Week 3 Haematology Flashcards

Question

Acquired haemolytic anaemia

Answer 1

1. **Autoimmnune** - Warm type (IgG) - Cold type (IgM) 2. **Isoimmune** (antibodies from something else .e.g mother) - haemolytic disease of newborn 3. **Non-immune** - fragmentation haemolysis

Answer 2

IgM autoantibodies bind to RBC membrane, leading to its destruction Causes: Primary (idiopathic) Secondary: Mycoplasma pneumoniae, infectious mononucleosis (glandular fever), lymphoproliferative disorders Clinical features: painful fingers/toes assoc with cold exposure Treatment: Mycoplasma - self limiting Keep warm

Answer 3

Autoantibody IgG attaches to RBC membrane, causing destruction. Damaged RBCs become spherocytic (RBCs round, rather than biconcave, no central pallor, smaller) and polychromatic. Phagocytosed by RES, esp. spleen, causing enlargement Causes: Idiopathic Lymphoproliferative disorders - CLL, Non Hodgkin's lymphoma Drugs e.g. cephalosporins SLE Management: Corticosteroids - Prednisolone Folic acid Blood transfusion Splenectomy Risks of splenectomy: increase risk of *Strep. pneumoniae, Haemophilus Influenzae, Neisseria Meningitidis* causing overwhelming post splenectomy infections - Penicillin prophylaxis required

Answer 4

Detects antibody on RBC surface Anti-IgG added to patient's RBCs Agglutination occurs, if there are RBCs are coated with IgG antibodies, present Postive - AIHA, HDN (haemolytic disease of newborn. IgG antibodies produced by mother, target antigens on RBCs of fetus)

Answer 5

Detect antibodies in serum Anti-IgG and test RBCs mixed with pt's serum. Agglutination occurs if serum antibodies present Blood transfusion - antibody screening, cross-matching

Answer 6

Myeloproliferative disorder BM filled with fibrous tissue

Answer 7

**1. Abnormalities of RBC membrane** Hereditary spherocytosis - AD, RBCs are spherocytic and polychromatic (increased reticulocytes) Jaundice Splenomegaly **2. Haemoglobinopathies** **3. Abnormalities in RBC enzymes** Pyruvate kianse deficiency anaemia - AR, extravasuclar haemolysis, ATP depletion Glucose 6 phosphate dehydrogenase deficiency: - X-linked recessive, acute episodic intravascular haemolysis - acute haemolysis from oxidative stress e.g. drugs - anti-malarials

Answer 8

IDA Thalassaemia ACD Siderblastic anaemia

Answer 9

Inherited conditions where there is a lack of globin chains due to absent genes (thalassaemias) or abnormal globin chain (sickle cell)

Answer 10

Globin chains produced on ribosomes Adult Hb (HbA) made up of 2 alpha and 2 beta chains - 4 alpha globin genes (chromosome 16) and 2 beta globin genes (chromosome 11) Feotal Hb (Hb F) made up of 2 alphas and 2 gammas

Answer 11

Beta thalassaemia major (missing 2 genes) - unable to make adult Hb - significant dyserythropoiesis Clinical features: Maxillary prominence Skulls thicker Enlarged spleen

Answer 12

Relative lack of globin genes Normally 4 alpha and 2 beta globin genes Alpha thalassaemias: A+thal trait (missing one gene): mild microcytosis Homozygous a+ thal trait (missing two): mild microcytosis, mild anaemia HbH disease (missing 3): significant anaemia, abnormal shaped RBCs Alpha thal major (missing 4): incompatible with life Treatment: Transfusion Iron chelators - as iron overload major cause of mortality

Answer 13

Missing 3 alpha genes As there is not enough alpha globin chains, causes excess beta globin chains Beta chains join up together becoming a tetramer (HbH) Blood transfusion required during stress

