Haematology Flashcards
FBC
Full blood count
WBC
White blood count
Leucocytes
White blood cells. Includes polymorphs, lymphocytes and monocytes.
Blood film
Stained smear for light microscopy inspection.
WBC differential
WBC differential may be obtained from inspection of the blood film or directly from the haematology FBC analyser. This determines the number of polymorphs, lymphocytes and monocytes in the total WBC.
Monocytes
Circulating phagocytic cells will become tissue macrophages.
Polymorph
The polymorphnuclear leucocyte.
Granulocyte
Cells with 2-5 nuclear lobes and granules in the cytoplasm. Staining characteristics of the granules identify:
NEUTROPHILS: neutral staining granules in cytoplasm.
BASOPHILS: basophilic granules. Basophils migrate to the tissues to become Mast cells.
EOSINOPHILS: eosinophils granules.
Neutrophilia
Increased neutrophils.
Neutropenia
Decreased neutrophils.
Lymphocytosis
Increased lymphocytes
Activated lymphocytes
Often seen in viral infections
Atypical mononuclear cells
Atypical reactive (CD8) lymphocytes in certain infections such as glandular fever and viral hepatitis.
Thrombocytopenia
Reduced platelets
Thrombocytosis
Increased platelets
Hypochromic microcytic
Poorly haemoglobinsed and small RBCs (decreased MCH, decreased MCV). Seen in iron deficiency, chronic disease and thalassaemia trait.
MCV/MCH
Mean corpuscular volume (RBC size). Mean corpuscular Hb content.
Reticulocytes
immature RBCs. Normally <2% of RBCs. No nucleus but some persisting RNA. Polychromatic (blue-purple) appearance in the blood film.
Rouleaux
RBC columns seen in samples with raised globulin or raised fibrinogen levels ie. myeloma, chronic inflammation/infection.
Target cells
RBC appearance frequently seen in liver disease (particularly in biliary obstruction), also seen in haemoglobinopathies
Spherocytes
Spherocytic RBCs seen in haemolysis particularly autoimmune haemolytic anaemia (AIHA) and hereditary spherocytosis
Howell-Jolly Bodies
Nuclear fragments in RBC in hyposplenic patients.
Macrocytes
Large RBCs (increase in MCV) seen in B12/folate deficiency, hepatic disease, hypothyroidism.
Anisopoiklocytosis
Abnormalities of RBC shape and size seen in B12/folate deficiency.
RBC fragmentation
Seen in mechanical haemolytic anaemias eg. prosthetic valve malfunction.
Haemoglobinopathy
Abnormality of globin synthesis.
Direct Coombs Test
Test to detect presence of antibody on RBC surface (positive in AIHA, HDN).
Erythroblasts
Nucleated RBC prescursors
Megaloblasts
The abnormal nucleated RBC precursors seen in B12 or Folate deficiency.
Megakaryocytes
Platelet precursors
Bone marrow aspirate
Aspiration of marrow granules to provide cellular detail.
Bone marrow trephine biopsy
Removal of core of bone and marrow provides detail of architecture and infiltration.
Leukaemic blasts
The abnormal primitive blast cells that are found in the bone marrow (and often also in the peripheral blood) in Acute leukaemia and poor prognosis myelodysplastic syndromes.
AML
Acute Myeloid Leukaemia (the more common acute leukaemia seen in adults).
ALL
Acute Lymphoblastic Leukaemia (more common in children).
CML
Chronic Myeloid Leukaemia
CLL
Chronic Lymphatic Leukaemia
Myelodysplastic syndromes
Describes the bone marrow appearance when abnormal (dysplastic) cell growth occurs. Previously called pre-leukaemic as MDS can progress to secondary AML.
Myeloproliferative
Describes proliferation of cells in the bone marrow with normal (non dysplastic) appearance. CML, polycythaemia Vera, Essential thrombocythaemia and myelofibrosis.
Myeloma
Malignant proliferation of plasma cells in the bone marrow. Note this is a lymphoproliferative disease NOT a myeloproliferative disease.
PT
Prothrombin time. Test of extrinsic pathway of coagulation sensitive to Warfarin and liver disease.
INR
International Normalised Ratio. Measure of warfarin activity.
PTT
Partial Thromboplastin Time. Also known as APTT (activated PTT) and KCCT (Kaolin Cephalin clotting time). Measure of intrinsic pathway sensitive to IV Heparin.
