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Phase 2a > Haematology > Flashcards

Haematology Flashcards

1
Q

What is polycythaemia (erythrocytosis)?

A

an increase in Hb, PCV and RBC

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2
Q

What is absolute polycythaemia?

A

true increase in red cell volume, primary or secondary

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3
Q

What is relative or stress/spurious polycythaemia?

A

normal red cell volume, decreased plasma volume, can occur in dehydration and burns

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4
Q

Is Hb or PCV a better indicator for polycythaemia?

A

PCV, as Hb could be low during iron deficiency

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5
Q

What is a normal PCV in the blood?

A

45%

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6
Q

Primary causes of polycythaemia?

A

polycythaemia rubra vera, epo receptor mutations, high oxygen affinity Hb

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7
Q

Secondary causes of polycythaemia?

A

increase in epo from hypoxia, smoking, high altitude, chronic lung disease, anoxia and tumour

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8
Q

What is polycythaemia rubra vera?

A

stem cell disorder with an alteration in the pluripotent progenitor cell, >95% in JAK2 mutations

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9
Q

What is the JAK2 gene?

A

a signal transducer, especially those triggered by haemopoetic growth factors

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10
Q

Symptoms of polycythaemia rubra vera?

A

tiredness, depression, vertigo, tinnitus, hypertension, angina, intermittent claudication, severe itching after hot bath, gout and peptic ulcer, plethora, deep dusky cyanosis, splenohepatomegaly, easy bleeding

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11
Q

What complications can polycythaemia lead to?

A

thrombosis

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12
Q

Treatment of polycythaemia?

A

venesection, chemo (IFN and hydroxyurea), low dose aspirin for thrombosis prophylaxis, anagrelide, radioactive 32P, surgery to prevent leukaemia (splenectomy), keep PCV and platelet count low, cytotoxic myelosuppresion hydroxycarbamide, regular removal of blood, phlebotomy to keep haematocrit

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13
Q

How many polycythaemia cases develop into myelofibrosis or AML?

A

myelofibrosis in 30%

AML in 5%

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14
Q

What will investigations show in polycythaemia?

A

raised haematocrit, Hb, RCC, MCV, raised WCC and platelets, neutrophil leucocytosis, o2 sat >92%, thrombocytosis, splenomegaly,

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15
Q

What will bone marrow show in polycythaemia?

A

bone marrow hypercellular with prominent megakaryocutes, low epo

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16
Q

What is the WHO diagnostic criteria for polycythaemia?

A

2 major and 1 minor or main major and 2 minor

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17
Q

What are the major criteria for polycythaemia?

A

Hb>16.5g/dL in women and 18.5d/dL in men

red cell mass >25% above normal

JAK2 617V F mutation

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18
Q

What are the minor criteria for polycythaemia?

A

BM biopsy showing hypercellularity

low serum epo

endogenous erythroid colony in vitro

increased serum uric acid and vit b12 and vit b12 binding protein

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19
Q

What is the prognosis of polycythaemia without treatment?

A

6-18 months

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20
Q

Why is uric acid increased in polycythaemia?

A

increased RBC breakdown, increases uric acid

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21
Q

Treatment of secondary polycythaemia?

A

phlebotomy to maintain circulation and reduce viscosity

treat underlying condition

o2 for hypoxia, weight loss, smoking cessation, surgery to correct AV shunts

hydroxyurea

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22
Q

What is disseminated intravascular coagulation?

A

widespread inappropriate fibrin deposition within the vasculature from increased tissue factor

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23
Q

What are the causes of DIC?

A

infection - meningococcaemia, septicaemia, malaria, varicella, CMV, HIV
malignancy - AML, mucin secreting adenocarcinoma
obstetric complications - amniotic fluid embolus, retained placenta, septic abortion
anaphylaxis
trauma, burns
liver failure
pancreatitis
heat stroke, acute hypoxia, blood loss, snake venom

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24
Q

Pathophysiology behind DIC?

A

activation of the coagulation pathway in response to infection, this uses up platelets and coagulation factors so secondary activation of fibrinolysis leading to fibrin degradation products which inhibit fibrin polymerisation, and no platelets left for other clotting

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25
Q

Clinical features of DIC?

A

acutely ill, shock, can be no bleeding or widespread haemorrhage, bleeding from mouth, nose, venepuncture

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26
Q

Where in the body is mainly affected by DIC?

A

skin, brain and kidneys

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27
Q

What will investigations show in severe DIC?

A 
prolonged PT, APPT, TT
low fibrinogen level
high FDPs and D dimer due to intense fibrinolytic activity, stimulated by the prescence of fibrin 
severe thrombocytopaenia
blood film shows fragmented RBC
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28
Q

What will investigations show in mild DIC?

A

without bleeding
raised FDPs
increased synthesis of coagulation factors and platelets
normal PT, APTT, TT and platelets

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29
Q

What is the treatment of DIC?

A

transfusion of platelet concentrates, FFP, cryoprecipitate and RBCs if bleeding
activated protein c concentrates
NO inhibitors of fibrinolysis as may cause fibrin deposition

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30
Q

Complications of DIC?

A

gangrene from thrombosis

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31
Q

Are PT and APTT intrinsic or extrinsic?

A

PT - extrinsic

APTT - intrinsic

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32
Q

What makes up cryprecipitate?

A

fibrinogen, factor VIII

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33
Q

What are the 2 main platelet disorders?

A

idiopathic thrombocytopenic purpura

thrombotic thrombocytopenic purpura

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34
Q

What is a petechia?

A

individual purple spots in a purpuric rash

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35
Q

What is thrombocytopenia?

A

a reduced platelet production in the bone marrow, excessive peripheral destruction of platelets or sequestrian in an enlarged spleen

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36
Q

What causes immune/idiopathic thrombocytopenia purpura (ITP)?

A

immune destruction of platelets after binding to Fc receptors on macrophages - caused by congenital thrombocytopenia (absent or malfunctioning MK in BM), infiltration of bone marrow (lymphoma, leukiemia, myeloma), reduced TPO production (liver disease), low platelet production (low B12/folate, low TPO, toxins), dysfunctional production of platelets (myelodysplasia)

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37
Q

What is the onset like for children and adults in immune/idiopathic thrombocytopenia purpura (ITP)?

A

acute in children

chronic in adults

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38
Q

At what age is immune/idiopathic thrombocytopenia purpura (ITP) most common in children?

A

2-6years

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39
Q

What are the symptoms of children immune/idiopathic thrombocytopenia purpura (ITP)?

A

mucocutaneous bleeding, severe bleeding (recent viral infection)

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40
Q

Is immune/idiopathic thrombocytopenia purpura (ITP) more common in males or females?

A

females

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41
Q

What other diseases is immune/idiopathic thrombocytopenia purpura (ITP) associated with?

A

autoimmune illnesses, CLL, solid tumours, HIV

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42
Q

Clinical features of immune/idiopathic thrombocytopenia purpura (ITP)?

A

rare major haemorrhage if severe, easy brusing, purpura, epistaxis, menorhagia, bleeding, splenomegaly

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43
Q

What will investigations show in immune/idiopathic thrombocytopenia purpura (ITP)?

A

isolated thrombocytopenia, bone marrow examination, platelet autoantibodies, increased or normal megakaryocytes in bone marrow, FBC, peripheral blood smear

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44
Q

Treatment of immune/idiopathic thrombocytopenia purpura (ITP) in children?

A

no treatment unless serious bleeding

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45
Q

Treatment of immune/idiopathic thrombocytopenia purpura (ITP) in adults?

A

1 - oral corticosteroids
IV IgG to raise platelet count
2 - splenectomy
3 - high dose corticosteroids, IV IgG, chemo

anti D immunoglobulin, immunosuppressants, platelet transfusion

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46
Q

When would you not have to treat immune/idiopathic thrombocytopenia purpura (ITP) in adults?

A

when platelets are >30x90^9/L unless they are having surgery

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47
Q

What can cause immune thrombocytopenia?

