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MBBS - Year 2 > Haematology - Coagulation and Bone Marrow in Health and Disease > Flashcards

Haematology - Coagulation and Bone Marrow in Health and Disease Flashcards

1
Q

Haematopoiesis

A

The process from which blood cells are produced and developed from a pluripotent stem cell

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2
Q

Where does haemopoiesis occur in the foetus

A

Foetal yolk sac, liver, spleen and lymph nodes

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3
Q

Where does haemapoiesis occur in babies in children

A

All bone marrow (red marrow —> yellow marrow)

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4
Q

Where does haemopoiesis occur in adults

A

Bone marrow of axial Skelton and proximal long bones

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5
Q

Extramedullary haematopoiesis

A

Haemaopoiesis occurring ourisde of the bone marrow e.g. liver and spleen

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6
Q

When does extra medullary haematopoiesis take place

A

Bone marrow disease e.g. myelofibrosis when marrow becomes occupied w/ fibrotic tissue

Yellow (fatty) marrow can also be recruited top produce blood cells

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7
Q

What may extramedulalry haematopoiesis lead to

A

Enlargement of liver +/- spleen

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8
Q

Erythropopiesis

A

Production and development of red cells

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9
Q

Production and development of granulocytes

A

Granulopoiesis

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10
Q

Thrombopoiesis

A

Production and development of platelets

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11
Q

Function of maegakaryocytes

A

Produce platelets and stay in bone marrow - does not pass into blood stream

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12
Q

Properties of haemopoeietic stem cells

A

Differentiation

Self-renewal

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13
Q

How long does it take for a stem cell to become a formed blood cell

A

2-3 weeks

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14
Q

How does the micorenevornment affects the function of haematopoietic stem cells

A

Growth factors

Interaction w/ neighbouring cells

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15
Q

Examples of growths factors stimulating different haematopoietic stem cells

A 
Epo
Tpo
IL-5, IL-6
G-CSF
M-CSF
GM-CSF
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16
Q

Composition of blood

A

Specialised connective tissue w/ 4 main components: RBC, WBC, plasma and platelets

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17
Q

Where are blood cells found in the blood

A

Suspended in plasma

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18
Q

Blood volume in M and F

A

5-6L in M

4-5L in F

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19
Q

Cells formed from myeloid progenitor cells

A

RBC
Platelets
Granulocytes - eosinophil, basophil, neutrophils

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20
Q

Cells formed from lymphoid progenitor cells

A

B cells
T cells
NK cells

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21
Q

When will affected cell lineage number go up in the blood

A

If the stem cells is ‘overactive’ either because of clonal genetic defect (mlaignancy) or because environment drives activity

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22
Q

Why must haematoppoiesis be regulated

A

Blood cell production must match blood cell destruction

Production may need to be increased in certain situation e.g. bleeding, infection

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23
Q

How do haematopoietic growth factors affect cell production

A

Stimulate increased production

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24
Q

Red cells and erythropoietin (epo) feedback loop

A

Low blood oxygen causes liver and kidney to please epo into bloodstream
This increases number of red cells and increases oxygen-carrying capacity

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25
Q

Why might a high blood count occur

A

Primary - abnormal bone marrow
Secondary - normal bone marrow

Red cell destruction due to asnet or poorly perfuming spleen (hyposplenism)

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26
Q

Which is the most common reason for high blood counts

A

Secondary causes

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27
Q

Primary causes of leucocytosis

A

Leukaemia
Lymphoma
Myeloproliferative disorders

Bone marrow must be treated/ managed

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28
Q

Secondary causes of leucocytosis and thrombocytois

A 
Infection 
Infl
Infarction 
Tumour
Stress/ trauma - leucocytosis only
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29
Q

Example of a condition causing primary thrombocytosis

A

Essential thrombocythemia

Treat/ manage bone marrow e.g. hydroxycarbamide

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30
Q

What is haematocrit (Hct)

A

Ratio of RBC to total blood volume

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31
Q

True erythrocytosis vs apparent polycythemia

A

True erythrocytes ‘polycythemia’ is an increased number of red cells (increased Hct)
Apparent polycythemia is caused by reduced plasma volume

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32
Q

Primary causes of erythrocytosis - clonal stem disorders

A

Polycythemia vera

Treat/ manage the bone marrow e..g venesection +/- hydroxycarbamide, plus aspirin

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33
Q

Causes of apparent polycythemia

A

Overweight
Smoking
Alcohol excess
Medications e.g. diuretics

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34
Q

Secondary causes of erythrocytosis - raised epo

A 
Low oxygen in the blood e.g COPD
Tumours 
Doping 
High affinity Hb - high altitudes
Polycystic renal disease 
L to R shunt in heart
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35
Q