Coagulation
Term to describe the coagulation cascade and the pathways (extrinsic and intrinsic) that lead to the conversion of Fibrinogen to Fibrin. Do not confuse with the term Agglutination which describes RBCs being stuck together (agglutinated) by RBC antibodies.
Purpura/Petechiae
Pin point bleeding on skin and mucous membranes. Usually due to thrombocytopenia or less commonly vasculitis (the glass test: purpura does not blanch on pressure. Telangiectasia will blanch).
Ecchymoses
Bruises
DIC
Disseminated Intravascular Coagulation. Consumption of coagulation factors and platelets.
Factor concentrates
Freeze dried coagulation factors. Can be prepared from donated plasma (ie. Beriplex: contains factors II, VII, IX, X for warfarin reversal) or by recombinant technology ie. Recombinant F VIII for Haemophilia A).
Group and screen
Determine ABO and Rh group. Screen plasma for immune RBC antibodies.
Packed RBCs
Units of blood from which most plasma has been removed.
FFP
Fresh Frozen Plasma.
PPS
Plasma Protein Solution (Albumin 5%).
20% Albumin
Salt poor high Albumin
Cryoprecipitate
Prepared from donated plasma. Rich in F VIII and fibrinogen.
Indirect Coombs Test
Test to detect the presence of RBC antibodies in plasma. This test is the basis of the cross match and antibody screen in group and screen.
What is the management plan of splenic injury?
Conservative, interventional radiology or splenectomy.
What is the definition of a ‘major haemorrhage’?
Loss of more than one blood volume within 24 hours (around 70mL/kg, >5litres in a 70kg adult). 50% of total blood volume lost in less than 3 hours. Bleeding in excess of 150ml/minute.
What is in a ‘major haemorrhage pack’?
6U PRC (packed red cells), 4U of FFP (fresh frozen plasma) and 1 pooled platelets.
What are some of the complications of major haemorrhage?
Hypothermia, acidosis, coagulopathy, hypocalcaemia.
Name some hereditary conditions that impair bone marrow function
Thalassaemia, sickle cell anaemia, fanconi anaemia, dyskeratosis congentia, hereditary leukemia (very rare).
Name some acquired conditions impairing bone marrow function
Aplastic anaemia, leukaemia, myelodysplasia, metastatic malignancy, infections, chemotherapy.
Name 3 classical myeloproliferative disorders
Polycythaemia rubra vera, essential thrombocytosis and myelofibrosis.
What are the high risk features for Essential Thrombocytosis?
Aged over 60 years old and one or more risk factors- platelets >1500x10^9/l, previous thrombosis or thrombotic risk factors eg. diabetes or hypertension.
What are the first and second line treatments for essential thrombocytosis?
First line= hydroxycarbamide and aspirin
Second line= anagrelide and aspirin
What are myelodysplastic syndromes?
Characterised by dysplasia and ineffective haemopoiesis in greater than or equal to 1 of the myeloid series. May be secondary to previous chemo pr radiotherapy. Often associated with cytogenic abnormalities.
What is the method of inheritance of Fanconi’s anaemia?
Autosomal recessive.
What are the characteristics of Fanconi’s anaemia?
Somatic abnormalities, bone marrow failure, short telomeres, malignancy, chromosome instability.
Autologous transplant “autograft”
Uses the patients own blood stem cells.
Allogenic transplant “allograft
Any transplant in which the stem cells come from a donor.
Syngeneic transplant
Transplant between identical twins.
Allogenic sibling
HLA identical
Haplotype identical
A half matched family member. Usually a parent or half matched sibling.
Volunteer unrelated
Also known as matched unrelated.
What are the main indications for autologous stem cell transplantation?
Relapsed Hodgkin’s disease, non-hodgkin’s lymphoma and myeloma.
How are autografts collected?
Patients receive G-CSF +/- chemotherapy to make the stem cells leave the bone marrow so that the can be collected from the blood. Mobilised peripheral blood stem cells are harvested by apheresis.
What are the main indications for an allogenic stem cell transplant?
Acute or chronic leukaemias, relapsed lymphoma, aplastic anaemia and hereditary disorders. Allografts can be full intensity “myeloablative” or reduced intensity “mini” transplant.
What are the advantages and disadvantages of umbilical cord blood transplant?
Advantages:
-More rapidly available than volunteer unrelated donor.
-Less rigorous matching to patient type as immune system naive.
Disadvantages:
-Small amount-adults will often require a double cord transplant.
