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HAEM/IMMUNOLOGY > Haematology > Flashcards

Haematology Flashcards

1
Q

How is anaemia defined?

A

Haemoglobin level below the lower limit of normal for age/sex

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2
Q

What are clinical features of anaemia?

A
  • Pallor
  • Weakness, fatigue, lethargy, dizziness, headache
  • tachycardia
  • older patients: HF, angina, claudication
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3
Q

What are the 3 broad groups under the morphological approach to anaemia?

A
  1. Hypochromic - reduced MCV and MCH
  2. Macrocytic - increased MCV
  3. Normochromic normocytic - normal MCV/MCH
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4
Q

What are examples of hypochromic microcytic anaemia?

A
  • iron deficiency
  • anaemia of chronic disease
  • thalassaemia
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5
Q

What are Macrocytic anaemia examples?

A
  • megaloblastic - B12/folate
  • hypothyroidism
  • pregnancy
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6
Q

What are examples of normochormic, normocytic anaemia?

A
  • anaemia of chronic disease
  • acute blood loss
  • some haemolytic anaemias
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7
Q

What are macro and microcytic anaemias associated with?

A

Macrocytic - problems in synthesis of RBC

Microcytic - deficiency in Hb production

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8
Q

How are these proteins involved in iron absorption?

  1. ferritin
  2. transferrin
  3. transferrin receptor
  4. ferroportin
A
  1. ferritin - iron storage protein found in serum
  2. transferrin - transport protein for iron
  3. transferrin receptor - cells absorb iron through internalisation of transferrin bound to transferrin receptor
  4. ferroportin - transports iron across cell membrane to plasma
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9
Q

What are the three categories of cause for iron deficiency?

A

XS blood loss
Decreased absorption
Increased utilisation of iron - pregnancy

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10
Q

What are some clinical features of iron deficiency?

A
  • anaemia
  • dietary cravings - pica
  • glossitis
  • angular stomatitis
  • brittle nails
  • koilonychia - spoon nails
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11
Q

What would be seen in a FBP of iron deficiency

A
  • reduced Hb, RCC, MCV

Blood film - hypo chromic microcytic red cells + pencil cells

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12
Q

What would be the findings in iron studies of someone with iron deficiency?

A
  • reduced ferritin
  • reduced transferrin saturation
  • increased transferrin
  • reduced serum iron
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13
Q

What is the management of iron deficiency?

A
  1. Oral iron - best absorbed as Fe2+ with vitC
  2. Parenteral iron therapy - non compliant or can’t absorb
  3. Blood transfusion of iron - for haemodynamically unstable
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14
Q

What is anaemia of chronic disease/inflammation?

A

Seen in patients with inflammatory or malignant disease - elevation of IL6 which stimulates hepcidin –> causes the internalisation of ferroportin which prevents iron from being absorbed in the GIT - functional iron deficiency because it cannot be accessed

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15
Q

What would a FBP and iron studies of anaemia of chronic disease show?

A 
FBP - mild anaemia, normal or reduced MCV
Iron studies:
- increased ferritin
- reduced transferrin saturation 
- reduced transferrin
- reduced serum iron
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16
Q

What is thalassaemia and what are the types?

A

Beta-thalassaemia - trait and major

Alpha thalassaemia - trait and major

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17
Q

What is the difference in presentation between beta major and trait thalassaemia?

A

Major (XS alpha globin)- homozygotes present between 3-12 months of age (transfer from foetal to adult Hb)
Trait - usually asymptomatic

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18
Q

What is megaloblastic anaemia?

A

Macrocytic anaemia resulting from inhibition of DNA synthesis - causing impaired RBC production
Commonly due to folate or B12 deficiency

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19
Q

What is vitamin B12 involved in and causes the deficiency?

A

B12 - involved in maintenance of myelin in NS and DNA formation and synthesis/cell division
Cause: malabsorption due to pernicious anaemia, coeliacs, pregnancy

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20
Q

What is pernicious anaemia?

A
  • macrocyclic anaemia caused by B12 deficiency
  • due to stomach atrophy and reduced Intrinsic factor secretion
  • results in reduced absorption of B12
  • Associated with AI diseases
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21
Q

How is the clinical presentation of B12 deficiency unique?