Answer 14

Includes Sickle cell disease, Hb C, D, E Sickle cell pathogenesis: Point mutation on beta globin chain (glutamine to valine) at position 6 leads to: - RBCs becoming rigid, and occluding blood vessels leading to tissue infarction - RBCs have reduced life span (10d) Clinical features: Brain - stroke, moya moya Lungs - pulmonary hypertesnsion Urogenital - priapism (maintain erection) Management: Hydration, analgesia, prophylactic vaccinations, O2, fluids, blood transfusion

Answer 15

Blood vessel damage, disrupts endothelium Exposure of tissue factor and collagen Primary haemostasis (platelets recriuted) Secondary haemostasis (coagulation factors activated)

Answer 16

**Primary haemostasis:** When endothelium damaged, exposes **collagen and tissue factor** Platelets have receptors (**GPIb**) which bind to **von Willebrand factor** allowing platelets to **adhere** to vessel wall Platelets release granular contents (ADP, thromboxane A2) ADP allows expression of **GPIIb/IIIa** on platelets, which allows them to **aggregrate** with each other, and with **fibrinogen,** forms a **weak platelet plug** Phospholipid is exposed on surface of platelets **Secondary haemostasis** Coagulation cascade is activated Events: Intiation - extrinsic pathway (due to TF) Propagation - instrinsic pathway (due to subenothlelial collagen) Thrombin generated, converts fibrinogen to fibrin, which is cross-linked to form stable platelet plug.

Answer 17

**Intrinsic pathway (PTT)** Subendothelial collagen Factor 12, 11, 9, 8 **Extrinsic pathway (PT)** Tissue factor Factor 7 **Common:** 10, 5, 2 (thrombin), 1 (fibrin) Factor 10, 5, 2 (prothrombin complex) Factor XIIIa (13a) allows crosslinking of fibrin Every step requires phospholipid and Ca2+

Answer 18

- Tissue factor pathway inhibitor: inhibits TF and Xa - Thrombomodulin activates protein C to APC (activated protein C) Protein C and Protein S inactivate factor V + VIII (5, 8) Antithrombin inactivates factor 7, 5, 2,

Answer 19

As fibrin made, stimulates uPA and tPA which activates plasminogen to plasmin Plasmin breaks down fibrin to fibrin degradation products e.g. D-dimer a2-antiplasmin: regulates plasmin production Plasminogen activator inhibitors: inhibits uPA and tPA TAFI (thrombin activateable fibrinolysis inhibitor): inhibits uPA and tPA, reduces breakdown of fibrin

Answer 20

Assess primary haemostasis in vivo: bleeding time ex vivo: FBC (platelet count), platelet function (assessed by light transmission aggregometry) Assess secondary haemostasis: Prothrombin time (PT) Activated partial thromboplastin time (APTT) Thrombin clotting time (TCT)

Answer 21

Take sample of blood, place in citrate tube (chelates Ca2+, stopping blood from clotting) Cetrifuged creating platelet poor plasma Ca2+ added to PPP Clot forms How long clot formed measured) **Prothrombin time - extrinsic pathway and common** (1.0-1.2) depends on: - Factors VII Factors X, V, II and fibrinogen INR (international normalised ratio) - standardised form of PT Activated partial thromboplastin time - intrinsic pathway depends on: - Factors XII, XI, IX, VIII - Factors X, V, II and fibrinogen Thrombin clotting time (TCT): measures conversion of fibrinogen to fibrin Depends on: - How much fibrinogen present - How well fibrinogen functions Prolonged by: Thrombin inhibitors (heparin) Inhibitors of fibrin polymerisation (paraproteins)

Answer 22

Anti-coagulants - inhibit coagulation factor Anti-platelets - inhibits platelet aggregration Fibrinolytic agents - Enhances lysis of fibrin clot

Answer 23

Inhbits formtion of fibrin clot Heparin - inhibits Xa, thrombin (IIa) Warfain - Vit K antagonist, inhibits II, VII, VIII, X DOACs: Dabigatran - inhibits thrombin (IIa) Apixaban, edoxaban - inhibits Xa