A

heparin induced, neonatal induced, post transfusion purpura

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48
Q

How do neonates cause immune thrombocytopaenia?

A

due to fetamaternal incompatibility for platelet specific antigens

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49
Q

How does blood transfusion cause thrombocytopaenia?

A

rare, but also occurs in patients previously immunised by blood transfusion of pregnancy

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50
Q

Where are platelets destroyed in immune/idiopathic thrombocytopenia purpura (ITP)?

A

in the spleen

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51
Q

What is thrombotic thrombocytopenia purpura (TTP)?

A

platelet consumption leads to profound thrombocytopenia

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52
Q

Causes of thrombotic thrombocytopenia purpura (TTP)?

A

familial or acquired

secondary to cancer, HIV, pregnancy, certain drugs, idiopathic

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53
Q

Treatment of thrombotic thrombocytopenia purpura (TTP)?

A

plasma exchange to increase ADAMTS-13, plasmapheresis, corticosteroids, rituximab

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54
Q

How can you monitor treatment in thrombotic thrombocytopenia purpura (TTP)?

A

platelet count and serum LDH

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55
Q

Where do micro thrombi from thrombotic thrombocytopenia purpura (TTP) usually affect?

A

kidneys, heart, brain

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56
Q

Neurological symptoms caused by thrombotic thrombocytopenia purpura (TTP)?

A

stroke, headaches, delirium, bizarre behaviour, hallucination

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57
Q

What anaemia occurs in thrombotic thrombocytopenia purpura (TTP)?

A

microangiopathic haemolytic anaemia - small blood clots damage RBC causing intravascular haemolysis

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58
Q

pathology behind thrombotic thrombocytopenia purpura (TTP)?

A

reduced ADAMTS-13 so reduced break down of ultralarge von willebrand factor multimers (ULVWM), so it accumulates, with platelet aggregation and clots in multiple organs

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59
Q

What conditions have microangiopathic haemolytic anaemia?

A

thrombotic thrombocytopenia purpura (TTP), DIC and HUS

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60
Q

complication of thrombotic thrombocytopenia purpura (TTP)?

A

AKI

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61
Q

clinical features of thrombotic thrombocytopenia purpura (TTP)?

A

fiond purpura, fever, fluctuating cerebral dysfunction, microangiopathic haemolytic anaemia, red cell fragmentation, AKI

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62
Q

How does thrombotic thrombocytopenia purpura (TTP) affect lactic dehydrogenase levels?

A

raises them due to haemolysis

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63
Q

What can cause over anticoagulation?

A

warfarin, heparin, rivaroxaban, dabigatran

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64
Q

What converts fibrinogen to fibrin?

A

thrombin

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65
Q

Anitdote of rivaroxaban and dabigatran?

A

none

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66
Q

antidote of heparin over anticoagulation?

A

protamin

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67
Q

What is thrombocytosis?

A

platelet count above 400x10^9/L leading to thrombosis

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68
Q

Causes of thrombocytosis?

A

splenectomy, malignant disease, inflammatory disorders, major surgery, post haemorrhagic, myeloproliferative disorders, iron deficiency

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69
Q

Treatment of thrombocytosis?

A

treat underlying cause, aspirin, hydroxycarbamide to reduce platelet count, dialysis

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70
Q

What does the liver produce to stimulate platelet production form magakaryocytes by binding to platelet and MK receptors

A

thrombopoietin

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71
Q

What is the charge on an activated platelets phospholipid surface

A

negative - to allow coagulation factors to blind

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72
Q

What produces thromboxane A2?

A

arachidonic acid in platelets via COX-1

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73
Q

function of thromboxane A2?

A

induces aggregation and vasoconstriction

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74
Q

What conditions consume platelets?

A

DIC, TTP, HUS, HELELP, major haemorrhage

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75
Q

What is heparin induced thrombocytopenia?

A

development of an IgG antibody against the complex form between platelets and heparin and instead binds to and activates platelets forming thrombosis and platelet consumption, most at risk after unfractioned heparin treatment or cardiac bypass surgery

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76
Q

What is Von Willebrand Disease?

A

deficiency of von villebrand factor leading to impaired platelet adhesions and aggregation

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77
Q

Treatment of heparin induced thrombocytopaenia?

A

alternative anticoagulation, never reexpose to heparin

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78
Q

How does heparin induced thrombocytopaenia present?

A

sharp fall in platelets 5-10 days after starting heparin treatment

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79
Q

What are the 2 types of P2Y12 receptor inhibitors?

A

thienopyridines and non thienopyridines

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80
Q

Types of thienopyridines?

A

clopidogrel - hepatic CYP2c19 conversion into active metabolite 2 step process

prasugrel - single CYP step therefore faster transformation into active metabolite, rapid action but greater risk of bleeding

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81
Q

Types on non theinopyridines?

A

ticagrelor - reversibly binding oral P2Y12 anatgonist, does not require metabolic conversion to an active form, so faster onset of action

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82
Q

Example of GP IIbIIIa inhibitors?

A

tirofiban - non peptide tyrosine derivative, rapid onset, rapid reversibility of anti platelet effect

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83
Q

Life span on platelets?

A

7-10 days

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84
Q

shape of platelets?

A

disc shape to allow them to flow close to endothelium

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85
Q

How are old platelets removed?

A

phagocytosed by splenic macrophages in red pulp

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86
Q

Function of thrombopoietin?

A

decrease in platelets, cause increase in TPO to increase binding to MK and platelet receptors to increase platelet production

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87
Q

Platelet physiology?

A

platelets adhere to damaged endothelium via collagen and vWF. Binding of collagen stimulates cytoskeleton shape change for increase in SA, releases ADP, fibrinogen, thrombin and Ca2+ from platelet granules. Aggregation of platelets by fibrin, coagulation factors bind.

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88
Q

What chromosome if vWF gene on?

A

12

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89
Q

What are the 4 types of vWF disease?

A

1 - poor quantitative deficiency (autosomal dominant)
2 - qualitative abnormality (autosomal dominant)
3 - near complete deficiency (autosomal recessive)
4 - type normandy

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90
Q

Clinical features of type 1 and 2 vWF disease?

A

bleeding post trauma or surgery, epistaxis and menorrhagia

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91
Q

Clinical features of type 3 vWF disease?

A

severe bleeding but rare joint and muscle bleed

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92
Q

Treatment of vWF disease?

A

desmopressin, plasma derived factor VIII concentration that contain vWF treat bleeding and surgery, cryoprecipitate

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93
Q

function of vWF?

A

binds to GpIb receptor on platelets to subendothelial collagen and transport of factor VIII

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94
Q

Causes of vit K insufficiency?

A

warfarin, malabsorption, alcholism, CF, CKI, cholestatic disease

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95
Q

Symptoms of vit K insufficiency?

A

inrease PT and PTT, bruising, haematuria, GI bleeding

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96
Q

Treatment of vit K insufficiency?

A

IV phylomenadione, vit supplements, vit k rich foods

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97
Q

What is haemophilia?

A

X linked recessive bleeding and bruising disorder

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98
Q

What is haemophilia A?

A

factor VIII deficiency, normal vWF

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99
Q

Clinical features of haemophilia A?

A

mild - bleeding after injury or surgery later in life
moderate - severe bleeding post injury, occasional spontaneous bleeds
severe - frequent spontaneous bleeding into joints and muscles lead to deformity

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100
Q

What are the factor VIII levels in haemophilia A?

A

normal = 50-150iu/dL
mild = >5
moderate = 1-5
severe =

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101
Q

What will investigations show in haemophilia A?

A

low factor VIII, coagulation factor assay, increased PTT, normal PT, increased APPT

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102
Q

Treatment of haemophilia A?

A

educate, counselling, testing, avoid anticoagulants
mild - desmopressin
severe - require IV replacement with plasma concentration factor VIII

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103
Q

What is the half life for factor VIII and therefore how many time is replacement necessary?

A

12 hours, twice a day

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104
Q

What complications can haemophilia A lead to?

A

patients immune system may start to reject the IV plasma factor VIII

joint destruction by recurrent bleeding

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105
Q

Which is more common haemophilia A or B?