What can polycythemia vera and essential thrombocythemia lead to in untreated

A

Thrombosis

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36
Q

Reasons for low blood counts

A

Underproduction

Reduced survival in the circulation

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37
Q

Reasons for leucopenia - underproduction

A

Drugs affecting stem cells e.g. chemo

Part of pancytpenia due to marrow failure

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38
Q

Reasons for leucopenia - reduced survival

A

Autoimmune
Drugs
Consumption - flu
Combi e.g viral hepatitis - both the virus and drugs used to treat cause reduced survival

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39
Q

Reasons for thrombocytopenia - underproduction

A

Drugs affecting stem cell
liver failure (tpo underproduction)
Part of pancytopenia due to marrow failure

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40
Q

Reasons for thrombocytopenia - peripheral destruction

A

Autoimmune (ITP)
Hypersplenism (hiding in the spleen)
Drugs
Infections/ infl/ sepsis increases consumption of platelets

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41
Q

Hypersplenism

A

Inappropriate removal of erythrocytes, granulocytes or playlets from blood

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42
Q

What do pts w/ hypersplenism characteristically have

A

Splenomegalyu
Destruction or pooling of 1/1+ by the cell —> release of immature cells in PB
Normal bone marrow

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43
Q

Drugs causing peripheral destruction of platelets

A

Penicillin
Furosemide
NSAIDs

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44
Q

Reasons for low blood counts caused by reduced production

A 
Myeloma - bone marrow overrun w/ functionally useless cells; normal cells incl stem cells crowded out 
Myelodysplasia 
Metastatic malignancy 
Myelofibrosis 
Leukaemia 
Lymphoma 
Aplastic anaemia 
Haematininc deficiency
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45
Q

Aplastic anaemia

A

Empty bone marrow cased by stem cell failure
Can be primary or most commonly secondary e.g. drug-induced, viruses
BM no longer produces blood cells

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46
Q

What does haematinic deficiency cause in blood counts

A

Pancytopenia

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47
Q

White cell malignancies divided by lineage

A

Myeloid cells - AML, myeloproliferative disorders and myelodysplasia
Lymphoid cels - ALL, CLL, lymphoma, myeloma

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48
Q

White cell malignancies of immature cells (blasts)

A

AML

ALL

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49
Q

White cell malignancies of mute cells

A 
Myeloproliferative disorders 
Myelodysplasia 
CLL
Lymphoma 
Myeloma
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50
Q

What are the myeloproliferative disorders

A

Polycythemia Vera (PV)
C/c myeloid leukaemia (CML)
Essential thrombocythemia (ET)
Myelofibrosis

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51
Q

Myledysplasia (MDS)

A

Haematopoietic stem cell malignancies, related to myeloproliferative disorders
Abnormal maturation as well as abnormal proliferation in BM
Dysplastic cells don’t get into blood

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52
Q

What does MDS present with on a FBC

A

Pancytopenia

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53
Q

What % of MDS pts evolve into AML

A

20%

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54
Q

Myelofibrosis

A

Malignant proliferation of reticulin fibres in bone marrow

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55
Q

Features of myekofibrosis

A

Anaemia
Leucoerythroblastic blood film
Splenomegaly

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56
Q

What can myelofibrosis dveelpi from

A

MPN or be primary

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57
Q

MPN

A

Myelo proliferative neoplasms

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58
Q

What can myelofibrosis transform into

A

AML

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59
Q

Causes of low blood counts w/ normal bone marrow (reduced cell survival)

A

Immune cellular destruction
Drugs
Haemorrhage
Hypersplenism

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60
Q

When would you see Auer rods on a blood film

A

Acute (myeloid) leukaemia - blasts

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61
Q

Causes of hyposplenism

A

Splenectomy e.g. therapeutic or due to trauma
Auto-infarction e.g SCD
Infiltration e.g metazoic malignancy
Under-functioning e.g. coeliac disease

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62
Q

Hyposplenism on a blood film

A

Howell-Jolly brides
Target cells
Acanthocytes

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63
Q

Causes of neutrophilia

A 
Bacterial infection  **
Infl cords 
Burns 
Cigarette smoking 
Steroids (glucocorticosteroids)
G- CSF
Solid tumours 
Myeloproliofertiave disorders e.g. CML *
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64
Q

General causes of lymohocytosis

A 
Viral infections e.g. EBV *
Hypospleinsim 
TB 
Brucellosis 
CLL 
Lymph. w/ 'spillover'
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65
Q

General causes of eosinophilia

A 
Allergic reaction - most common 
Vasculitis 
Drugs 
Worm infestations 
Cancer (esp solid tumours and lymphoma)
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66
Q

Most common causes of microcytic anaemia

A

IDA

ACD

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67
Q

Most common cause of microcytic anaemia

A

Vit B12 or folate déficiency - causes pancytopenia

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68
Q

What addn info can we get from a blood film

A

Morphology of rd cells, white cells and platelets
Morphology of any abnormal cells incl blasts
Blood borne infections e.g. malaria
Roleuax (stacking of RBCs), agglutinates, fibrin clots, platelet clumping