-Slower engraftment
-If relapse, cannot go back for donor lymphocyte infusion
How does graft vs. host disease most commonly manifest?
As a skin rash, jaundice or diarrhoea.
What is the difference between acute versus chronic GvHD?
Acute is less than 100 days since transplant and chronic is over 100 days since transplant.
What clotting factors are vitamin K dependent?
Factors II, VII, IX and X (2,7,9 and 10). Vitamin K is found in green vegetables, liver and eggs.
What is primary haemostasis?
Recruitment of platelets to the site of damage.
What is secondary haemostasis?
Activation of coagulation factors. Initiation- extrinsic pathway. Propagation- intrinsic pathway. Thrombin generation. Fibrin production- the clot.
What makes up the prothrombinase complex?
Activated factor 5 and factor 10.
What is light transmission aggregometry used for and how does it work?
Used to assess platelet function.In the aggregometer, PPP is stirred in a cuvette at 37°C and the cuvette sits between a light course and a photocell. When an agonist is added the platelets aggregate and absorb less light and so the transmission increases and this is detected by the photocell.
How can you assess primary haemostasis?
In vivo- bleeding time (old fashioned). Ex vivo- FBC (platelet count) and platelet function tests- light transmission aggregometry.
How can you assess secondary haemostasis?
Prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin clotting time (TCT_ and individual coagulation factor assays.
What is the prothrombin time (PT) testing and how is it done?
PT stimulates the activation of the extrinsic pathway. Thromboplastin is added to patients plasma, warm to 37 degrees, add calcium and calculate time to form clot. Normal range 10-13 seconds. Normal ratio 1.0-1.2.
What is the International Normalised Ratio (INR)?
Standardised form of prothrombin time. A patients INR is identical in any lab. Result is factored by International Sensitivity Index.
What is the activated partial thromboplastin time (APTT) testing and how is it done?
APTT stimulates activation via the intrinsic pathway. Patients plasama, add contact factor (Kaolin or silica) and phospholipid ‘partial thromboplastin’. Warm to 37 degrees. Add calcium, calculate time taken to clot. Normal 26-38 seconds.
What is the Thrombin Clotting Time (TCT) test and how is it done?
Measurement of conversion of fibrinogen to fibrin clot. Patients plasma plus bovine thrombin (less calcium or phospholipid dependent), time to clot. Normal 10-16 seconds.
What is a normal APTT time?
26-38 seconds.
What is a normal PT time?
10-13 seconds.
What will prolong the thrombin clotting time?
Inhibitors of thrombin (heparin, dabigatran), FDPs, inhibitors of fibrin polymerisation (paraproteins).
What are the 3 types of antithrombotic agents?
1) Anticoagulants- inhibit one or several components of the coagulation cascade.
2) Fibrinolytic agents- enhance lysis of fibrin clot.
3) Anti-platelet agent- inhibit platelet activation or aggregation.
What do anticoagulants do?
Inhibit one or several components of the coagulation cascade- inhibit formation of fibrin clot. Heparin and Fondaparinux. Warfarin. DOACs.
Heparin MOA
Given as an injection. Augments activity of endogenous antithrombin. Does not cross the placenta. Has a short half life. Can be unfractioned (UFH) or low molecular weight (LMWH).
DOACs
Direct Oral Anti-Coagulants (DOACs). Factor IIa inhibitor= dibigatran. Factor Xa inhibitors= rivaroxaban, apixaban, edoxaban.
What are the contraindications for all DOACs?
Pregnancy and breast feeding, liver disease with cirrhosis +/- coagulopathy and some drugs.
What drug reverses Dabigatran (DOAC, factor IIa inhibitor)?
Idarucizumab
What are the 2 main types of fibrinolytic drugs?
1) Kinases eg. streptokinase, urokinase
2) Tissue plasminogen activators (tPA) eg. Alteplase, Tenectaplase, Reteplase
What breaks down fibrin into fibrin degradation products?
Plasmin
MOA of kinases
Bind to plasminogen (both clot bound and free) to release plasmin and break down fibrin. Since it releases plasmin throughout body it increases the bleeding risk significantly. Half life short 15-20 minutes. Give a bolus dose then infusion.
Streptokinase
A fibrinolytic. Derived from streptococci bacteria. Antigenic- recent strep infection/previous use of streptokinase can lead to use of streptokinase being ineffective.