A

A

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106
Q

What is haemophilia B?

A

factor IX deficiency (xmas disease)

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107
Q

Treatment of haemophilia B?

A

educate, counselling, testing, avoid anticoagulants, desmopressin, IV infusion of factor IX, gene therapy

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108
Q

What is the half life of factor IX and how often is a given in haemophilia B?

A

18 hours, twice a week

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109
Q

Complications of haemophilia B?

A

joint destruction by recurrent bleeding

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110
Q

What is malaria?

A

an infectious disease caused by parasitic Plasmodium, spread by the female Anopheles mosquito

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111
Q

What are the 4 species of the plasmodium infection?

A

plasmodium falciparum, plasmodium virax, plasmodium ovale, plasmodium malariae

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112
Q

Which plasmodium species causes a more severe illness?

A

plasmodium falciparum

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113
Q

Which plasmodium species is most likely to relapse after many years?

A

plasmodium virax and plasmodium ovale

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114
Q

Symptoms of malaria?

A

fatigue, night sweats, flu like symptoms, fever of 41, diarrhea, nausea, vmiting, anaemia, splenomegaly, siezures

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115
Q

Complications of malaria?

A

cerebral malaria, anaemia, DIC, blackwater fever, jaundice, splenic rupture, tertian fever, quartan fever

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116
Q

What is Tertian fever?

A

fever that recurs every second day for 48 hours

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117
Q

What is Quartan fever?

A

fever that recurs every fourth day

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118
Q

What does cerebral malaria cause?

A

decreased consciousness, confusion, convulsions, coma

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119
Q

What is blackwater fever?

A

widespread intravascular haemolysis causing dark urine

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120
Q

If a patient presents with fever and foreign travel, what should you think of?

A

malaria

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121
Q

When does mortality increase with malaria?

A

if less than 3 years or pregnant

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122
Q

When do malaria symptoms usually present?

A

within a month of bite

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123
Q

What is used for malaria diagnosis?

A

thick and thin blood films - look at the number of infected cells to detect level of parasitaemia

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124
Q

What medications are given for malaria prophylaxis?

A

atovaquone with proguanil or quinine with doxycycline

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125
Q

What does the treatment of malaria depend on?

A

type of malaria, severity and where is was caught

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126
Q

What medications are used to treat malaria?

A

atovaquone with proguanil or quinine with doxycycline

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127
Q

contraindications for atovaquone-proguanil?

A

pregnant/breast feeding, severe kidney problems

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128
Q

Side effects of atovaquone-proguanil?

A

stomach upset, headaches, skin rash, mouth ulcers, expensive

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129
Q

Why are Chloroquineand proguanil not prescribed for malaria as much now?

A

largely ineffective against plasmodium falciparum, but good in places where that species is less common

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130
Q

Investigations for malaria?

A

bloods
blood film - parasites on Giemsa stained thick/thin film
renal time PER
antigen detection kits
lumbar puncture to exclude bacterial infection

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131
Q

What disease protects against malaria?

A

sickle cell disease (and lacking the Duffy antigen)

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132
Q

What malaria species causes anaemia and hepatosplenomegaly?

A

p.vivax, p.ovale

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133
Q

How does a mosquito infect a human with malaria?

A

female mosquito is infected after taking a blood meal containing gametocytes and the protozoa develop in the mosquito and the sporozoites migrate to the salivary glands so inoculate a human when biten

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134
Q

Where do sporozoites migrate to in the mosquito in malaria?

A

salivary glands

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135
Q

What happens to sporozoites once inoculated in a new human host?

A

travel to liver, infect hepatocyts, and multiply then from schizonts and then merozoites, the hepatocytes then rupture so merozoites released into the blood stream, continue to replicate until RBC ruptures which can then be transferred to feeding mosquito

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136
Q

How could vaccines prevent malaria?

A

maintain high antibody levels to prevent infection

can prevent transfer

can prevent progression of disease

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137
Q

What drug inhibits haem metabolism?

A

lumfantrine

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138
Q

What drug inhibits falciporum sarcoplasmic?

A

endoplasmic reticulum calcium ATPase

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139
Q

What drug inhibits haem polymerase?

A

chloroquine, and quinine

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140
Q

What drug inhibits plasmodial protein synthesis?

A

doxycycline

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141
Q

What measure help prevent malaria?

A

mosquito eradication, bed nets, insect repellent, antimalarial prophylaxis

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142
Q

Management of uncomplicated malaria?

A

chloroquine
artemisnin based drug
primaquine to eradicate hepatic hyponozoiles to prevent relapse
artemisinin based combination therapy

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143
Q

Management of severe malaria?

A

IV artesunate, ICU for ventilation, blood tranfusion, monitor fluid balance, treat complications e.g. hypoglycaemia

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144
Q

What is hyperreactive malarial splenomegaly?

A

exaggerated immune response to repeated infections causing anaemia, massive splenomegaly, elevated IgM levels

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145
Q

What is anaemia?

A

reduced red cell mass w/wo reduced Hb concentration

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146
Q

What is the normal Hb conc for male and female?

A 
male = 13.1-16.6g/dL
female = 11-14.7d/dL
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147
Q

What is a normal MCV?

A

82-96fl

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148
Q

Life span of RBC?

A

120 days

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149
Q

Where are RBC produced and removed?

A

produced in bone marrow, removed in spleen, liver, bone marrow and blood loss

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150
Q

What are the 3 sizes of RBC?

A

microcytic
normocytic
macrocytic

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151
Q

What does anaemia cause?

A

reduced O2 transport, tissue hyposxia, increase tissue perfusion, increase O2 transfer to tissues

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152
Q

What investigations show be done for anaemia?

A

WBC. platelet, reticulocute, blirubin, blood film, ferritin, transferritin

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153
Q

Anaemia symptoms?

A

tired, malaise, reduced exercise tolerance, SOB, angina, claudication, symptoms of underlying cause, palpitations

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154
Q

Signs of anaemia?

A

pallow, pale mucous membranes and palmar creases, glossitis, angular stomatitis, kylonichia

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155
Q

What is the most common form of anaemia?

A

microcytic

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156
Q

what causes microcytic anaemia?

A

iron deficiency, chronic disease, sideroblastic anemia, thalassaemia

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157
Q

What foods have iron in?

A

vegetables and grains

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158
Q

Where is haem iron absorbed?

A

proximal intestine via the intestinal haem transporter HCP1 in the duodenum (upregulated in iron deficiency and pregnancy)

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159
Q

Is haem iron or non haem iron more rapidly absorbed?

A

haem

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160
Q

What is haem used for?

A

Hb production

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161
Q

What causes lack of iron?

A

use more, lose more, lack of it in diet, bleeding

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162
Q

What is the usual serum iron level?

A

13-32umol/L

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163
Q

How is iron transported in the body?

A

2 ferric ions bound to transferrin, normally only 1/3 saturated, iron then binds to erythoblasts and reticulocytes in marrow and removed

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164
Q

How much iron is stored in the HB?

A

2/3rds

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165
Q

When is other iron stored?

A

reticuloendothelial cells, hepatocytes and skeletal muscle cells and plasma

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166
Q

How is iron lost?

A

faeces, urine, sweat, menstruation

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167
Q

What conditions cause an increase in iron?

A

hereditary haemochromatosis (mutation in HFE gene) and secondary haemochromatosis (iron overload from blood transfusion)

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168
Q

What causes iron deficiency?

A

blood loss from GI or uterus, hookworm, poor diet

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169
Q

Clinical features of iron deficiency?

A

brittle nails, spoon shaped nails, atrophy of papillae of tongue, angular stomatitis, brittle hair, dysphagia and glossitis

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170
Q

What will investigations show in iron deficiency anaemia?

A

microcytic hypochromic RBC, decreased iron, increase binding sites, decreased serum ferritin, increased serum soluble transferrin receptors

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171
Q

What is the treatment of iron deficient anaemia?