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69
Q

Rouleaux on blood film

A

Stacking of RBCs

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70
Q

When does rouelaux occur

A

In infection
Reaction condns
Myeloma

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71
Q

Lymphoma

A

Cancer of the lymph nodes

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72
Q

Classification of lymphoma

A

Hugh grade or low grade
B-cell or (less commonly) T cell
Hodgkin or Non-Hodgkin

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73
Q

What do lymphoma pts px with

A

(Painless) swellings - lymphadenopathy
+/- B symptoms

May be incidental finding on MRI

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74
Q

B symptoms seen in lymphoma

A

Night sweats
Fever
Unintentional wt loss >10% in 6/12

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75
Q

What may lymphoma pts present with

A

Hepatosplenomegaly
Symptoms related to cytopenias
Symtoms related to lumps in/compressing important structures e.g. kidneys, lungs, bowel
Pruritus

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76
Q

Hx of high grade vs low grade lymphoma

A

Short vs longer or ‘no’ hx

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77
Q

Growth of high grade vs low grade lymphoma

A

Quickly vs slowly

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78
Q

Which lymphoma pts are symptomatic

A

High grade

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79
Q

Difference in approach to treating high grade vs low grade lymphoma

A

Treatment always required immediately vs watch and wait

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80
Q

Which lymphoma in a lifelong illness

A

Low grade - not curable

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81
Q

Which lymphoma. treatment involves intensive chemo

A

High grade

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82
Q

How many curative opportunities are there in high grade vs low grade lymphoma

A

One change in high grade (or maybe two) Bute low grade can usually be treated again and again

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83
Q

Staging of lymphoma

A

Ann Arbor

Stage I (best) - IV (worst)
Looks at LN and organ involvement

A: absence of B symptoms
B: B sx

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84
Q

How is lymphoma diagnosed

A

Bx of lump - core bx ro whole node excision

NOT fine needle aspirate (FNA)

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85
Q

Burkitt lyphoma

A

Very rapidly growing subtype of high-grade B-cell NHL

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86
Q

Genetic cause of Burkitt’s lymphoma

A

t(8; 14) - translocation of chromosome 8 to 14

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87
Q

What is endemic Burkitt’s lymphoma associated w/

A

EBV infection

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88
Q

Is Hodgkin lymphoma low-grade or high-grade

A

High

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89
Q

Epidemiology of Hodgkin lymphoma

A

Most common in young adults and 60+

M > F

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90
Q

What infection is associated w/ Hodgkin lymphoma

A

EBV

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91
Q

Px of Hodgkin lymphoma

A

Pruritus
Often present w/ mediastinal mass - SVC obstruction, bronchial compression (cough, SOB, stridor)
Alcohol-induced LN pain

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92
Q

Dx of Hodgkin lymphoma

A

Bx - scattered Reed Sternberg (owl eyes) cells and reactive cells

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93
Q

Treatment and prognosis of Hodgkin lymphoma

A

Different chemo to NHL

Prognosis particularly good

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94
Q

Imaging for lymphoma staging and response

A

PET scan

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95
Q

In which lymphoma is extra-nodal disease common

A

NHL

GI tract - gastric MALT lymphoma in c/c H. pylori infection, small bowel lymphoma
Skin- mycosis fungoides

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96
Q

Most common leukaemia

A

CLL

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97
Q

Usual findings of CLL

A

incidental lymphocytosis on FBC

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98
Q

If there is only lymphadenopathy and NO lymohocytosi, what should be suspected

A

Small lymphocytic lymphoma (SLL), low grade NHL

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99
Q

Diagnosing CLL

A

FBC, blood film (leucocytosis and smear cells)
Examination findings
Immunophenotyping - monoclonal antibody w/ immunological marker for CD5 and CD19

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100
Q

When would you treat CLL immediately

A

Bulk disease e.g. lymphadenopathy
Disease obstructing major organ
Bone marrow failure
B sx

‘Watch and wait’ approach is usually used

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101
Q

Drug treatment for CLL

A

Monoclonal antibody + chemo e.g. rituxumab, fludarabine and cyclophosphamide
B-cell signalling inhibitors (tablets) e.g. ibrutinib

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102
Q

Epidemiology of CLL

A

Usually >70 yrs

Generally slowly progressive

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103
Q

Genetic cause of CML

A

t(9:22) - ‘philadelphia chromosome’

Codes for a anew protein, BCR-ABL, a tyrosine kinase

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104
Q

Why is CML always treated when diagnosed

A

Can progress to AML

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105
Q

CML px

A

Incidental - neutrophilia w/ granulocyte precursors
Sx related to anaemia and splenomegaly e.g. pain and early satiety
B sx

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106
Q

Dx of CML

A

FBC (neutrophilia and presence of myelocytes) and blood film
FISH to look for Philadelphia chromosome
Bone marrow bx to assess phase

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107
Q

FISH

A

Fluroscent in-situ hybridisation

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108
Q

Treatment of CML

A

Tyrosine kinase inhibitor e.g, imatinib
Daily tablets lifelong
Aim for low levels of BCR-ABL, use PCR