Tissue plasminogen activators MOA
Activates plasminogen. Plasmin cleaved from plasminogen. Relatively selective for clot bound plasminogen= minimal unwanted fibrinogenolysis.
When are tPAs used?
- For acute MI when patients not suitable for PCI- within 12 hours of onset.
- Ischaemic stroke (alteplase)-within 4.5 hours of onset
- Massive PE with haemodynamic instability (alteplase)- reduces thrombus size and cardiac strain.
What is the main side effect of tPAs?
Significant risk of haemorrhage, any organs- particularly intracerebral.
List some absolute contraindications to thrombolysis
- Haemorrhagic stroke history
- Ischaemic stroke in previous 6 months
- CNS damage
- Major trauma/surgery/head injury within past 3 weeks
- GI bleeding within last month
- Aortic dissection
What are the pros to using catheter directed thrombolysis?
Smaller doses, administered directly into vessel containing thrombosis, less systemic effect. Can be used in acute limb ischaemia, massive DVT, blocked central venous catheter.
MOA of Clopidogrel (anti-platelet)
Irreversibly blocks ADP receptor. This decreases expression of GPIIIb/IIIa a receptor which binds fibrinogen. Lower expression means reduced binding of fibrinogen.
MOA of Abciximab or Tirofiban (anti-platelet)
GPIIb/IIIa antagonists. They are monoclonal antibodies that antagonise the GPIIb/IIIa receptor. Leads to reduced platelet aggregation and reduced binding of fibrinogen.
MOA of aspirin.
Irreversible inhibition of cyclooxygenase. Blocks the conversion of arachidonic acid into thromboxane A2. Leads to decreased platelet activation.
MOA of Dipyridamole
Phosphodiesterase III inhibitor. Increased platelet concentration of cAMP. cAMP leads to platelet responsiveness to ADP. Reduced platelet aggregation.
Indications for anti-platelet drugs
CV disease, Acute MI, secondary prevention CVD. Cerebrovascular disease (without AF), peripheral vascular disease, acute stroke/TIA/secondary prevention.
What is Disseminated Intravascular Coagulation (DIC)?
Condition in which small blood clots develop throughout the bloodstream, blocking small blood vessels. The increased clotting depletes the platelets and clotting factors needed to control bleeding, causing excessive bleeding.
Causes of Disseminated Intravascular Coagulation?
Sepsis, malignancy, massive haemorrhage, severe trauma, pregnancy complications eg. pre-eclampsia, placental abruption, amniotic fluid embolism.
What can we do when INR is too high?
Stop warfarin or reduce dose. Give vitamin K (oral or IV). Give coagulation factors (II, VII, IX, X). Prothrombin complex concentrates- beriplex, octaplex.
What is Haemathrosis?
Haemarthrosis is a bleeding into joint spaces. It is a common feature of Hemophilia.
Haemophilia A
Classical haemophilia. Factor VIII deficiency. Incidence 1/20,000. X-linked inheritance. Prolonged APTT.
What is the role of Von Willebrand factor?
Facilitates platelet adhesion and aggregation in primary haemostasis and binds FVIII and prolongs its half life in plasma (influences secondary haemostasis).
Von Willebrand disease
Most common mild bleeding disorder. Mostly autosomal dominant with variable penetrance. Mucosal type bleeding pattern. Reduced VWF +/- reduced platelet aggregation +/- reduced FVIII.
Primary classification of Von Willebrand disease
Type 1- partial quantitive deficiency (not enough made).
Type 2- qualitative deficiency of VWF (made but doesn’t work).
Type 3- virtually complete deficiency of VWF.
How do you treat bleeding in patients with inherited platelet disorders?
Pressure, tranexamic acid/desmopressin. Platelet transfusion (HLA matched), rFVIIa.
Bernard Soulier Syndrome
Inherited platelet disorder. Absent/defective GP IIb/V/IX. Macrothrombocytopenia.
Glansmanns thrombasthenia
Absent/defective GP IIb/IIIa. Normal platelet count.
Inherited thrombophilia
1) Deficiencies of natural anticoagulants- antithrombin, protein C, protein S.
2) Specific genetic mutations- factor V Leiden, Prothrombin gene mutation.
Lupus anticoagulant
Phospholipid dependent antibody. Causes prolonged APTT. If persistent may be associated with prothrombotic state. Persisting lupus anticoagulant + thrombosis (or recurrent fetal loss)= antiphospholipid syndrome.
What enzymes contain iron?