A

treat the cause, ferrous sulphate 200mg, treat for 3 months post resolving

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172
Q

Side effects of ferrous sulphate medication?

A

constipation

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173
Q

What chronic diseases cause anaemia?

A

TB, Crohn’s, RA (inflammatory disease)

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174
Q

How does chronic disease cause anaemia?

A

high levels of hepadin, lack of erythropoetin and renal disease cause decrease of iron from bone marrow to erythroblasts, inadequate erythropietin response to the anaemia and decreased RBC survuval

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175
Q

What is normocytic anaemia?

A

seen in anaemia of chronic disease, endocrine disorders and some haemotological disorders

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176
Q

What are the two types of macrocytic anaemias?

A

megaloblastic and non megaloblastic depending on bone marrow findings

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177
Q

What is a megaloblastic anaemia?

A

presence of erythroblasts with delayed maturation due to defective DNA synthesis in bone marrow

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178
Q

What causes folate deficiency?

A

poor intake, excessive utilization, malabsorption

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179
Q

What are the clinical findings of folate deficiency?

A

asymptomatic, anaemia symptoms, symptoms of underlying cause, glossitis

180
Q

What investigations are done for folate deficiency?

A

serum and red cell folate

181
Q

What is the treatment of folate deficiency?

A

5mg of folic acid/day to replace body stores

prophylactic folic acid if planning pregnancy

182
Q

What is the treatment of B12 deficiency?

A

hydroxocobalamin 1000ug IM, oral B12 mg/day

183
Q

What are B12 and folate used for?

A

DNA synthesis

184
Q

What does B12 and folate deficiency cause?

A

pancytopenia

185
Q

Where is folic acid broken down?

A

upper GI

186
Q

What is the form of folic acid in the body?

A

methyl THF monoglutamate in the serum

187
Q

In what foods in folate found?

A

green vegetables

188
Q

In what foods in B12 found?

A

meat, eggs, fish

189
Q

Where is B12 stored?

A

liver

190
Q

Where does macrocytic anaemia manifest first?

A

bone marrow

191
Q

Causes of macrocytic anaemia?

A

liver disease, alcohol, hypothyroid, B12 and folate deficiency

192
Q

Where is B12 absorbed?

A

terminal ileum

193
Q

What is the most common cause of B12 deficient anaemia?

A

pernicious anameia

194
Q

What is pernicious anaemia?

A

an autoimmune disorder where there is atrophic gastritis with loss of parietal cells, causing decreases intrinsic factor and B12

195
Q

In who is pernicious anaemia most common in?

A

fair haired, blue eyes, type a blood, females, over 60 (rarely congenital in children with early onset)

196
Q

what two antibodies are seen in pernicious anaemia?

A

parietal cell antibodies and intrinsic factor antibodies

197
Q

What are the 2 types of intrinsic antibodies?

A

inhibits intrinsic factor binding to B12

inhibits B12 intinsic factor complex to receptor site on ileum

198
Q

What are the parietal cells and chief cells replaced with in pernicious anaemia?

A

mucin secreting cells

199
Q

Treatment of pernicious anaemia?

A

corticosteroid therapy

IM hydroxycobalamin

200
Q

Clinical features of pernicious anaemia?

A

lemon/yellow colouring, glossitis, red tongue, angular stomatitis, nerulogical changes

201
Q

Clinical features of pernicious anaemia in serious cases?

A

symmetrical paraethesiae in fingers and toes, early loss of vibration sense and proprioception, progressive weakness and ataxia

202
Q

What do investigations show in pernicious anaemia?

A

megablastomic, increased serum bilirubin, increased LDH, serum methylmalonic acid, homocysterine, decreased serum vit b12, increased serum folate levels, megaloblasts in bone marrow, low Hb, wcc and platelets

203
Q

What is the absorption test called to find the cause of pernicious anaemia and what does it involve?

A

Schilling test - oral radioactive B12 and IM non radio-active IM

normal = >10% of oral dose in urine

abnormal if not - so redo with intrinsic factor capsules, if it is normalised, then it is pernicious anaemia

if still abnormal then lesion in terminal ileum or bacterial overgrowth

204
Q

What is macrocytosis without megablastic change?

A

raised MCV with normoblastic

205
Q

What is the cause of macrocytosis without megablastic change?

A

pregnancy, alcohol, liver disease, drugs, reticulocytosis, hyperthyroidism, some haemotological disorders, cold agglutinin due to autoagglutinations of red cells

206
Q

What will investigations show in macrocytosis without megablastic change?

A

normal B12 and folate

increased lipid deposition in red cell membrane and increased in reticulocytes leading to increased MCV

207
Q

What is aplastic anaemia?

A

pancytopenia with hypocellularity (aplasia) of the bone marrow

208
Q

Cause of aplastic anaemia?

A

immune mechanisms, activated cytotoxic T cells in bone marrow and blood, cytotoxic drugs, NSAIDs, inherited fancous anaemia, aplastic anaemia, transient eythroblastopenia, parvovirus B19 infection, malignancy

209
Q

Why can’t bone marrow repopulate in aplastic anaemia?

A

reduction in pluripotential stem cells and a fault in the remaining ones

210
Q

What can aplastic anaemia lead to?

A

myelodysplasia, paroxysmal nocturnal haemoglobinuria, AML

211
Q

Clinical features of aplastic anaemia?

A

anemia, bleeding, infection

212
Q

What will investigations show in aplastic anaemia?

A

pancytopenia, virtual abscence of reticulocytes, hypocellular bone marrow with increased fat spaces, negative coombs and normal bilirubin, absent red cell precusors on bone marrow examination

213
Q

Treatment of aplastic anaemia?

A

steroids, supportive care and treatment to accelerate bone marrow recovery, transfusions, prevent infection, bone marrow transplantation, immunosuppressive therapy

214
Q

What is haemolytic anaemia?

A

caused by increased destruction of RBCs in the macrophages of the bone marrow, liver and spleen, normal or increased RBC production

215
Q

Is haemolytic anaemia more common in intra or extravascular?

A

extravascular

216
Q

What is the difference between intra and extravascular haemolytic anaemia?

A

e - RBCs are emoved from circulation by macrophages

i - RBCs destroyed in circulation and haemoglobin is liberated to be reabsorbed by renal tubules and broken down and deposited as haemosiderin

217
Q

What can be used to estimate RBC survival?

A

IV 51Cr labelled red cells

218
Q

What does pernicious anaemia lead to?

A

achlorydia and b12 malabsorption

219
Q

Congenital causes of haemolytic anaemia?

A

heriditary spherocytosis, sickle cell disease, thalassaemia, sideroblastic anaemia, enzyme disorders

220
Q

Acquired causes of haemolytic anaemia?

A

immune autoantibodies against RBC, mechanical

221
Q

What is hereditary spherocytosis?

A

RBC are sphere shaped, varies from mild-severe

222
Q

Symptoms of hereditary spherocytosis?

A

anaemia, jaundice, enlarged spleen, gall stones, leg ulcers

223
Q

Treatment of hereditary spehrocytosis?

A

folic acid and spelnectomy

transfusion or steroids in aplastic crisis

224
Q

What is sideroblastic anaemia?

A

a ringed sideroblast, caused by congenital of leukaemias due to not being able to incorporate iron into Hb

225
Q

What is the treatment of sideroblastic anaemia?

A

treat if symptomatic, RBC transfusion with iron chelation therapy, avoid alcohol, reduce vit C intake as it can increase iron absorption

226
Q

What do investigations show in sideroblastic anaemia?

A

high serum iron and transferritin saturation

227
Q

What are the 4 types of normocytic anaemia?

A

acute haemorrhage, anaemia of chronic disease, aplastic anaemia, haemolytic anaemia

228
Q

What do investigations show in acute haemorrhage anaemia?

A

normocytic normochromic anaemia, increased reticulocytes, normal bilirubin

229
Q

pathophysiology of anaemia of chronic disease?

A

IL-6 are increasing hepcidin, causing a decreased response to EPO and decreased production over time

230
Q

What are the 4 types of haemolytic anaemia?