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109
Q

A/c leukaemia px

A

Consequences of cytopenias e.g. bleeding, anaemia, infections
Short hx - treatment required quickly

ALL pts sometimes have lympadenopathy or hepatosplenomegly at dx

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110
Q

Dx of a/c leukaemia

A

Blasts on blood film or BM (> 20%)

Dx confirmed w/ immunophenotyping (distinguishes AML from ALL)

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111
Q

Epidemiology of a/c leukaemia

A

ALL more common in children (little people)

AML more common in elderly (mature people)

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112
Q

APML

A

A/c promyelocytic leukaemia

Subtype of AML associated w/ DIC (medical emergency)

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113
Q

Treatment options for a/c leukaemia

A

Intensive chemo, may involve allogenic stem cell transplant (may be curative, v toxic)
Low intensity chemo (may prolong life but not curatiev, still toxic)
Palliative care - sx control at home

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114
Q

Aside from chemo , what else to a/c leukaemia pts need

A 
Hickman line 
Prophylactic antimicrobials 
Transfusions (Red cells, platelts)
Treatment of neutropenic sepsis
Pian control 
Antiemetics 
Psychological support
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115
Q

Haemostasis

A

The arrest of bleeding

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116
Q

What does a hyperocagulable state lead to

A

Thrombosis

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117
Q

What does reduced coagulation lead to

A

Bleeding disorder

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118
Q

Phases of CML

A

C/c
Acceleration
Blast - crises

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119
Q

Rule of 1/3 in CLL

A

1/3 don’t progress
1/3 progress lowly
1/3 undergoes Richter’s transformation to become aggressive high-grade lymphoma.

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120
Q

Features of all types of leukaemia

A

BM failure causing pancytopenia
B sx
Generalised painless lymphadenopathy
Hepatosplenomagly

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121
Q

Sx of thrombocytopenia

A

Bleeding
Ecchymoses (bruises)
No-blanching petechiae (smaller)/ purpura (bigger)

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122
Q

Specific sx of AML

A

Infiltration –> gum hypertrophy, skin infiltration

DIC in APML

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123
Q

Specific sx of ALL

A

Children w/ FTT
CNS involvement
Painless unilateral testcular swelling
Renal enlargement

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124
Q

CNS involvement in ALL

A

Inc cranial nerve palsies and meninges due to mets to meninges –> neck stiffness and papilloedema

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125
Q

Papilloedema

A

Optic disc swelling

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126
Q

Stages of haemostasis

A

Tissue injury –> thrombus formation -> tissue repair –> dissolution of the thrombus

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127
Q

How does haemostasis work?

A

Vasoconstriction - limits blood flow to the injured region
Formation of platelet plug
Formation of fibrin mesh - to stabilise the thrombus
Clot dissolution - through the action of plasmin

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128
Q

Steps of formation of platelet (primary haemostatic) plug

A

Adhesion - platelets come into contact w/ damaged sub endothelium
Activation - vWF factor causes platelets to adhere to ECM collagen
Aggregation - platelet-platelet interaction via fibrinogen

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129
Q

Examople of primary haemostasis

A

Von Willebrand disease

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130
Q

Features of Von Willebrand disease

A

Usually pattern = mucosal haemorrhage
Bleeding at time of trauma/ surgery
Menorrhagia
Nose bleeds

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131
Q

What do the symptoms of Von Willebrand disease vary according to

A

Amount of vWF (most commonly mild form of disease)

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132
Q

Secondary haemostasis

A

Stabilisation of platelet plug

Fibrin acts like gun giving the platelet mass strength allowing to function as a secure patch and protect the base to allow repair and healing

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133
Q

Purpose of coagulation

A

To produce a stable haemostat plug via localised fibrin clot formation at the site of vessel injury

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134
Q

Mechanism of blood coagulation

A

Enzymatic cascade of series of coagulation proteins sequentially activated and a plied which results in a fibrin clot

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135
Q

Coagulation pathways

A

Intrinsic
Extrinsic
Common

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136
Q

Factors in intrinsic coagulation pathway

A

XII —> XIIa
XI —> XIa
IX —> IXa

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137
Q

Factors in extrinsic coagulation pathway

A

VII
VII + TF —> VIIa: TF

Tissue factor released when vessels are injured

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138
Q

Factors in common coagulation pathway

A

X —> Xa: Va
II (prothrombin) —> IIa (thrombin)
III (fibrinogen) —-> fibrin (IIIa)

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139
Q

Congenital disorder of 2’ haemostasis

A

Low blood clotting factors - Haemophilia A or B

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140
Q

Haemophilia A vs B

A

A - lack of factor VIII

B - lack of factor IX

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141
Q

Usual pattern of haemophilia

A

Joints/ soft tissue bleeding

Bleeds into ‘target’ joints –> arthritis joint
Retroperitoneum
Bleeding at times of trauma/ surgery