Cytochromes, peroxidases, xanthine oxidase, catalases, RNA reductase.
What is hepcidin and how does it work?
It is the ‘low iron’ hormone. It reduces the levels of iron in plasma. Hereditary hameochromatosis due to loss of hepcidin. Hepcidin binds ferroportin and degrades it- reducing iron absorption (enterocyte) and decreasing iron release from RES. Hepcidin is synthesised in the liver.
What are the causes of hypochromic microcytic red blood cells?
1) Iron deficiency anaemia- not enough hame
2) Thalassaemia- not enough globin
3) Anaemia of chronic disease
4) Sideroblastic anaemia (particularly congenital SA).
What is latent iron deficiency?
When serum ferritin is low, RES iron stores are low but haemoglobin is normal. 20% of females have this.
When might it be difficult to diagnose iron deficiency anaemia?
If someone has RA/IBD as ferritin is an acute phase protein which can be raised in these patients event though the patient has IDA.
Signs of IDA
Koilonychia, atrophic glossitis, angular stomatitis.
Causes of IDA
1) Dietary- premature neonates and adolescent females.
2) Malabsorption (eg. in coeliac)
3) Blood loss (major cause)
What sort of drugs can cause iron loss from bowels?
Aspirin and NSAIDs.
When would you give IV iron as a treatment for IDA instead of oral iron?
Intolerant of oral iron, if you worry about their compliance, if they are on renal replacement.
What is anaemia of chronic disease and what are its causes?
It is failure of iron utilisation- iron is trapped in the RES. Hepcidin levels are high. Causes:
- Infection
- Inflammation eg. Crohn’s disease
- Neoplasia
Anaemia of chronic renal failure
Anaemia of chronic disease and low levels of erthyropoetin.
How is B12 absorbed?
Binds to intrinsic factor. Absorbed in terminal ileum. Binds to transcobalamin.
What is a dietary source of folate?
Green veg (destroyed by cooking).
What is ineffective erythropoiesis?
Death of mature cells whilst still in marrow. Due to B12 or dietary folate deficiency.
What does clinical B12 deficiency cause?
Megaloblastic anaemia (sometime leucopenia, thrombocytopenia). Bilateral peripheral neuropathy or demyelination of the posterior and pyramidal tracts of the spinal cord.
What is pernicious anaemia?
The most common cause of vitamin B12 deficiency in the UK. Pernicious anaemia causes your immune system to attack the cells in your stomach that produce the intrinsic factor, which means your body is unable to absorb vitamin B12.
Causes of B12 deficinecy
Not enough dietary intake, pernicious anaemia, removal of stomach, Crohn’s affecting terminal ileum-prevents absorption.
What are thalassaemias?
Relative lack of normal globin chains due to absent genes.
Beta thalassaemia major
Missing both beta globin genes. Autosomal recessive. Unable to make adult haemoglobin. Significant dyserythropoiesis (defective development of RBC). Often have big spleens. Transfusion dependent from early life.
Pathogenesis of sickle cell disease
Single amino acid substitution on Beta globin gene at position 6 (chrom 11). Glutamine to valine= HbS. End up with 2 alpha and 2 beta (sickle) chains= a2Bs2
What is the clinical result of sickle cell anaemia?
Reduced red cell survival (might only last 10 days) and vaso-occlusion- tissue hypoxia/infarction. It’s a multisystem disease- can affect everywhere.
What is haemolytic anaemia?
Anaemia related to reduced RBC lifespan. No blood loss, no haematinic deficiency.
What is a compensated haemolytic state?
Red cell lifespan is reduced (20-100 days) but haemoglobin is maintained at a normal level.
What is hereditary spherocytosis?
Abnormality of RBC membrane- congenital haemolytic anaemia. Autosomal dominant. RBC spherocytic and polychromatic. Don’t always need treatment but if so splenectomy and hyposplenic prophylaxis.
What are the types of congenital haemolytic anaemia?
1) Abnormalities of RBC membrane
2) Haemoglobinopathies
3) Abnormalities of RBC enzymes
Glucose 6 phosphate dehydrogenase deficiency
Congenital haemolytic anaemia. Acute episodic intravascular haemolysis. X linked recessive. Acute haemolysis from oxidative stress: Favism (Fava beans) and drugs: anitmalarials, sulphonamides and others.
Acquired haemolytic anaemias
1) Autoimmune- warm type (IgG), cold type (IgM).