A

membrane defect - hereditary spherocytosis
enzyme defect - G6PD deficiency
haemoglobinopathy - sickle cell disease, thalassaemia
immune haemolytic anaemia

231
Q

Features of haemolytic anaemia?

A

increased serum unconjugated bilirubin, increased urinary urobilinogen, increased faecal stercobilinogen, spelomegaly, reticulocytosis, expansion of bone marrow

232
Q

What is the consequence of sphere shaped RBC in hereditary spherocytosis?

A

they are more rigid and less deformable so unable to pass through the splenic microcirculation so have a shortened lifespan

233
Q

What do investigations show in hereditary spherocytosis?

A

anaemia, spherocytes on blood film, eviden haemolysis, increased lysisity, negative antiglobulin test

234
Q

What is hereditary elliptocytosis?

A

red cells are elliptical from protein deficiency leading to weakness of horizontal protein interaction and membrane defect

235
Q

What is hereditary stomaocytosis?

A

When RBC have pale central area appearing slit like, due to membrane defect or excess alcohol

236
Q

What is thalassaemia?

A

autosomal inherited recessive condition producing microcytic aaemia due to problem in globin chain production which alters Hb synthesis

237
Q

What is B thalassaemia?

A

mutation in b globin chain on chromosome 11 which causes an increase in globin production

238
Q

What are the 3 types of b thalassaemia?

A

minor (heterozygous)
intermediate (homozygous b and a)
major (cooleys anaemia)

239
Q

Symptoms of B thalassaemia minor?

A

asymptomatic, mild/absent anaemia, increase in HbA2 and HbF, Carner state

240
Q

Symptoms of B thalassaemia intermediate?

A

moderate anaemia, no transfusions, splenomegaly and bone deformities, recurrent leg ulcers, gallstones and infections

241
Q

Symptoms of B thalassaemia major?

A

severe anaemia, cranial bossing due to extra medullary haematopoiesis, bone marrow expansion in hand, failure to thrive and recurrent bacterial infection

242
Q

Is B thalassaemia mutation or deletion?

A

point mutation

243
Q

What is A thalassaemia?

A

an a globin gene mutattion causing gene deletion and a globin synthesis, results in excess B globin production

244
Q

On what chromosome is the mutation in A thalassaemia?

A

chromosome 16

245
Q

Is A thalassaemia mutation of deletion?

A

deletion

246
Q

What is the effect of each deletion in A thalassaemia?

A

1 - no significant anaemia
2 - microcytosis w/wo mild anaemia
3 - HbH disease - it does not carry O2 and precipitate everything in erythroblasts leading to moderate anaemia and splenomegaly
4 - has no a chain and only y4 so leads to still born (Barts hydrops fetalis)

247
Q

What will investigations show in A thalassaemia?

A

A thalassaemia on blood film, microcytic, hypochromic anaemia, decrease MCV and MCH, iron and ferritin normal, Hb electrophoresis shows increases HbA2 and increased HbF, high performance liquid chromatography, x ray show bone abnormalities

248
Q

Complications of A thalassaemia?

A

galls stones, iron overload, splenomegaly, increased risk of infection, HF, arrhythmias, bone abnormalities (cranial bossing)

249
Q

What is HbH?

A

4 B chains, low HbA and Y4 and reduced HbA2

250
Q

Treatment of thalassaemia?

A

education, genetic counselling, based on symtpoms, transfusions if Hb

251
Q

pathophysiology of B thalassaemia?

A

homozygous state, point mutation in B glbin gene, decrease in B globin chain production, excess of a chains, causing decrease in HbA and increase in HbA2 and HbF, leading to haemolysis

heterozygous state (carrier) is asymptomatic or mild anaemia, increases HbA2

252
Q

What is G6PD deficiency?

A

a decrease in G6PD, causing reduced glutathione and acute oxidant induced haemolysis from drugs, surgery and infection, broad beans

253
Q

What do investigations show in G6PD deficiency?

A

decreased G6PD enzyme assay levels, increased bite cells, blister cells and heinz bodies on blood film, reticulocytes, evident haemolysis, G6PD normal immediately after attck

254
Q

Treatment of G6PD deficiency?

A

avoid precipitants, blood transfusion, treat underlying cause

255
Q

Symptoms of G6PD deficiency?

A

acute drug induced haemolysis, favism, chronic haemolytic anaemia, neonatal jaundic, infections and acute illness caused by rapid intravascular haemolysis

256
Q

What is sickle cell anaemia?

A

HbS is caused by mutations of adenine to thymine, changing a B globin chain, in sickle cell anaemia, both b genes are abnormal, trait is just one chain abnormal

257
Q

At what age does sickle cell anaemia develop?

A

6 months old

258
Q

pathology behind sickle cell anaemia?

A

deoxygenated HbS molecules are insoluble, polymerizable under deoxygenated conditions and eventually become sickle like in appearance becoming irreversible due to dehydration from K+ leaving the RBC, decreased RBC survival and impairs passage through vessels leading to blockage

259
Q

Cause of sickle cell anaemia?

A

infection, dehydration, cold, acidosis, hypoxia

260
Q

What are the 3 types of sickle cell anaemia?

A 
homozygous HbSS (most severe)
combined heterozygosity HbSC (intermediate)
heterozygous HbAS (no symptoms)
261
Q

Symptoms of sickle cell anaemia?

A

acute pain in hand and feet from small vessel vaso occlusion, severe pain in bones, fever, pulmonary hypertension, anaemia, bone marrow aplasia, acute chest syndrome, splenic sequestrain and painful enlargement, splenic pooling of RBC and hypovalaemia, liver sequestrain

(heterozygous individuals have no symtpoms except for when in hypoxic enviroment)

262
Q

What do investigations show in sickle cell anaemia?

A

increased reticulocytes, hyposplenism, turbid appearance due to HbS, No HbA, parents have sickle cell trait, electrophoresis identifies individuals wthether HbAS or HbSS

263
Q

Treatment of sickle cell anaemia?

A

avoid/treat precipitating factors, supportive therapy with IV fluids and analgesia, o2 and antibiotics, folic acid, penicillin, blood transfusions, splenectomy, stem cell transplantation, hydroxycarbamide to increase HbF concentrations and reduces pain acute chest syndrome, counselling, prognosis varies

264
Q

Long term problems of sickle cell anaemia?

A

delayed growth, development and menstruation, infections in tissues, leg ulcers, cardiomegaly, arrhythmias, cardiomyopathy, pigment stones, chronic tubulointerstitial nephritis, background retinopathy, impaired placental blood flow causing abortion and intrauterine growth retardation, priapism (painful erection), transient ischaemic attack, stroke, fits

265
Q

What is sickle cell trait?

A

one abnormal b globin chain

266
Q

symptoms of sickle cell trait?

A

no symptoms, extreme cases cause anorexia

267
Q

Investigations of sickle cell trait?

A

60% HbA, 40%HbS, blood count, film nromal, positive sickle test, Hb electrophoresis

268
Q

Which is more serious, sickle cell trait or sickle cell aneamia?

A

sickle cell anaemia

269
Q

What does a combination of TB and sickle cell trait resemble?

A

sickle cell anaemia

270
Q

symptoms of HbE heterozygotes?

A

asymptomatic, normal Hb, microcytic red cells causing mild microcytic anaemia

271
Q

Symptoms of HbE and B thalassaemia?

A

causes variable anaemia, can be severe as B thalassaemia major

272
Q

Who would be offered prenatal screening?

A

for offspring of patients who have both B thalassaemia or sickle cell trait as 25% will have either of these, involves counselling, pregnent women screened for anaemia, partners should be tested, foetal DNA

273
Q

What kind of inheritance is sickle cell anaemia?

A

autosomal recessive

274
Q

What is vaso occlusive crisis?

A

triggered by hypoxia, infection, dehydration

coagulation in the microvasculature lead to CNS infarction, breathing difficulties, bone pain

275
Q

Treatment of vaso occlusive crisis from sickle cell anaemia?

