10^9/L

Neutrophils (60%)
Lymphocytes (30%)
Monocytes
Eosinophils
Basophils
154
Q

Common features of B12 deficiency ?

A

Megaloblastic anaemia, mild jaundice, glossitis/angular stomatitis, weight loss, sterility

155
Q

What is the FAB classification used for?

A

AML - looks at morphological features

156
Q

What is relative polycythemia?

A

Decreased percentage of plasma e.g dehydration from drinking alcohol

157
Q

Which CMPD shows variable cytopenias and splenomegaly?

A

Myelofibrosis

158
Q

What is Ann Arbor staining used to stage?

A

Lymphoma - think about which side of diaphragm the lymph node groups are

159
Q

Which lymphoma has a bimodal incidence?

A

Hodgkin’s lymphoma - 20s & & 70s

160
Q

Which lymphoma presents with Reed-sternberg cells on histological sections?

A

Hodgkin’s lymphoma

161
Q

Which lymphoma are B symptoms a clearer negative prognostic indicator for?

A

Hodgkin’s lymphoma

162
Q

Which lymphoma has raised paraprotein levels?

A

Non hodgkin’s lymphoma

163
Q

What does antithrombin III bind to on endothelium in order to destroy thrombin, FXa, FIXa?

A

Heparin sulphate which is on all endothelial cells.

164
Q

What binds to thrombomodulin?

A

Thrombin - results in activation of protein C which destroys FVa & FVIIIa

165
Q

What are vitamin K dependant clotting factors?

A

II, VII, IX & X

166
Q

What does FXIIIa do?

A

Cross linking of fibrin molecules

167
Q

What cleaves plasminogen into plasmin?

A

tissue plasminogen activator

168
Q

Which test is used to test the extrinsic pathway of the coagulation cascade?

A

Prothrombin time

169
Q

APTT is used to measure what?

A

Intrinsic pathway

170
Q

How do you test vWF function?

A
  • vWF:FVIII binding
  • vWF:platelet binding
  • vWF:collagen binding
  • multimer formation
  • vWF count
171
Q

What drugs inhibits thromboxane and so prevents platelet adhesion?

A

Aspirin

172
Q

Which factors does LMWH act on?

A

FX & some FII

173
Q

How do you reverse Life threatening haemorrhage due to too much anticoagulation?

A

Give Vit K IV and give four factor concentrate

174
Q

What is epistaxis?

A

Nose bleeds

175
Q

Difference between petechiae and purpura?

A 
Petechiae = small red/purple spots
Purpura = large purple patches
176
Q

Is retroperitoneal bleeding due to a defect in coagulation or platelets?

A

Coagulation

177
Q

What can desmopressin be used to treat?

A

vWD type 1 & mild Haemophilia A

178
Q

Why vaccinate against Hep A & B in vWD & Haemophilia patients?

A

More likely to require blood transfusions through which hepatitis may be transmitted

179
Q

Causes of vitamin K deficiency?

A
  • obstructive jaundice
  • prolonged nutritional deficiency
  • broad spectrum antibiotics
  • neonates
180
Q

Disease of what organ can cause impaired haemostasis? Inc risk of severe bleeding, thrombocytopenia, excessive plasmin activity

A

Liver - cirrhotic coagulopathy

181
Q

What is massive transfusion syndrome?

A

Transfusion of a volume equal to the patients blood volume in less than 24 hours OR 50% blood volume within 3 hours

182
Q

Disruption in the physiological balance of procoagulant and anticoagulant mechanisms = what name?

A

DIC

183
Q

Acute causes of DIC?

A
  • sepsis
  • obstetric complications
  • trauma
  • acute intravascular haemolysis
  • liver disease
184
Q

Chronic causes of DIC?

A
  • malignancy
  • end stage liver disease/cirrhosis
  • retained dead foetus
185
Q

Which one is heterozygous - sickle cell trait or sickle cell disease?

A

Sickle cell trait (HbA/S) - no problems except for extreme hypoxia or dehydration

186
Q

Which one is homozygous - thalassaemia minor or thalassaemia major?

A

Thalassaemia major - fatal if untreated

187
Q

Treatment of thalassaemia major?

A

Transfusion 3-4 wks from 1st year of life. to prevent iron overload = iron chelation therapy

188
Q

During pregnancy; anaemia or polycythemia? Leukocytosis or leukocytopenia? Thrombocytosis or thrombocytopenia? Pro-coagulant or anti-coagulant?

A
  • anaemia
  • leukocytosis
  • thrombocytopenia
  • pro-coagulant = pro-thrombotic state
189
Q

Which coagulation factors increase in pregnancy?

A

Factors V, VII, VIII, FX, FXII + plasma fibrinogen and vWF

190
Q

At birth what percentage of our haemoglobin is HbF?

A

55-65%

From Flashcardlet (22 decks)

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