2) Isoimmune- haemolytic disease of newborn (HDN).
3) Non immune- fragmentation haemolysis.
What is the Direct Coombs test used for?
To detect the presence of antibodies (+/- complement) on RBC surface in warm haemolytic anaemia. Positive in AIHA but also in haemolytic disease of the newborn..
What is haemolytic disease of the newborn?
Also known as erythroblastosis fetalis, is an alloimmune condition that develops in a peripartum fetus, when the IgG molecules produced by the mother pass through the placenta.
What are Auer rods?
Auer rods are clumps of azurophilic granular material that form elongated needles seen in the cytoplasm of myeloid leukemic blasts. Seen in acute myeloid leukemia.
What is lymphoma?
Malignancy derived from lymphocytes: B lympocytes, T lymphocytes, natural killer cells. Unlike leukemia it generally presents with a tumour mass. most commonly develops in lymph nodes.
What are the risk factors for lymphoma?
Immuno-suppressive disorders/treatment (organ transplantation, HIV). Infections (EBV, H. pylori). Age. Having a close relative with lymphoma.
What is a Reed Sternberg cell and when is it found?
Large, abnormal lymphocytes that may contain more than one nucleus type of cell that appears in people with Hodgkin disease. The number of these cells increases as the disease advances.
What is plasma cell myeloma?
Plasma cells are immunoglobulin producing cells. Plasma cell myeloma is a neoplastic proliferation of plasma cells in bone.
How do you stage lymphoma?
Ann-Arbor classification system. Stages 1-4 plus minus A/B.
What is follicular lymphoma?
Commonest subtype of low grade lymphoma- associated with t14;18 translocation. B cell lymphoma. Often presents with stage 4 disease. Indolent clinical course, usually incurable.
How do you treat follicular lymphoma?
Early stage 1A and some 2A- localised radiotherapy. Advanced stage- asymptomatic, no bulk- watch and wait. Advanced stage- symptomatic and/or organ compromise- immunochemotherapy. Rituximab (anti CD20) and chemo. Followed by maintenance rituximab.
What is diffuse large B-cell lymphoma?
High grade lymphoma. Commonest subtype of NHL. Biologically heterogeneous group of B cell lymphomas- associated with various translocations and genetic abnormalities; complex karyotype. Wide variation in presentation. Aggressive but curable in over 50%.
What is R-CHOP chemotherapy and for what condition is it used?
R: Rituximab C=Cyclophosphamide H=Adriamycin (Doxorubicin) O=Vincristine P=Prednisolone Used in the treatment of diffuse large B cell lymphoma. It is given on day 1 of a 21 day cycle.
What is Burkitt lymphoma?
High grade lymphoma. Characterised by translocations involving MYC gene. Usually short history, marked B symptoms, rapidly growing tumours with massive tumour bulk. Most cases present with extranodal disease.
Tumour lysis syndrome in Burkitt’s lymphoma
A prototype of high grade non-Hodgkin lymphoma characterized by high tumor burden. It is exquisitely chemosensitive, and responds well to treatment. Rapid cell lysis leads to release of massive amounts of breakdown products giving rise to the so called “tumor lysis syndrome” with acute renal failure (ARF).
Classic Hodgkin Lymphoma presentation
Bimodal age incidence, usually presents with painless lymphadenopathy. Spreads from one nodal group to immediately adjacent nodes then later haematogenenous spread to liver, lungs, BM. May have B symptoms. Itch may precede diagnosis for many months.
What chemo is given in Hodgkin lymphoma?
A= Adriamycin (doxorubicin) B=Bleomycin V=Vinblastine D=Dacarbazine Given on days 1 and 15 of 28 day cycle.
What is a ‘paraprotein’?
An abnormal ‘monoclonal protein’ produced by abnormal plasma cells in myeloma. Also called an ‘M’ protein.
What is the classical triad of myeloma?
1) Increased plasma cells in bone marrow
2) Clonal immunoglobulin or paraprotein
3) Lytic bone lesions
What do bisphosphonates do in myeloma?
Given for the lytic bone lesions. Reduces pain, reduces pathological fractures, reduces hypercalcaemia, reduces need for radiotherapy.
MGUS
Monoclonal gammopathy of undetermined significance
What are the potential immune complications of chronic lymphocytic leukaemia?
Autoimmune haemolytic anaemia= 5-10%. Autoimmune thrombocytopenia <5%. At presentation or precipitated by treatment.