A

hydroxycarbamide - breaks down cells that are prone to sickle and therefore reduced the frequency of vasoocclusive attacks

276
Q

What are the 4 types of leukaemia?

A

AML, ALL, CML, CLL

277
Q

In who is ALL most common?

A

children

278
Q

In who is CML most common?

A

elderly

279
Q

What is the general treatment of leukaemia?

A

chemotherapy (induction, consolidation and maintenance), bone marrow transplant for poor prognosis or relapse

280
Q

What is leukaemia?

A

rare neoplasm of blood or bone marrow, occuring at any age

281
Q

What are the complications of leukaemia?

A

death, increased infection risk, haemorrhage, pulmonary intracranial, depression

282
Q

Symptoms of anaemia?

A

breathlessness, fatigue, angina, claudication, pallow, cardiac flow murmur

283
Q

Symptoms of neutropenia?

A

infections, fever, mouth ulcers

284
Q

Symptoms of thrombocytopenia?

A

bleeding, bruising, petechiae, gum bleeding, fundal haemorrhage

285
Q

What are blast cells?

A

immature precursor cells

286
Q

What are myeloblasts?

A

immature precursor of myeloid cells

287
Q

What are lymphoblasts?

A

immature precursors of lymphoblasts

288
Q

In who are blast cells seen?

A

not in normal individuals, they are suggestive of chronic disease or leukaemia beginning to transform into an acute disease

289
Q

What is diagnostic for AML on microscopy?

A

Auer rods

290
Q

What are smudge cells?

A

lymphocytes that lack an identifiable cytoplasmic membrane and nucleus

291
Q

When do smudge cells develop?

A

develop due to fragile lymphocytes in CLL

292
Q

On what chromosome is the BCR gene?

A

22

293
Q

On what chromosome is the ABL gene?

A

9

294
Q

What is the Philadelphia chromosome?

A

contains ABL and BCR gene, it is 22- chromosome

295
Q

What causes ALL?

A

lymphoblasts are over produced in the marrow, immature lymohocytes are produced and inhibition of other white blood cells due to lack of space and nutrients so there are less of them in the blood, and lymphoblasts infiltrate other tissues

296
Q

Risk factors for ALL?

A

downs syndrome, ionising radiation, pregnancy, benzenes, environmental triggers, with genetic susceptibility

297
Q

symptoms of ALL?

A

reflect the underproduction of healthy RBCs, platelet and WBCs

general fatigue, weakness, dizziness, frequent fever, injection, weight loss, bruising, bone pain, SOB, purpura, night sweats

298
Q

How is ALL diagnosed?

A

exclude other causes e.g. coagulation to exclude DIC

blood smears show blasts in peripheral blood

csf sample shows if there has been invasion into brain and CNS

medical imaging shows invasion into other tissues

cardiac function for planning therapy

299
Q

How is ALL classified?

A

B or T cell lineage, association with philadelphia chromosome

300
Q

Treatment of ALL?

A

induce remission with dexamthasone, vincristine, anthracycline antibiotics and cyclophosphamide

maintain with methotrexte, mercaptopurine, cytarabine, hydrocortisone

continued oral/IV chemo at less frequent rate

immunotherapy/marrow transplant

301
Q

What is the survival and prognosis for ALL?

A

5yr survival is 85%, prognosis based on age, race, gender, genotype

302
Q

What is leukaemia chemotherapy treatment stages based on?

A

remission induction, consolidation/intensification and maintenance therapy

303
Q

What is the function of the remission stage in ALL chemo?

A

acheieves absence of blasts in peripheral blood and

304
Q

What is the function of consolidation in ALL chemo?

A

further reduction of cancerous cells

305
Q

What is the function of maintenance therapy in ALL chemo?

A

killing any residual cells not killed by previous therapy, lasts years

306
Q

Where about on your body can radiotherapy be used?

A

painful bony areas

307
Q

In who is CLL mainly seen?

A

> 60

308
Q

Cause of CLL?

A

gradual accumulation of B lymphocytes from blood/bone marrow and lymph glands

309
Q

What are the symptoms of CLL?

A

asymptomatic, bone marrow failure, non tender lymphadenopathy, malaise, weight loss, night sweats, anaemia, fever, recurrent infection

310
Q

How do lymph nodes appear in CLL?

A

enlarged, rubbery, soft tender lymph nodes, slowly enlarge over time

311
Q

How do ALL and CLL symptoms differ?

A

similar but CLL may be asymptomatic and diagnosis can be by chance

312
Q

What is CLL prognosis like?

A

1/3 progress slowly, 1/3 progress rapidly, 1/3 never progress

313
Q

What will investigations show in CLL?

A

positive ZAP-70 marker (worse prognosis), decreased Hb and plateletsm increased WBC, lymphocytosis, small lymphocytes, lymphocyte infiltration

314
Q

Treatment of CLL?

A

chlorambucil, fludarabine, rituximab, prednisolone, cyclophosphamide, monoclonal antibodies, transplant, targeted therapy, transfusion

315
Q

What is the most common leukaemia in adults?

A

AML

316
Q

Symptoms of AML?

A

same as ALL, with hepatosplenomegaly and gum hypertrophy, bone marrow failure, malaise, weight loss, night sweats

317
Q

What is the diagnosis for AML?

A

auer rods, blood film, bone marrow and lymph node biopsy, immunotyping, genetic, FAB classification

318
Q

Risk factors of AML?

A

myeloproliferative disease, alkylating agents, ionising radiation exposure, downs syndrome

319
Q

What is AML treatment if younger than 60?

A

chemo w/anthracycline and cytarabine or methotraxate - given 5 cycles of 1 week blcoks

prophylatic cover for bacteria, viruses and fungi as infection is a major risk

320
Q

What is AML treatment if older than 60?

A

palliative anthracycline, cytarabine or mitoxantrone

bone marrow transplant if poor prognosis

321
Q

Which leukemia has the strongest association with the philadelphia chromosome?

A

CML

322
Q

clinical features of CML?

A

bone marrow failure, gout, bruising, hepatosplenomegaly, malaise, weight loss, night sweats, pallor, extramoddallar, soft tissue leukaemic diposit chlooma

323
Q

What is the Philadelphia chromosome?

A

t(9;22) (in 80% of CML cases) forms bcr-abl fusion gene

324
Q

What do investigations show in CML?

A

neutrophilia, mature myeloid precursors, increased basophils and eosinophils, decreased Hb, increased WBC

bone marrow aspiration shows increased cellularity, and increased myeloid precursors

325
Q

Risk factors of CML?

A

ionising radiation exposure

326
Q

What is the main treatment for CML?

A

imatinib

327
Q

Treatment of CML?

A

imatinub

328
Q

What is the difference between leukaemia and lymphoma?

A

leukaemia - bone marrow proliferative disorder (myeloid of lymphoid lineage)

lymphoma - neoplastic disease of mature lymphocyes in lymphoid tissue - solid tumour

329
Q

What happens in cells in acute and chronic stages?

A

acute - excess of blast cells, multipotent cells, rapidly dividing causing acute onset

chronic - cells tend to be more mature and have a more functional role, less rapidly dividing, so less acute onset of disease

330
Q

Which leukaemia is associated with downs syndrome?

A

ALL

331
Q

Why does hepatomegaly and splenomegaly occur in ALL?

A

higher basal metabolism so hep

excess defective cells have to go to spleen to be destroyed so sple

332
Q

What causes marrow failure in ALL?

A

replacement of marrow cells with blast cells

333
Q

What are the 3 stages of CML?

A

chronic (asymptomatic), accelerated (bleeding and splenomegaly) and blast phase (bone pain and AL signs)

334
Q

What are the two types of lymphoma?

A

Hodgkin’s and non-Hodgkin’s

335
Q

What are B symptoms?

A

temperature of >38, weight loss >10% of body weight in last 6 months, symptoms due to enlarge mass e.g. cough

336
Q

What is Non Hodgkin’s Lymphoma?

A

malignancies of B cell or T cell origin, and it is classified by the stage or maturation

337
Q

What 2 things can lymphoid progenitor cells become in the bone marrow?