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142
Q

What do the sx of haemophilia vary accord to

A

Amount of factor 8/9 - lower levels, worse the bleeding

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143
Q

Acquired disorder of 2’ haemostasis

A

Warfarin, liver disease (clotting factors produced in liver)

Much more common than congenital

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144
Q

What stops the coagulation process from forming thrombi throughout the circulation

A

Coagulation inhibitors

Fibrinolysis - breakdown of the fibrin clot by plasmin

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145
Q

Coagulation inhibitors in body

A

Antithrombin
Protein C
Protein S

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146
Q

How does fibrinolysis stop the coagulation process from forming thrombi throughout the circulation

A

Plasminogen —> palms

Fibrin breaks down into fibrin degradation products (FDPs) AKA D-dimers which stabilises 1’ haemostatic plug

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147
Q

Blood used in lab coagulation tests

A

Anticoagulated blood - coagulation proteins inactivated by anticoagulant (citrate) - blue bottle
Clotted blood - Coagulation proteins not present, no anticoagulant - yellow bottle

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148
Q

Coagulation testing

A 
Measurement of time intakes to for a fibrin clot in plasma 
As the coagulation factors have been invited, an 'activator' is added to start the coagulation 
Different pathways (and coagulation factors) can be assessed by added different activators
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149
Q

Coagulation screen

A 
Prothrombin time (PT)
Activated partial thromboplastin time (APTT)
Thrombin time (TT) - less commonly used
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150
Q

Prothrombin time

A

Tissue factor is added too ample of plasma along w/ Ca

Time until fibrin formation is measured by shining a light (initial solution is transparent)

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151
Q

What pathway does PT look at

A

Extrinsic and common

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152
Q

What factors does PT look at

A

VII

V, X, prothrombin, fibrinogen

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153
Q

Normal clotting time for PT

A

10-13s

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154
Q

When is PT abnormal

A

Liver disease
Warfarin
DIC

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155
Q

Activator in APTT

A

‘Contact activator’

Phospholipid and Ca

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156
Q

What pathway does APTT look at

A

Intrinsic and common

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157
Q

What clotting factors does APTT look at

A

VIII, IX, XI, XII

V, X, prothrombin, fibrinogen

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158
Q

Normal clotting in AOTT

A

24-38 s

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159
Q

When is APTT abnormal

A

Haemophilia A/B
DIC
Lupus anticoagulant

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160
Q

Activator in TT

A

Thrombin

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161
Q

Pathway measured in TT

A

Fibrinogen to fibrin

162
Q

Factors TT look at

A

Fibrinogen

163
Q

Normla clotting time for TT

A

14-16

164
Q

When is tT abnormal

A

Low fibrinogen states

165
Q

Causes of over coagulation

A

Too many cells
Deficiency of natural anticoagulants
Other coagulation abnromlaities

166
Q

Too many cells causing over coagulation

A

Increased platelets

Increased RBCs

167
Q

Other coagulation abnormalities causing overcoagulation

A

Factor V Leiden variant - factor V which is resistant to inactivation by Protein C
Prothrombin gene variant - elevated levels of prothrombin

168
Q

What can bleeding disorders arise due to

A

Problems w/ blood vessel wall
Problems w/ vWF
Problems of platelets
Problems w/ the coagulation factor cascade

169
Q

Inherited vascular defects that can cause bleeding disorders

A

Hereditary haemorrhage telangiectasia

CTD

170
Q

Acquired vascular defects that can cause bleeding disorders

A

Senile purpura
Steroids
Scurvy
Amyloid

171
Q

Causes of low platelets causing bleeding disorders

A

Inherited - rare

Acquired - immune (ITP, TTP), bone marrow failure, drugs

172
Q

Causes of functional platelet abnormality leading to bleeding disorders

A

Inherited - rare

Acquired - drugs e.g. aspirin, clop, uraemia (renal failure)

173
Q

Inherited problems w/ the coagulation cascade

A 
Haemophilia A (factor VIII deficiency)
Haemophilia B (factor IX deficiency)
174
Q

acquired problems w/ the coagulation cascade (factor deficiencies)

A

Drugs e.g. warfarin, heparin, DOACs
Severe liver disease
DIC
Massive blood loss

175
Q

TTP

A

Thrombotic Thrombocytopenia purpura

176
Q

Genetic cause of TTP

A

Absent ADAMTS13 (due to an antibody), leads to ultra large vWF multimer which binds platelets in the microcirculation

177
Q

What does TTP cause

A

Micro thrombi and consumption of platelets

Ischaemia in critical organs

178
Q

Classical pentad of TTP

A 
Fever
MAHA
Renal impairment 
Fluctuating neurological signs - blood clots in microcirculation of brain 
Thrombocytopenia
179
Q

MAHA

A

Microangiopathic Haemolytic Anaemia

180
Q

Is TTP a haematological emergency

A

Yes - remove plasma w/ multimers

181
Q

What is anticoagulant therapy

A

Using drugs to treat and/or prevent thrombosis

Conventionally doesn’t incl antiplatelets e.g. aspirin

182
Q

Common indication for anticoagulants

A 
Prevention of CVA in AF 
Treatment of VTE 
Prevention of recurrent VTE 
Prevention of valvular thrombosis/  embolism in metallic heart valves 
Treatment of ACS 
Thromboprophylaxis
183
Q