A

Neurological - peripheral neuropathy and subacute degeneration of posterior columns of spinal cord

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22
Q

What is the treatment for B12 deficiency?

A

Replacement of B12 via IM injection of 1000ug cyanocobalamin or hydroxocobalamin

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23
Q

What are causes of folate deficiency?

A
  • reduced dietary intake
  • reduced absorption
  • increased folate use
  • increased folate loss
  • drugs
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24
Q

What is the treatment for folate deficiency?

A

Reversing the underlying cause/taking oral supplements

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25
Q

What is haemolysis and what are the clinical features?

A

Haemolysis - increased RBC destruction and reduced lifespan and leads to compensatory increased EPO and RBC production
Clinical features:
increased RBC destruction - inc bilirubin, lactate hydrogenase, dark urine
Compensatory increased production of RBC - increased reticulocytes, reduced folate stores

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26
Q

What are the causes of RBC haemolysis?

A

RBC abnormalities:

  1. membrane abnormalities - hereditary spherocytosis or eliptocytosis
  2. enzyme deficiencies - G6PD
  3. Hb abnormalities

Extrinsic to RBC

  1. AI haemolytic anaemia
  2. infection
  3. mechanical trauma
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27
Q

What is Autoimmune haemolytic anaemia? How is it diagnosed?

A

Auto-antibodies produced against RBC’s causing agglutination and haemolysis
Diagnosis:
-normocytic/macrocytic anaemia
- increased RCC
- increased bilirubin
+ve direct antiglobulin test (DAT)/Coomb’s

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28
Q

What are the subtypes of AIHA?

A

IgG - warm antibody AIHA

  • antibodies more active in body temp
  • therapy - steroid, rituximab, splenectomy, immunosuppressant

C3d - cold antibody AIHA

  • more active at room temp
  • therapy - rituximab
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29
Q

What happens after disruption to the vascular endothelium?

A
  1. platelets bind and form unstable clot
  2. TF n sub endothelium activates FVII
  3. Clotting cascade - thrombin production
  4. large scale thrombin production
  5. Fibrinolysis is activated to localise the clot
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30
Q

What are the causes of accelerated bleeding?

A
  1. abnormalities of vasculature
  2. defects of primary haemostats - platelet disorders
  3. defects of secondary haemostats - procoagulant protein deficiency
  4. accelerated breakdown of clot
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31
Q

What are disorders of primary homeostasis?

A
  1. abnormal platelet number - thrombocytopenia
    - impaired BM
    - Hypersplenism
    - increased destruction - infection/ITP
    - drug induced
  2. Abnormal platelet function
    - congenital - bernard solider, glanzmanns, VWD
    - Acquired - drugs
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32
Q

What is the normal function of platelets?

A

Involves adhesion, shape change causing platelet activation, granule release and recruitment of more platelets - aggregation and platelet plug!

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33
Q

What is Von Willebrand’s disease?

A

Defective or missing VWF
Autosomal disease affecting primary haemostasis as VWF is needed for platelet binding AND it is also a carrier protein for FVIII - secondary haemostasis

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34
Q

What are the types of VWD?

A

Type 1 - decreased quantity VWF
Type 2 - decreased function VWF
Type 3 - rare, severe deficiency of VWF due to 2 defective genes

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35
Q

What is the laboratory diagnosis of VWD?

A

Potentially prolonged APTT - due to FVII and VWF

VW screen for VWF antigen, function and FVII levels

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36
Q

What is the management of VWD?

A

Desmopressin (DDAVP) - releases endogenous stores of VWF
Tranexamix acid tablets - stop clot breakdown
Biostate - for severe VWD or non-responders to DDAVP

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37
Q

How does vitamin K deficiency effect bleeding? How is it diagnosed?

A

VitK is essential for clotting and activation of FII, VII, IX, X.
Diagnosis - prolonged INR, normal fibrinogen and normal/prolonged APTT that corrects on mixing with normal plasma

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38
Q

How does liver disease affect coagulation?