Answer 24

Enhances activity of antithrombin Anti-IIa and anti-Xa activity Doesn't cross placenta Given parenterally LMWH has superior pharmacokinetic profile, side effect profile, can be used in out-patients (as doesn't need monitoring) But more expensive Not readily reverisble (UF can be reversed by protamine) Indications: Immediate, short acting effect Acute DVT, PE (LMWH) Cardiac bypass (UFH)

Answer 25

Inhibits Vit K oxide reductase, inhbitiing Vit K Inhibits II, VII, VIII, X Delayed onset/offset (takes 5-7 days for steady state - full anticoagulable effet) Narrow therapeutic window Requires INR monitoring Indications: AF, Acute DVT, PE, prosthetic heart valve NOT for immediate anti-coagulation

Answer 26

Dabigatran: inhibits IIa (thrombin, preventing conversion of fibrinogen to fibrin) Apixababn, edoxaban: inhibits Xa (prevents conversion of prothrombin to thrombin) Indications: prophylaxis venous thromboembolism Don't require monitoring Contra-indications: pregnancy, breast feeding, liver disease, drugs (CYP3A4 inhibitors) Warfarin vs DOACs **Warfarin:** slow onset/offset dosing are individualised INR monitoring Many food, drug interactions Renal impairment may increase bleeding risk Rapid reversal with Vit K **DOACs:** rapid onset offset dosing based on CrCl annual monitoring Few food, drug interactions Renal impairment contra-indicated No rapid reversing

Answer 27

Enhances lysis of fibrin clot 2 classes: Kinases e.g. Urokinase Tissue plasminogen activators: Tenecteplase

Answer 28

Streptokinase, Urokinase Binds to plasminogen - increases plasmin and directly increases breakdown on fibrin clot - Causes fibrinolysis and fibringenolysis Streptokinase: - Made from streptococci bacteria - Antigenic: can cross react with anti-streptococcal antibodies Urokinase: - Made from renal cells in culture so not antigenic Indications: MI Problems: significant bleeding risk, streptokinase antigenic

Answer 29

Tenecteplase, Alteplase Activates plasminogen Selective for clot bound plasminogen, so minimal unwanted fibrinolysis effects Tenecteplase: short half life **Indications** - MI - Ischaemic stroke (alteplase) PE with haemodynamic instability (alteplase) **Side effects:** Risk of haemorrhage Contra-indications Haemorrhagic stroke Major trauma

Answer 30

Catheter passes through to site and fibrinolytic drugs infused Pros: Smaller doses Less systemic effects Uses: Acute limb ischaemia DVT

Answer 31

Inhibits platelet activation, platelet aggregration **Clopidogrel** - irreversibly blocks ADP mediated platelet aggregration - decreases expression of **GPIIb/IIIa** receptors leading to reduced binding of fibrinogen **Abciximab** - monoclonal antibodies which antagonise GPIIb/IIIa. Causes reduced platelet aggregration, and binding of fibrinogen **Aspirin** - irreversibly binds to cyclooxygenase (blocks conversion of arachidonic acid to thromboxane A2) leading to decrease platelet activation **Phosphodiesterase inhibitor III e.g. Dipyridamole** - Increased platelet conc of cAMP, decreased responsiveness to ADP leading to decrease platelet aggregration Thromboxane synthetase inhibitors (Picotamide) Thromboxane receptor blockers (Ifetroban) Indications: Cardiovascular disease Acute MI - aspirin, clopidogrel (up to 12 months) Cerebrovascular disease (no AF) Acute stroke (clopidogrel)