Types of DOACs

A

Factor Xa inhibitors - apixaban, rivaroxaban, edoxaban

Thrombin inhibitors - dabigatran

184
Q

Parenteral thrombin inhibitor

A

Argotroban

Bivalirudin

185
Q

MOA of warfarin

A

Competitivlh natganoised vit K, which is necessary for production of clotting factors II, VII, IX and X

186
Q

Speed of warfarin onset of actin

A

Slow, several days until therapeutic

187
Q

INR calculation

A

INR = (PT pt/ PT control)^ thromboplastin ISI

188
Q

Why are pts on warfarin monitored w/ INR

A

High inter-pt variation

189
Q

Strength of warfarin tablets

A 
1mg = brown
3mg = blue 
5mg = pink
190
Q

Warfarin monitoring

A

Regular monitoring needed
Pts provided w/ a yellow book
Target INR:: 2.5 (range 2-3) is the standard intensity - some indications have higher target INR range

191
Q

What is the incidence of haemorrhage proportional to

A

INR - BUT can occur within target range

192
Q

Factors affecting INR

A

Individual variation/ genetic
Drugs (incl alcohol) can potentiate the effects of warfarin
Diet e..g. vit k
Intercurrent illness
Mistaken dose e.g elderly, visually impaired

193
Q

Implication of drugs potentiating warfarin

A

INR must be checked within 5 days of starting/ stopping new drugs

194
Q

Types of heparins

A 
Unfractoinated heparin (UFH)
LMWH e.g. dalteparin, tinzaparin, enoxaparin
195
Q

Administration of heparins

A

IV or s/c

Destroyed by gastric acid so oral administration not possible

196
Q

What is UFH a mixture of

A

Different wt heparin molecules

197
Q

MOA of UFH

A

Potentiates antithrombin increasing anticoagulant effect

198
Q

Clinical uses of UFH

A

Initial treatment of VTE

Anticoagulant ‘bridging therapy’ to cover surgery in Hugh thrombotic risk pts

199
Q

How does UFH affect clotting screen

A

Prolongs APTT - if used at treatment doses requires regular monitoring of APTT

200
Q

Time for UFH onset of action

A

Immediate but large doses required for full therapeutic anticoagulant (continuous IV infusion)

201
Q

When are small doses of UFH given

A

Thromboprophylaxis (s/c injection)

202
Q

Monitoring for UFH

A

Large inter-person variability - measure APTT

203
Q

Plasma half-life fo UFH

A

Short (20-120 MINS)

204
Q

Potential side effect of UFH

A

Heparin induced thrombocytopenia (immune reaction)

205
Q

Reversal agent for UFH

A

Protamine

206
Q

MOA of LMWH

A

Majority of effect is anti Xa (indirectly through antithrombin)
Lesser degree of thrombin inhibition

207
Q

When would you give a higher over a lower dose of LMWH

A

High dose for full anticoagulation

Lower dose used for VTE prophylaxis

208
Q

Can APTT be used to assess LMWH effect

A

No

Variable effect of APTT - may be normal

209
Q

Onset time of LMWH

A

Immediate

210
Q

Monitoring for lMWH

A

Non required

Unless severe renal failure or extremes of body wt - can use anti Xa

211
Q

What is treatment dose for LMWH based on

A

Wt

212
Q

Excretion of LMWH

A

Renal - will accumulate in renal failure

213
Q

Which has a longer plan a half-life out of UFH and LMWH

A

LMWH - so can be given for most indications

214
Q

What is the risk of HIT with LMWH

A

Much lower than UFH

215
Q

Reversal agent for LMWH

A

None available

216
Q

APTT target for pts being anticoagulants w/ UFH

A

2.0

Measure APTT ration every 6 hrs until stable

217
Q

MOA of fondaparinoux

A

Effect mediated by antithrombin

Only inhibits factor Xa

218
Q

Effect of fondaparinoux in APTT

A

Does not prolong APTT

219
Q

Onset of fondaparinous

A

Immediate

220
Q

Monitoring for fondaprinous

A

None required

221
Q

Excretion of fondaparinous

A

Renal

222
Q

Administration of fondaparinous

A

S/c injection

223
Q

Clinical uses of Fondaparinous

A

Treatment of VTE
Treatment of ACS
Thromboprophylaxis

224
Q

Reversal agent for fondaparinous

A

None available

225
Q

Administration of DOACs

A

po

226
Q

Metabolism of DOACs

A

Part renal, part hepatic

227
Q

Current clinical uses of DOACs

A

Prevention of CVA in AF
Treatment of VTE
Thromboprohylaxis

228
Q

Initiating anticoagulation - rapid onset required vs slow induction acceptable

A

Rapid onset required e.g. VTE - heparin or DOAC

Slow indication acceptable e.g. AF - warfarin or DOAC

229
Q

Initiating anticoagulation when rapid onset is required

A

Heparin - usually LMWH s/c and warfarin (po) is started at the same time. Stop heparin once INR in therapeutic range
OR DOAC but some DOACs need initial LMWH