A
  • reduced synthetic function
  • reduced vitK absorption
  • reduced clearance of clotting factors
  • hyprfibrinolysis
  • thrombocytopenia
  • acquired platelet dysfunction
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39
Q

What is a massive transfusion and the clotting problems associated with it?

A

Transfusion of >50% of blood volume within 24 hours. Packed cells contain diluted amount of clotting factors and platelets

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40
Q

What is disseminated intravascular coagulation?

A

When blood is exposed to pro-coagulant factor (TF e.g.) causing massive thrombin generation, widespread coagulation and then fibrinolysis and depletion of clotting factors

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41
Q

In DIC what is the most common presentation and how is it confirmed?

A

Feature: bleeding - acute spontaneous from cannula site
Confirmation:
- prolonged INR and APTT that correct on mixing
- low fibrinogen, platelets
- RBC fragmentation, raised D-dimers

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42
Q

What are the bleeding symptoms in platelet disorders?

A
  • Mucocutaneous bleeding, oral, GI etc
  • bleeding after minor cuts
  • petechia common
  • immediate bleeding in procedures
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43
Q

What are the bleeding symptoms in clotting factor deficiencies?

A
  • deep tissue bleeding, joints, muscles
  • may develop hematomes
  • delayed bleeding
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44
Q

What are acquired, inherited and other risk factors for VTE?

A

Acquired - previous VTE, trauma, surgery, cancer, nephrotic syndrome, immobility
Inherited - antithrombin deficiency, protein S/C deficiency, prothrombin gene mutation
Other - elevated FVIII

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45
Q

What is antiphospholipid syndrome?

A

Acquired thrombophilic syndrome

  • evidence of antiphospholipid antibodies
  • venous or arterial thrombosis
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46
Q

What does thrombophilia screen involve?

A
  • antithrombin
  • protein C and S
  • prothrombin gene mutation
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47
Q

What is antithrombin involved in and what causes deficiency?

A

Majori inhibitor of thrombin and and factor Xa
Deficiency - autosomal dominant condition, results in 10x increase in thrombosis risk (can also be an acquired condition)

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48
Q

How is protein C involved in coagulation?

A

VitK dependent Anticoagulant protein that is enhanced by protein S, has anti-inflammatory actions, protects endothelial barrier function and enhances fibrinolysis
- autosomal dominant disorder = deficiency

49
Q

What is Factor V leiden mutation?

A

Point mutation that prevents protein C from inactivating factor V = constantly high Va levels

50
Q

What are clinical features of DVT?

A
  • swelling, redness, tenderness, pitting edema
51
Q

How can d-dimer be used in the diagnosis of DVT?

A

D-dimer not a specific test for VTE because elevated in infectionn, DIC, malignancy
Negative d-dimer can exclude CVT
Positive d-dimer - cannot confirm DVT

52
Q

Clinical features of PE

A
  • Chest pain
  • SOB
  • Cough/haemoptysis
  • Palpitations/syncope
53
Q

What are the treatment aims of VTE?

A
  • relieve symptoms
  • prevent PE
  • prevent death
  • prevent recurrence
  • prevent complications
54
Q

Complication of DVT

A

Post-phlebitic syndrome - chronic edema, pain and swelling in the leg causing ulceration and increased susceptibility to infection

55
Q

Complication of PE

A

Pulmonary HTN - will affect heart and lung function

56
Q

What are treatment options in DVT/PE?

A
  1. Parenteral anticoagulants:
    - unfractionated heparin (inpatient)
    - low molec weight heparin (outpatient)
    - fondaparinux
  2. Oral anticoagulants:
    - warfarin
    - new oral agents: dabigatran, rivaroxaban
  3. Aspirin
57
Q

What are the steps prior to blood transfusion to find a compatible donor?

A

Group, screen, crossmatch

58
Q

What is involved in grouping?

A

Tube agglutination - antiserum added to patient RBC and check for agglutination

Column agglutination - pre made cartridge of serums, add drop of RBC to each one (faster)

59
Q

What does screening involve?