Answer 32

Pathological activation coagulation cascade Formation of micro-thrombi leading to ischaemia, infarction, and organ failure Depletion of coagulation factors leading to bleeding **Causes:** - sepsis e.g. meningococcal septicaemia due to nisseria meningitidis) - malignancy e.g. acute promyelocytic leukaemia - severe trauma - pre eclampsia **Symptoms**: Multiple bleeding sites, petechiae, bruising of skin **Investigations** FBC+film, **platelets (reduced),** RBC fragmentation Coagulation: PT (prolonged), APTT(prolonged) **D-dimer (increased)** Management: Treat underlying case Fresh frozen plasma+/- platelets Heparin Anti-thrombin concentrate

Answer 33

Stop warfarin, reduce dose Give Vit K Give coagulation factors (II, XII, XIII X)

Answer 34

Poor coagulation factor synthesis (as liver produces coagulation factors) Vit K deficient (which leads to deficient factors (2, 7, 9, 10) Poor clearence of activated coagulation factors DIC

Answer 35

Haemophilia A: Factor VIII deficiency Haemophilia B: Factor VIIII deficiency X-linked **Prolonged APTT** (as factor 8 and 9 due to intrinsic pathway) PT normal (extrinsic pathway) Treatments: Education Desmopressin Replacement therapy - FFP

Answer 36

AD Most common anti-coagulation disorder Reduced **vWF** +/- reduced platelet aggregration **reduced VIII** (as vWF binds to VIII and prolongs its half life) Mucosal type bleeding pattern Clinical features: epistaxis (nose bleed), mennorhagia, GI bleeding, haemoptyis

Answer 37

AR Mucosal type bleeding pattern **Bernard Soulier Syndrome (defective GPIb/V/IX)** - platelet adhesion impaired, macrothrombocytopenia (englarged platelets) on blood smear (as produces immature platelets) **Glansmanns thrombasthenia (defective GPIIIa/IIb)** - platelet aggregation impaired Management: Pressure Desmopressin Platelet transfusion

Answer 38

Deficiencies of natural anticoagluants: - Anti-thrombin - Protein C - Protein S Specific genetic mutations: Factor V leiden: mutation in V, stopping activated protein C to cleave factor 5, leading to increase in blood clotting Prothrombin gene mutation - increase prothrombin and thrombus formation

Answer 39

Antibody that binds to phospholipids, leading higher chance of blood clotting Anti-phospholipid syndrome: persisting Lupus anticoagulant + thrombosis Investigations APTT prolonged APTT 50:50 mixing partially corrects DRVVT ratio prolonged

Answer 40

Perform 50:50 mix - combine 1 part normal plasma and 1 part patient's sample If APTT fully corrects: prolongation due to factor deficiency (as normal plasma replaced the factors) If APTT partially corrects: inhibitor(e.g. lupus anticoagulant)

Answer 41

Hyercoagulable state due to another condition E.g. Antiphospholipid syndrome - presence of antiphospholipid antibodies e.g. Lupus anticoagulant, anti cardiolipin antibodies Disrupts Annexin 5 shield, exposes excess phospholipid Clinical scenario: - Venous/arterial thrombosis - Recurrent miscarriage

Answer 42

Self limiting postviral illness where immune system destroys platelets Most common in children Presents with purpuric , epistaxis, mennorhagia, (spleen not enlarged) Treatment Steroids, IVIG

Answer 43

EBV infection resulting in lymphocytic leukocytosis (increase lymphocytes as fighting infection) - comprising of CD8 T cells Clinical features: fever, tonsilitis, cervical lymphadenopathy. splenomegaly Tests: monospot test - detects heterophile antibodies (produced during EBV reaction which reacts with animal (sheep, horse) antibodies causing blood to agglutinate) EBV titres Treatment Self limiting Amoxicillin should not be given as due to virus not bacteria, and can cause amoxicillin rash Complications: Can become dormant in B cells

Answer 44

SLE Prolonged anti-coagulant due to lupus anticoagulant Pt has increased thrombotic tendency (different to what laboratory tests shows)

Answer 45

Due to E.coli 0517 Symptoms: bloody diarrohea Clinical features: anaemic, thromocytopenic, uraemia RBCs look fragmented Coagulation not affected