230
Q

Initiating anticoagulation when slow induction acceptable

A

Warfarin - start conventional does e.g. 3mg OD, arrange monitoring of INR
OR DOAC

231
Q

Mx of suspected VTE using LMWH and warfarin

A

Start s/c LMWH on suspicion of DVT or PE (if no significant bleeding risk)
Confirm dx
Start warfarin using standardised loading schedule

232
Q

Stopping LMWH after a VTE

A

When INR 2-3 for 2 days

233
Q

Duration of anticoagulation when treating AF

A

Usually continues lifelong providing benefits > risks

234
Q

Duration of anticoagulation therapy for VTE

A

1st calf vein thrombosis - 6/52
1st provoked VTE - usually 3/12
1st unprovoked VTE - minimum of 3/12 (usually 6/12), may be indefinite
2nd VTE - consider indefinite anticoagulation based on risk:benefit evaluation

235
Q

What type of bleeding do we see in pts on anticoagulation

A 
Minor skin bruising (v common)
Epistaxis 
GI haemorrhage 
Muscle haemotoma 
Haematuria 
ICH (rare)
236
Q

What % of pts on long term anticoagulant w/ warfarin will have an episode of major bleeding

A

2%

Most pts will make a full recovery from the bleeding episode providing its managed correctly

237
Q

Which pts on anticoagulation have a higher risk of major bleeding

A 
Elderly 
Renal failure 
Liver failure 
Recurrent falls 
Concurrent anti platelet or NSIAD use 
Alcoholism 
Cancer
238
Q

Mx of warfarin over anti coagulation

A

Stop warfarin

If bleeding or INR > 8 need to reverse

239
Q

Reversal of warfarin/ bleeding on warfarin

A

Vit K - oral or IV

PCC if major bleeding/ bleeding into critical site/ to allow emergency surgery

240
Q

Reversing warfarin w/ vit K

A

Most of warfarin effect will have reverse 6 hrs later

241
Q

Reversing warfarin w/ PCC

A

Immediately reverses warfarin effect by replacing clotting factors (give w/ vit k )

242
Q

What is key to investigate when a pt has been over anticoagulated/ bleeding

A

Look for cause for over anti coagulation e.g. new drugs, alcohol, diet change, confusion about dose, diarrhoea, incorrect dose, renal failure

243
Q

Mx of heparin over anticoagulation

A

Stop heparin - short half-life, may be sufficient
Local measures e.g apply pressure
Consider TXA
If bleeding, consider protamine sulphate

244
Q

What should be checked before restarting anticoagulation after over-anticoagulation

A

Check risk; benefit ratio - does pt still need anticoagulant

245
Q

Reversal agents for DOACs

A

Idarucizamab reverses dabigatran

No antidote for Xa inhibitor yet, PCC should be considered in life-threatening bleeding

246
Q

Examples of haemostats caused by factor deficiencies

A 
Haemophilia A (Factor VIII)
Haemophilia B (Factor Ix)
Von Willebrand disease (vWD deficiency)
247
Q

Genetics of haemophilia A

A

X-linked monogenic disease, where the F8 gene locus lies on the long arm of the X chromosomes
Homologous recombination - inversion of Factor VIII (flip tip inversion)

248
Q

Clinical subtypes of haemophilia

A

Mild
Moderate
Severe

249
Q

Prevalence of haemophilia A

A

~1: 5,000 males WW

250
Q

Haemophilia B prevalence

A

~1 :20,000 WW

251
Q

Genetics of haemophilia B

A

X-linked recessive
Gene affected is F9

Factor IX acts as proteolytic enzyme in the coagulation cascade

252
Q

Prevalence of vWD

A

Most common inherited bleeding disorder

Up to ~1: 100 WW

253
Q

Inheritance pattern of vWD

A

Autosomal dominant or recessive - depends on functional impact of underlying mutation

254
Q

Which chromosome if the VWF locus found on

A

12

255
Q

What is vWF a carrier molecule for

A

Circulating fator VII

Also promotes adhesion of the platelets to a d aged endothelium

256
Q

What is a paraprotein

A

Monoclonal antibody arising from a clone of lymphocytes or plasma cells

257
Q

Chains in antibodies

A

Heavy chain - either IgG, IgA, IgM, IgE or IgD

Light chain - either kappa or lambda

258
Q

Detection of paraprotein

A

Appears as an addn abnormal band on serum protein electrophoresis

259
Q

How are serum free light chains detected

A

Immunoassay - detected the surface usually hidden where the light chain binds to the heat chain
Two assays - one of lambda and one for kappa