A

Screen patient’s plasma for antibodies: patient plasma mixed with O RBC’s with antigens (Rh, Kel, Duffy etc)

60
Q

What is involved in the crossmatch?

A

Donor RBC mixed with patient plasma

61
Q

When should packed cells be tranfused?

A

When Hb <70 always transfuse, if 70-100 transfuse if symptomatic (normal

62
Q

What does fresh frozen plasma contain? does it need to be grouped?

A

Clotting factors fibrinogen, vWF - indicated for reduced factor production, XS factor consumption
- needs to be ABO grouped but not RhD grouped (AB suitable for all groups as there are no a/b)

63
Q

Which blood groups are the universal donor and recipient?

A

Universal donor - type O RhD -v

Universal recipient - type AB RhD +ve

64
Q

What are the immune complications of blood transfusion?

A
  1. febrile non-haemolytic transfusion reaction: cytokines a/b to donor WBC
  2. Acute haemolytic transfusion reaction: ABO/RhD incompatible blood
  3. Delayed haemolytic transfusion - a/b from previous alloimmunisation
  4. Allergic reaction: hypersensitivity to plasma proteins from donor
65
Q

What are less common but serious immune reactions to blood transfusion?

A
  1. TRALI - lung neutrophils activated by donor a/b - fever + resp distress
  2. Transfusion associated graft vs host disease
66
Q

What are non immune complications with blood transfusion?

A
  1. transfusion associated circulatory overload
  2. transmitted bacterial infection
  3. transmitted viral infection
67
Q

What percentage of blasts in the blood and bone marrow is normal?

A

blood - none

BM - 2-5%

68
Q

What are -ve and +ve symptoms in haematology?

A 
Negative
- no WBC - frequent infection
- no RBC - anaemic
- no platelets - bleeding, petechiae 
Positive
- Type B symptoms - weight loss, fever, night sweats seen in lymphoma and acute leukaemia
69
Q

What is left shift?

A

increase in the number of immature neutrophils in the peripheral blood, usually in the form of band neutrophils
- myeloblasts only in blood of those with cancer

70
Q

What are myeloproliferative disorders?

Examples

A

Hyperplasia disorders where there is an over-production of blood cells usually along one lineage due to acquired KINASE MUTATIONS

  • polycythaemia rubra vera
  • essential thrombocythaemia
  • myelofibrosis
  • chronic myeloid leukaemia
71
Q

What is polycythaemia rubra vera?

A

Myeloprolif: High haematocrit (too many RBC)

JAK2 kinase mutation in 95%

72
Q

What is essential thrombocythaemia?

A

Myeloprolif: too many platelets causing risk of bleeding and thrombosis

73
Q

What is myelofibrosis?

A

Fibrosis of the bone marrow

  • overgrowth of stromal cells
  • haematopoesis shifted to spleen - splenomegaly
74
Q

What is CML?

  • features
  • cause
  • treatment
A

Myeloprolif: high neutrophil count
- raised WCC with left shift
- weight loss, fatigue, headache
- massive splenomegaly
Cause: mutation on BCR-ABL gene of philadelphia chromosome
Treatment: Imatinib - competitively binds kinase domain of abnormal BCR-ABL, preventing further proliferation

75
Q

What are the types of acute leukaemia?

A

Neoplasia of BM stem cell

  1. acute myeloid leukaemia
    - acute promyelocytic L is a subtype where there is abnormal accumulation of immature granulocytes (promyelocytes)
  2. acute lymphoblastic leukaemia
76
Q

What is lymphoma and what are the common features?

A

Cancer of the immune system

  • almost always present with lump anywhere on the body
  • symptoms can mimic infection - B symptoms
77
Q

What proportion of lymphomas are B and T cell origin?

A

B cell - 80%

T cell - 20% and more chemo resistant

78
Q

Which lymphoma incidence doubled between 1980 and 2010? suggesting modern lifestyle is stressing our immune system

A

Non-hodgkin lymphoma

79
Q

What are causes of non-hodgkin lymphoma?

A 
Chemo/radiation
Immunosuppression 
AI disease
Infections 
Environmental
80
Q

Which chromosomal translocations are commonly associated with lymphoma? and what do they encode?