Answer 46

Malignancy from mature B cells. Characterised by presence Reed Sternberg cell (large, lots of cytoplasm, bilobed nucleus. Owl's eye appearence) Staging: History for B symptoms (systmeic symptoms - weight loss, night sweats, pyrexia), lymphadenopathy - physical examination - CT - BM to determine stages 1-4 (1=localised, 2= 2 or more sites on same side of diaphragm, 3=both sides of diaphragm, 4=widespread)

Answer 47

Chronic lymphoid leukaemia (CLL) Monoclonal B cells Different from chronic myeloid leukaemia (CML), as doesn't change to acute leukaemia (whereas CML can become AML or ALL)

Answer 48

Definition: Loss of more than one blood volume (\>5L in 70kg adult) within 24 hours Loss of 50% total blood volume in 3 hours Bleeding excess of 150mL/min **Management:** A, B, C O2 IV access Bloods - FBC, coagulation factors, fibrinogen Tranexamic acid Bloods - O neg, use group specific where possible **Complications** Hypothermia, acidosis, coagulopathy

Answer 49

Proliferation of myeloid blast cells in BM (which can't differentiate into RBCs, neutrophils, platelets leading to BM failure) Most common leukaemia in adults Death within days/weeks if untreated **Aetiology** Unknown, chemo, genetic e.g. Faconi's syndrome, blood disoders e.g. MPS, MDS **Clinical features:** Rapid onset symptoms, fatigue, infection, bleeding, bone pain, hepatosplenomegaly **Diagnosis:** FBC: Anaemia, thrombocytopenia, neutropenia, increased WBCs Blood smear: blast cells, granualated with Auer Rods Bonr marrow biopsy (definitive diagnosis): \>20% blast cells (large, little cytoplasm with punched out nucleus) t(15:17) - acute promyelocytic leukaemia (can also cause DIC) **Management** High dose chemo +/- SCT (\<60) Low dose chemo (\>60) Supportive treatment (elderly) Chemo - Anthracycline, cytarabine

Answer 50

Malignant clonal disorder characterised by increase in lymphoid blast cells (mostly B cells) 80% childhood leukaemias **Clinical features:** lymphadenopathy (enlarged lymph nodes), pupuric rash, bone pain, CNS symptoms (can cause meningeal leukaemia), testicular infiltration **Investigations** FBC: Anaemia, neutropenia, thrombocytopenia, leukocytosis (increased WBCs) Bone marrow trephine biopsy: **\>20% lymphoblasts in BM** High nuclear:cytoplasm ratio **Cytogenetics:** hyperploidy (excess chromosomes) good prognosis t(4:11), t(9:22) poor prognosis **CSF:** cell count high, glucose low, blast cells - meningeal leukaemia **Managment:** Chemo Supportive treatment: blood transfusion, FFP, antibiotics (increase risk of infections) - for older pts Those with poor prognosis, relapsed considered for BMT Silbings have 1/4 chance of being HLA matched

Answer 51

Increase in mature myeloid cells (neutrophils, basophils, eosinophils) More in middle-aged Causes: radiation **Clinical features:** asymptomatic, lethargy, night sweats, weight loss, splenomegaly **Investigations** FBC: Increased WBCs, anaemia, increased/decreased platelets Blood smear: mature myeloid cells basophil count \>20% would diagnose them in blast phase BM biopsy: Granulocytic hyperplasia Cytogenetics, PCR: BCR-ABL (required for diagnosis) **Stages:** Chronic - accelerated - blast crisis (AML/ALL) **Pathogenesis** Philidelphia chromosome - translocation between ch. 9 and 22 t(9:22) leading to fusion of BCR-ABL gene, creating abnormal tyrosine kinase **Treatments:** Imatinib (Tyrosine kinase inhibitor)