A

Precursor T cell of precursor B cell

338
Q

In Non Hodgkin’s Lymphoma, are maligancies of B cell or T cell more common?

A

B cell (80%)

339
Q

Where do precursor T cells mature to become thymocytes?

A

In the thymus

340
Q

Why are T cells double negative?

A

Because they can become CD8+ or CD4+

341
Q

Where do naive T cells become activated?

A

In the lymph node

342
Q

What enzymes help precursor B cells undergo VDJ recombination of light and heavy chains to become naive B cell?

A

RAG1/RAG2

343
Q

What do naive B cells have?

A

IgM

344
Q

Where do naive B cells travel to?

A

lymph node

345
Q

What happens when a B cell comes across an antigen?

A

Phagocytoses the antigen and presents it on its surface until it comes across a T cell

346
Q

What happens in co stimulation of T and B cells?

A

naive CD4 T cell stimulates the B cell and vice versa to produce activated T cell and B cell

347
Q

What do T cell cytokines cause the B cell to do?

A

proliferate into centroblasts, undergo somatic hyper mutation by the AID enzyme, allowing point mutation so there are many centroblast with different IgM antibodies as their variable regions have slightly changed, so there can be increased or decreased affinity to that antigen

348
Q

Where do centroblasts move through after somatic hyper mutation?

A

through the germinal center to where there are many follicular dendritic cells which are presenting many antigens on its surface, also T helper cells there, they become centrocytes

349
Q

What do centrocytes need to survive and mature and how do they get this?

A

cytokines - so they sample the antigens from the dendritic cells using their specific IgM antibodies to then present to the T helper follicular cell to proliferate and differentiate

350
Q

What happens to centrocytes that have a decreased affinity for the antigens?

A

they will die through apoptosis

351
Q

What can centrocytes proliferate into?

A

memory B cell or undergo class switching plasmoblast which can become plasma cells that secrete antibodies

352
Q

What is the process called that allows B cells to change IgM into IgE, IgG etc/?

A

class switching

353
Q

What are thymic B cells?

A

B cells that reside in the thymus

354
Q

What is lymphoma?

A

tumour of the lymph from B and T cell development - heterogenous, with proliferation of lymph tissue

355
Q

How do lymphomas differ?

A

different cellular origin, morphology, immunophenotype, cytogenic and molecular abnormalities and response to treatment and prognosis

356
Q

How common is Non Hodgkin’s Lymphoma?

A

6th most common cancer, increasing prevalence

357
Q

Risk factors for Non Hodgkin’s Lymphoma?

A

family history, genetic polymorphism (SCID), immunological autoimmune disease, virus, HTLV-1, H.pylori, HHV-8, HBV+EBV, HIV, peticides, herbicides and smoking

358
Q

What lymphomas can T cells in the thymus give rise to?

A

precursor T cell neoplasm

359
Q

What lymphoma can T cells in lymph node give rise to?

A

peripheral T cell neoplasm

360
Q

When can T cell lymphomas arise?

A

during genetic rearrangement of the T cell lymphoma and during positive and negative selection in the thymus which can then lead to precursor of peripheral T cell neoplasms

361
Q

Why are B cell lymphomas more common then T cell?

A

as they go through more genetic changes

362
Q

What lymphomas can B cells give rise to?

A

mantle cell lymphomas, chronic lymphocytic leukemia and small lymphocystic lymphoma, Burkitt’s lymphoma, Germinal centre B like lymphoma (DLBCL), follicular lymphoma, activated B cell like DLBCL, primary mediastinal DLBCL

363
Q

What is the prognosis like for germinal center DLBCL?

A

60% 5yr survival

364
Q

What is the prognosis like for activated DLBCL?

A

35% %yr survival

365
Q

What are the most common Non Hodgkin’s Lymphoma?

A

DLBCL and follicular

366
Q

What neoplasms can plasma cells give rise to?

A

multiple myeloma - caused by too many plasma cells being produce

367
Q

How do lymphomas arise?

A

translocation of chromosomes and genetic mutations during rearrangement

368
Q

What chromosomes are translocated in lymphoma?

A

Bcl-2 and Bcl-6 genes

369
Q

What mutations and amplifications occur in lymphoma?

A

p53, Bcl-2, Bcl-6, MYC

370
Q

How do Non Hodgkin’s Lymphoma present?

A

painless lymphadenopathy, unintentional weight loss, fever, dyspnoea, hepatosplenomegaly, lymph node mass

371
Q

What is the Ann Arbor classification?

A

for lymphoma classification from lymph node biopsy

1-single lymph node region, lymphoid structure or extranodal site
2-two or more lymph node regions one side of diaphragm
3-two or more lymph node regions both side of diaphragm
4-diffuse or disseminated involvement of on of more extralymphatic organs

372
Q

What is the main diagnostic difference seen in Non Hodgkin’s Lymphoma and Hodgkin’s Lymphoma?

A

Hodgkin’s Lymphoma has Reed Sternberd cells

373
Q

What is the treatment of Non Hodgkin’s Lymphoma?

A

R-CHOP regimin

cisplarn, etoposide, methotrexate

374
Q

What does R-CHOP stand for?

A 
rituximab
cyclophosphamide
hydroxydaunomycin
oncovin
prednisolone
375
Q

What is the second most common Non Hodgkin’s Lymphoma and when does it mainly occur?

A

follicular lymphoma - in mid-late life - has bone marrow infiltration

376
Q

Treatment of follicular lymphoma?

A

field megavoltage irradiation, chemotherapy, R-CHOP, radioimmunotherapy, myeloblative consolidation in younger patients, HSCT

377
Q

Which is the most common Non Hodgkin’s Lymphoma in children?

A

Burkitt’s

378
Q

What are the 3 types of Burkitt’s?

A

endemic (EBV associated), sporadic (30% EBV related), AIDs related

379
Q

Which is the most rapidly proliferative lymphoma?

A

Burkitt’s

380
Q

How does Burkitt’s lymphoma present?

A

rapidly gorwing jaw tumour, abdominal mass with bone marrow involvement, mass in CNS, kidney, testis

381
Q

In who is DLBCL most common?

A

adults, male >female

382
Q

What prognostic index fatcors decrease prognosis in DLBCL?

A

> 60, stage 3/4, high serum lactate dehydrogenase level, performance status 2, 1 or more extended site

383
Q

Treatment of DLBCL?

A

allopurinol, RCHOP, chemoimmunotherapy, interum PET scanning, intrathecal methotrexate, palliative chemo and radiation, peripheral blood stem cell harvest and autograft

384
Q

In who is mantle cell lymphoma most common?

A

late life, male >female

385
Q

Treatment of lymphoblastic lymphoma?

A

plasmapheresis to reduce paraprotein, blood transfusions and if young bone marrow transplant

386
Q

What is primary extranodal lymphoma?

A

lesion or mass at site, normally in CNS, stomach and skin

387
Q

What is primary CNS lymphoma usually seen?

A

DLBCL in immuno-competent and immuno-suppressed

388
Q

What is primary gastric lymphoma?

A

extanodal marginal zone lymphoma of mucosa associated tissue or DLBCL on a background of MALT lymphoma

389
Q

symptoms of primary gastric lymphoma?

A

gastric ulceration, mass, indigestion, bleeding, endoscopic biopsy

390
Q

Treatment of primary gastric lymphoma?

A

regular endoscopys, heliobactor eradication therapy, irradiation to gastric bed, chemoimmunotherapy

391
Q

What lymphoma can be T or B cell?

A

primary cutaneous lymphoma, both arise singly and multiply in the skin and persue a very long natural history

392
Q

Complications of lymphoma?

A

increased infection risk, recurrence and metastases, chemo complications, neuro complications

393
Q

How do Reed Steinburg cells appear and what causes them in Hodgkin’s Lymphoma?

A

giant cells, owl appearance

due to eosinophilic inclusions in the nuclei

394
Q

What are popcorn cells?