A 
Encode: immunoglobulin
Chromosomes - 2, 14, 22
•2p12 ->  light chain gene (IgK)
•14q32.3 -> heavy chain gene (IgH)
•22q11 ->  light chain gene (IgG)
81
Q

How is the germinal centre involved in lymphoma?

A

Germinal centres: mature B cells proliferate, differentiate and produce antibodies using Kappa, gamma, heavy chain. Immune system then determines if they have favourable binding, if not they apoptose.
- sometimes this goes wrong and during rapid proliferation, B cell picks up another gene resulting in lymphoma

82
Q

What were problems with the international working formulation in classifying lymphomas?

A
  • site of disease
  • B vs T cell origin
  • defining low grade NHL
  • new entities
83
Q

How did WHO/REAL classify B-cell neoplasms?

A
  1. precursor B cell neoplasm
  2. mature B cell neoplasm
    - - follicular lymphoma (35%)
    - - diffuse large B cell lymphomas (25%)
84
Q

What are the stages of lymphoma?

A

I - one lymph node region/lymphoid structure
II - 2+ lymph node regions on same side of diaphragm
III - lymph nodes on both sides of diaphragm
IV - involvement of extra nodal sites

85
Q

What investigations are done in lymphoma to determine staging?

A
  • open biopsy
  • blood tests
  • imaging PET
  • bone marrow biopsy
86
Q

What is the clinical spectrum of NHL? (0,2,6,10)

A

0 - small lymphocytic lymphoma (CLL)
2 - Follicular B cell NHL
6 - Diffuse large cell NHL
10 - Burkitt’s lymphoma

87
Q

What is the commonest type of lymphoma?

A

Follicular B cell NHL

  • incurable (7-15 year prognosis)
  • symptoms uncommon
88
Q

What is diffuse large B-cell lymphoma? and what does the international prognostic index measure to assess severity?

A 
Commonest aggressive lymphoma (many subtypes)
IPI:
A - age
P - performance status 
L - LDH (raised)
E - extra nodal disease (2+ sites)
S - stage (II, IV)
89
Q

What is the translocation causing Burkitt’s lymphoma and where does it commonly present?
Treatment?

A

t (8, 14) - associated with EBV
Rapidly growing mass in head, neck , abdomen in young adults
Treatment: intensive chemo = 80% cure

90
Q

How does mucosal associated lymphoid tissue lymphoma develop?

A

Chronic pylori infection causes lymphocytes to accumulate and they start to grow independently of H. pylori stimulation –> turns into MALT lymphoma

91
Q

What is the treatment for NHL?

A

Rituximab is a humanised antibody that binds CD20, which is expressed on B cells at most of their stages of development

92
Q

What is hodgkin lymphoma?

A

B cell lymphoma not expressing B cell surface antigens, presents with itch and large mediastinal mass
- large inflammatory response with Reed-Sternberg cells

93
Q

For HL and NHL, which is common, who is affected, and what % is nodal disease?

A

HL - uncommon, reed-sternberg cells, young and elderly, 90% nodal

NHL - common, elderly, varied cells, 60% nodal

94
Q

How does HL and NHL spread?

A

HL - contiguously

NHL - haematogenously

95
Q

What is the cure rate for HL?

A

> 80%

96
Q

What is multiple myeloma?

A

Neoplastic proliferation of plasma cells involving >10% of bone marrow with lytic bone lesions, hypercalcemia and renal failure
Usually presents as tumours masses spread throughout the skeletal system

97
Q

What do malignant plasma cells secrete? (in 95% of cases hence absence does not exclude diagnosis)

A

Monoclonal immunoglobulin called M protein

98
Q

What do the factors secreted by neoplastic plasma cells mediate?

A
  1. bone destruction/resorption

2. leads to hypercalcaemia

99
Q

What are the clinical features of MM?

A
  • Leukopenia, anaemia, thrombocytopenia (prolif. of plasma cells interferes with other cell production)
  • aberrant antibodies lead to impaired humeral immunity
100
Q

What is the CRAB presentation of MM?