Answer 52

Commonest leukaemia Incidence rises with age Proliferation of neoplastic mature, lymphoid cells ( naive B cells) Cells co-express CD5 (normally expressed on T cells) and CD20 **Clinical features:** aymptomatic, lethargy, night sweats, weight loss, lymphadenoapthy, anaemia, SOB Insiduous **Complications** Autoimmune haemolytic anaemia - (as when try to make immunoglobulins, do a crap job) Neutropenia Pulmonary infections (strep. pneumoniae, pneuomocystis jirovecii) - as B cells don't mature into plasma cells so increased infection **Diagnosis**: Most are incidental FBC - increased WBC **with lymphocytosis** (increased no. lymphocytes), anaemia Blood smear: **smudge cells** (looks like cell has been smash) **Clinical Staging: BINET** Stage A: \< 3 involved lymphoid tissue (nodes, spleen, liver) Stage B: \> 3 involved lymphoid tissue Stage C: Anaemia, thrombocytopenia **17p deletions** Aggressive disease del 17p causes loss of p53

Answer 53

Neoplastic disorders which causes clonal expansion of lymhoid cells involving lymoh nodes, and lymhoid tissue e.g. MALT, spleen Divided into Hodgkin's lymphoma (25%) and Non-Hodgkin's lymphoma (75%) Clinical features: Lymphadenopathy (painless, rubbery), B symptoms, splenomegaly, anaemia **Investigations** History: B symptoms Clinical examination: lymph nodes Blood tests - FBC, U&Es, ESR Imaging - CT BM - aspirate (sucking out marrow), trephine (BM core) Staging (Ann Arbor classification) Stage 1: 1 lymph node group Stage 2: more than 1 LN group but same side diaphragm Stage 3: more than 1 LN group different side diaphragm Stage 4: extranodal involvement e.g. liver, spleen A and B - indicates absence (A), presence (B) of B symptoms

Answer 54

Group of malignant disorders involving lymphoid cells More common than HL Split into B and T cell Each split into Indolent and Agressive Low grade (indolent) lymphoma - low rate prolfieration/apoptosis. Uncurable High grade (aggressive) lymphoma - neoplastic cells large, prominent nucleoli, high rate cell divison/death. Often curable. B cell indolent: follicular lymphoma B cell aggressive: diffuse large B-cell lymphoma, Burkitt's lymphoma Clinical features: Painless lymphadenopathy, B symptoms, cytopenias (due to marrow failure), abdominal disease

Answer 55

Indolent (low grade) B cell lympoma Neoplasm of B cells that makes follicle like nodiles Characterised by translocation **t(14:18)** leading to **upregulation** of **BCL2** (anti-apoptotic protein) Slow growth but reduced apoptosis Incidence increases with age Clinical presentation: Late adulthood, **painless lymphadenopathy** Complications: Can progress to diffuse large B-cell lymphoma Treatment: Aimed at symptom control Early stage - **radiotherapy** Advanced stages: **Rituximab**

Answer 56

Hetergenous group of B cell lymphomas High grade B cell lymphoma Resembles activated B-cells **Commonest** subtype of Non-Hodgkin's lymphoma Clinical features: Aggressive Lymphadenopathy - rapidly enlarging LN mass Extra-nodal presentation: Waldeyer's ring, GI, skin B symptoms Treatment: R-CHOP (rituximab, cyclophosphamide, adriamycin, vincristine, prednisolone)

Answer 57

High grade B cell lymphoma (highly aggressive) Neoplasm of B cells in germinal centre - Mostly in children Characterised by translocations involving **MYC gene t(8:14)** leading to high rate of proliferation, apoptosis - can cause **tumor lysis sydrome** (cancer cells release intracellular contents when destroyed leading to arrthymias, sudden death) **Clinical features:** short history, marked B symptoms, rapidly growing tumor **Extranodal disease:** - Jaws (African form), facial bone - Ileocoecal region of GI tract (sporadic form) - CNS involvement Histology: - starry sky appearence Treatment: CODOX-M / IVAC CODOX-M: (**c**yclophosphamide, (O) vincistine, **dox**orubicin, **m**ethotrexate)