A

small cell with hyperlobulated nuclues and small nucleoli, a variant of reed steinberg cells

395
Q

When does Hodgkin’s Lymphoma usually occur?

A

young adults and elderly

396
Q

Symptoms of Hodgkin’s Lymphoma?

A

B symptoms, hepatosplenomegaly, alcohol induced pain, mediastinal lymphadenopathy, enlarged non tender rubbery nodal

397
Q

Causes of Hodgkin’s Lymphoma?

A

male, exotoxin exposure, infection with EBV, immunosuppresed, previous infection with mononucleosis HL

398
Q

Do systemic symptoms suggest Hodgkin’s or non Hodgkins Lymphoma?

A

Hodgkin’s Lymphoma

399
Q

What is the staging of Hodgkin’s Lymphoma called?

A

Cotsworld staging

400
Q

Treatment of Hodgkin’s Lymphoma?

A

educate, macmillan, chemo (ABVD) following by radiotherapy

401
Q

Who does G6PD deficiency mainly affect?

A

african, middle east, mediterranean, X linked so male, but women can also be affected

402
Q

How is G6PD deficiency diagnosed?

A

by a screening test for NADPH

403
Q

What is G6PD deficiency crisis characterised by?

A

haemolysis, jaundice and anaemia

404
Q

Important drug interactions in G6PD deficiency?

A

primaquine, sulphonamides, nitrofurantoin, quinolones, dapsone

405
Q

In who does parovirus occur in?

A

children in epidemics (also called slapped cheek syndrome)

406
Q

What does the parovirus cause?

A

decreased RBC production, so dramatic Hb drop

407
Q

Do elliptocytosis and spherocytosis have horizontal or vertical interactions?

A

e - horizontal

s - vertical

408
Q

Function of G6PD?

A

protects from damage as it provides fuel for RBC and generates redox capacity to protect it, so without it leads to shortened RBC lifespan from oxidative damage

409
Q

What is classed as febrile neutropenia?

A

temp >38 and neutrophil count

410
Q

What is hyperviscosity?

A

increase in whole blood viscosity due to raise Ig from malignant clone of plasma cells

411
Q

Effect of hyperviscosity?

A

sludging and lack of perfusion through the microvasculature leading to leukaemia, myeloma, polycythaemia, waldenstroms macroglobulinaemia

412
Q

How does hyperviscosity present?

A

lethargy, headaches, confusion, visual disturbance, cranial nerve defects, ataxia, retinal haemorrhage, dyspnoea, cough

413
Q

Treatment of hyperviscosity?

A

plasmapheresis, leucopheresis, stumbling blocks, avoid blood transfusions, chemo

414
Q

What is tumour lysis syndrome?

A

life threatening matabolic derangement leading to renal, cardiac and neuro complications

415
Q

When does tumour lysis syndrome occur?

A

in leukaemia and non hodgkins lymphoma

416
Q

Treatment of tumour lysis syndrome?

A

aggressive IV hydration, cheo, prevent hyperuricaemia, allopurinol, treat hyperkalaemia, refer for dialysis, control electrolytes

417
Q

Problems with blood provision?

A

donor population are mainly white british, sickle population is normally diverse background, often multiple transfusions needed, high risk of raising antibodies, may be difficult to provide large number of matched units quickly, infrom NBS early

418
Q

What is acute sickle chest syndrome?

A

HbSS inheriting 2 cpies of beta chain mutation, polymerisation of Hb cascade of effects, reducing blood flow to tissue leading to infarction, causes hypoxia, raised RR, chest pain, fever

419
Q

Treatment of acute sickle chest syndrome?

A

red cell exchange transfusion, cross match patient for 8 units of blood, usually require central access, liase with apheresis team, terminate the viscous cycle by reducing HbS, o2, opiates

420
Q

What is myeloma?

A

malignant disease of plasma cells in the bone marrow

421
Q

How common is multiple myeloma?

A

second most common haematological cancer

422
Q

Who does multiple myeloma usually affect?

A

older people

423
Q

Symptoms of multiple myeloma?

A

back pain, RTI, anaemia, tiredness, fatigue, renal failure, proteinuria, fractures, dehydration

424
Q

What will investigations show in multiple myeloma?

A

proteinuria, lytic bone lesions

425
Q

How is the vertebra affected in multiple myeloma?

A

undergoes lytic bone lesions and haematopoesis

426
Q

pathophysiology of multiple myeloma?

A

increase in plama cell production so >10% plasma cells in bone marrow, so produce abnormal antibodies (IgG and IgA) in 75% of cases, and only produce only light chains (paraproteins)

427
Q

What cells make and break down bone?

A

osteoblasts build

osteoclasts break down

428
Q

What are bone marrow stromal cells?

A

regulates haematopoesis

429
Q

What do osteoblasts secrete?

A

osteoids and minerals (calcium and phosphate) to form strong bones

430
Q

What do osteoclasts secret?

A

HCl, causing release of calcium and phosphate form the bone to enter the blood

431
Q

What activates osteoclasts?

A

osteoblasts that express RANKL which stimulates osteoclast activity and OPG decreases osteoclast activity

432
Q

What happens to bone marrow stromal cells in multiple myeloma?

A

interact with cancerous cells through receptos and cytokines, resulting in cytokine mediated cell growth, survival, drug resistance and migration, allowing the multiple myeloma cells to survive, leading to increased osteoclast activity and reduced osteoblast activity

433
Q

What do multiple myeloma cells secrete?

A

cytokines

e.g. IL-3 - inhibiting osteoblast activity

DKK1 - inhibitng OPG production so increases osteoclast activity

MIP1a - stimulates osteoclast activity

434
Q

How can osteoclasts stimulate themselves?

A

through IL-6

435
Q

What does an increase in osteoclatic activity lead to?

A

bone fractures and lesions and more calcium entering the body so hypercalcaemia, leading to dehydration and nerve proteins

436
Q

What effect does paraproteins produced by multiple myeloma have?

A

leads to renal failure and light chains present in urine (Bencejones proteins)

437
Q

How does multiple myeloma cause anaemia?

A

shift from myeloid progenitor to lymphoid progenitor, overproduction of plasma cells so lack of RBC production, kidney failure, so decrease erypotietin production

438
Q

Investigations in multiple myeloma?

A

blood and urine

anaemia, paraproteinuria, hypercalcaemia, decrease normal antibodies, increased blood urea and nitrogen, increase in creatinine (renal incompentence), bence jones proteins, increased alkaline phosphatas

439
Q

What will bone investigations show in multiple myeloma?

A

bone aspiration, bone marrow biopsy, >10% plasma proteins, osteoporosis, lytic lesions in bone and soft tissue, pepper pot skull, vertebral collapse, hyperviscosity is rare

440
Q

Diagnosis of multiple myeloma?

A 
prescence of monoclonal plasma cells in bone marrow >10%, monoclonal antibodies in serum or urine and one or more of the following: (CRAB)
hypercalcaemia
renal insuffieciency
anaemia
lytic bone lesions
441
Q

Treatment of multiple myeloma?

A

chemotherapy and radiotherapy of vertebra etc

NSAIDs, bisphosphonates, EPO transfusion, IV Ig infusion, immunoparesis

442
Q

What is virchows triad?

A

slowing of blood flow, hypercoagulability, vessel wall damage

443
Q

At what age does multiple myeloma occur?

A

70 years

444
Q

What is the main cause of death in multiple myeloma?

A

renal failure

445
Q

What are the 4 classes of multiple myeloma?

A

symptomatic - significant paraproteinaemia or increase bone plasma cell, evidenceof organ damage

asymptomatic - significant paraproteinawmia, or increased bone plasma cells but no organ damage

monoclonal gammopathy of undetermined significance - monoclonal paraprotin in seum but not amm or smm

plasmacytoma - tumour of neoplastic plasma cells

446
Q

What happens in a serum electrophoresis and immunofixation for multiple myeloma?

A

proteins move across a gel according to their charge, separate out according to size

paraprotein produces a band in HTE Ig region

tall spikes represent large amounts of single paraprotein immunoglobulin

Phase 2a (15 decks)

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