A

hyperCalcaemia
Renal failure
Anaemia
Bone lesions

101
Q

Clinical scenario in which to consider MM?

A
  • unexplained normocytic anaemia
  • unexplained renal impairment
  • low trauma fracture
  • lytic bone lesion
  • unexplained hypercalcaemia
102
Q

How does MM affect neurological processes?

A
  • muscle weakness and pain
  • vertebral fracture - radiculopathy
  • spinal cord compression
103
Q

What are general processes in MM that affect the body?

A
  1. Amyloidosis - accumulation of free light chains that infiltrate any system
  2. Hyperviscocity - headaches, stroke, angina
  3. Weight loss
104
Q

How is the diagnosis of MM made?

A
  1. serum or urinary monoclonal protein
  2. presence of clonal plasma cells in BM or plasmacytoma
  3. Presence of end-organ damage related to plasma cell abnormalities
105
Q

What is the treatment for MM?

A

Its non-curative

  • improve quality of life, slow progression and complications
  • autologous stem cell transplant
106
Q

Which patients with MM are transplant eligible? and what do they receive?

A

patients if <70 yrs and no major comorbidities

- chemotherapy, proteasome inhibitor and autologous transplant

107
Q

What is chronic lymphoblastic leukaemia?

A

Indolent disease with clonal malignancy of mature B-cells (>5000 lymphocytes per mm3)

108
Q

What is the difference between CLL and small lymphocytic lymphoma (SLL)?

A

CLL - blood and bone marrow involved

SLL - lymph nodes involved, minimal blood or bone marrow involvement

109
Q

What are the clinical features of CLL?

A
  • 25% asymptomatic
  • Lymphadenopathy, hepatomegaly and splenomegaly common
  • 5-10% have B symptoms
  • immune disregulation
  • bone marrow failure
110
Q

What would CLL investigations show?

A

FBC - clinical ppn of CLL lymphocytes >5x10^9/L
Blood film - small lymphocytes
Bone marrow aspirate - >30% nucleated cells are lymphocytes

111
Q

What is the diagnostic criteria for CLL, SLL and monoclonal B cell lymphocytosis?

A

CLL: B cell >5x10^9/L in peripheral blood

SLL: B cell <5x10^9/L in peripheral blood + lymphadenopathy + splenomegaly

Monocloncal B cell lymphocytosis: B cell < 5x10^9/L in peripheral blood, no lymphadeno. or splenomegaly + no disease related symptoms

112
Q

What is the prognosis of CLL determined by?

A

Rai staging
Cytogenetic status

Low risk -> lymphocytosis in blood and bone marrow only

Intermediate risk -> lymphocytosis with enlarged nodes in any site or splenomegaly, hepatomegaly

High risk -> lymphocytosis with disease-related anaemia (<110 g/L) or thrombocytopenia (<100 x 109/L)

113
Q

What are the complications of CLL

A
  1. impaired cell mediated and humeral immunity
  2. Autoimmune cytopenias
  3. Transformation to high grade lymphoma
114
Q

Treatment for CLL

A
  • most don’t require treatment
    Indications for treatment: disease related symptoms, progressive marrow failure/lymphadenopathy/splenomegaly
  • although incurable, symptomatic patients treated with chemo, immunotherapy with antibodies against proteins on CLL cells

Young/fit: FCR fludarabine + cyclophosphamide + rituximab
Old/unfit: BR bendamustine + rituximab

115
Q

Blood film and bone marrow findings in macrocytic anaemia

A

Blood film - low RCC, Macrocytosis, hyperhsegmented neutrophils

Bone marrow - giant pronormoblasts and metamyelocytes

116
Q

Which leukaemia is more common in children and adults?

A

Children - ALL

Adults - AML

117
Q

Role of JAK-2 and which conditions it is often mutated in

A 
Pathway signalling, EPO binding, stem cell differentiation 
Hyperplasia/myeloproliferative disorders
- PRV
- ET
- MF
118
Q

What is pathognomonic to CLL/SLL

A

Activated lymphocytes gather in loose aggregates called proliferation centres

HAEM/IMMUNOLOGY (5 decks)

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