Answer 58

Haematological malignancy from mature B cells. Characterised by **Reed-Sternberg cells** (bi-lobed, prominent nucleolus, gives owl's eye appearence) Strong expression of CD30 Assoc. with EBV infections Incidence peaks at 20-30, then 50 **Clincal features:** painless lymphadenopathy (cervical common), cough, SOB, itch can precede diagnosis, alcohol related pain Subtypes: Classical Hodgkin's lymphoma (90%) and **nodular lymphocyte predominant** Classical Hodgkin's lymphoma split into: **Nodular sclerosing** (most common) - collagen bands divide LN into nodules. Uusally young, female, has cervical lymphadonapthy **Lymphocyte rich** - large no. of lymphocytes **Mixed cellularity** - fewever lymphocytes, more RS cells. Lots of eosinophils **Lymphocyte depleted** - few lymphocytes, lots of RS cell. Worst prognosis Spreads from one nodal group to adjacent group. Later, haemotological spread to liver, lungs CXR: can show widening of mediastinum, pleual effusion Complications: risk of Br. Ca in females, cardiovascular disease, infertility **Treatment** **ABVD** (adriamycin, bleomycin, vinblastine, dacarbazine) 1 and 15 of 28 day cycle

Answer 59

Neoplasm of mature **plasma** cells Abnormal plasma cells produce paraprotein (monoclonal protein) or only light chain of immunoglobulin produced (light chain myeloma) IgG most common Neoplastic cells resemble plasma cells - Mostly in elderly **Clinical presentation:** CRAB hyperCalaemia, renal insufficiency (as light chains deposit in renal tubules), Anaemia, Bone lytic lesions (as plasma cells leads to OC activation) Classical triad: increased plasma cells in BM, paraprotein, lytic bone lesions **Investigations:** Blood tests: FBC (rouleaux), ESR, serum electrophoresis (spike in M band (monoclonal protein: IgG or IgA) Urine tests - light chains (Bence Jones protein (light chains)) BM aspirate (increase no. of plasma cell) Imaging: MRI (bone lytic lesions, pepper pot skull) Complications: SC compression **Diagnosis:** \>10% plasma cells in BM + at least one of CRAB symptoms **Treatment:** Asymptomatic (smoudlering) - observe Symptomatic: Chemo inc. steroids + thalidomide Radiotherapy Supportive treatment: bisphosphonates

Answer 60

\<10% plasma cells in BM Serum M protein \<30 Bence Jones protein rare No symptoms characteristic of plasma cell myeloma (anaemia, hypercalcaemia, renal dysfunction, lytic bone lesions) Can progress to myeloma

Answer 61

Clinical features: pupura, mucosal bleeding Causes: BM failure ITP (idiopathic thrombocytopenia purpura) hypersplenism (overactive spleen) Henoch Schonlein purpura (normal platelets)

Answer 62

Folic Acid

Answer 63

E.coli Increases risk of Strep. pneumoniae, haemophilus influenzae, nisseria meningitidis

Answer 64

Leukaemia: malingnancy of leucocytes in BM or blood Lymphoma: malignancy of leucocytes in LN or lymphoid tissue e.g. MALT. Usually presents as a tumor mass

Answer 65

Single localized tumor of monoclonal plasma cells

Answer 66

SALTI Sideroblastic anaemia Anaemic of chronic dissease Lead poisoning Thalassaemia Iron deficiency anaemia

Answer 67

Autoimmune disease against platelet antigens (GPIIb/IIIa) which are consumed by splenic macrophages Most common cause of thrombocytopenia Acute form in children, weeks afer viral infection, self-limiting Clinical features: peteichae, epistaxsis, menorrhagia Complications: intra-cranial bleeding No splenomegaly Labs: Decreased platelet count PT, aPTT normal megakaryocytes on biopsy Treamtent: Steroids, splenectomy

Week 3 Haematology Flashcards

(92 cards)