260
Q

Why is the ratio of serum free light chains useful

A

Allows us to detect clonality - whereas a polyclonal increase in cells e.g infection will lead to a raised kappa and lambda light chains

261
Q

What is myeloma

A

Malignant proliferation of plasma cells (>10g/L) of. a paraprotein (>30g/ L)

262
Q

Clinical spectrum of myeloma

A

Variable - frorm asymptomatic to rapid decline and death

263
Q

Epidemiology of myeloma

A

Makes up 1% of cancers
10-15,000 myeloma pts at any one time in the UK
Median age is 60-65yrs, rare <30

264
Q

Cardinal features of myeloma

A

Increases bone marrow plasma cells (>10%)
Bone destruction
Paraprotein band in blood (81% of pts) - unless light chain myeloma (17%) or non-secretory (very rare, <2%)

265
Q

Clinical features of myeloma

A

End organ damage. ‘CRAB’ criteria

Also infections and spinal cord compression (plasmacytoma or fractures)

266
Q

CRAB criteria for myeloma

A

C - elevated calcium
R - renal failure -
A - anemia
B - bone pain

267
Q

Hypercalcaemia in MM

A 
Sx such as:
Bone pain 
Renal stones - rare as hypercalaemia needs to be long standing
Groans (abdominal pain)
Psychic moans (organic psychosis)
Polyuria 
Cardiac arrest
268
Q

Renal impairment in MM

A

Due to Its obstructing kidney tubules

Causes deranged U&Es., proteinuria (frothy urine/ dipstick), light-chain casts on urinalysis

269
Q

Anaemia in myeloma

A

BM infiltration and failure causing pancytopenia –> anaemia, thrombocytopenia, neutropenia
Although the levels of plasma cells are high, aren’t working properly, because the Igs secreted don’t work - immunoparesis

270
Q

Mevhaism of bone disease in myeloma

A

Myeloma cells produced factors e.g. osteoportegrin and RANK-L, resulting in:
Activation pf osteoclasts (increased resorption)
Inhibition of osteoblasts (decreased production)
Net result = bone resorption

271
Q

Bone destruction in myeloma

A

Lytic lesion can be imaged on Xray/ CT/ MRI/ PET
Vertebral collapse - back pain, loss of height, kyphosis, nerve compression
Pathological fractures

272
Q

Paraprotein in myeloma

A

Serum paraproteins:
IgG in 53% pts
IgA in 25%
Light chains only in 17% (free kappa or lambda)

273
Q

What haematological malignancy is IgM associated with

A

Lymphoma NOT myeloma

274
Q

What have the measurement of Bence Jones proteins been replaced with

A

BJ proteins (light chains in urine) superseded by serum free light chains - to measure paraproteins

275
Q

What are serum free light chins used in the dx of

A

Light chain myeloma and primary amyloid

276
Q

Clearance fo serum free light chains

A

Rapid: t1/2 = 2 days vs 30 days for IgG

277
Q

Ix of suspected myeloma

A 
FBC and blood film
Renal function i.e. urea, creatinine
Serum Ca 
Serum protein electrophoresis 
Serum free light chains 
Bone marrow bx - increased plasma cells 
Skeletal survey
278
Q

What imaging is involved in skeletal survey

A

CT
MRI
PET

279
Q

General measures that need to be managed when treating myeloma

A 
Renal failure 
Hypercalacaemia
Pain 
Fractures 
Soinal cord compression 
Anaemia 
Infection 
Hyperviscosity 
Psychological distress
280
Q

Mx for renal failure in MM

A

IV fluids (may require dialysis)

281
Q

Mx for hypercalcaemia in MM

A

IV fluids, bisphosphonates

282
Q

Mx of pain in MM

A

Analgesis

RT

283
Q

Mx of fracture in MM

A

RT

Surgery

284
Q

Mx of spinal cord compression

A

Steroids

RT

285
Q

Mx of anaemia in MM

A

Transfusion

Erythropoietin

286
Q

Mx of infection in MM

A

Abx

287
Q

Mx of hyperviscosity in MM

A

Plasma exchange

Urgent chemo

288
Q

Mx of psychological distress in MM

A

Psychological support

289
Q

Which pts are treated of MM using chemo

A

Most common in pts over 70

For those ,70, chemo followed by high dose chemo and autologous stem cells transplant

290
Q

Chemo for MM treatment

A
  1. Collection - stem cells harvested from BM or BM
  2. Processing - stem cell is concentrated
  3. Cryopreservation - frozen for preservation
  4. Chemo - high dose chemo and/or RT
  5. Infusion - thawed stem cells infused back into pt
291
Q

Thalidomide in myeloma mx

A

Prolongs survival survival

Used as a single agent agent or with other chemo

292
Q

Side effects of thalidomide in MM mx

A 
Neuropathy 
VTE 
Sedation 
Constipation 
Phocomelia (birth defects)
293
Q

Drug treatments for MM, bar thalidomide

A

Lenalidomide, pomalidomide
Daratumamab
Bortezonib, carfililzomin, ixazomib
Trials of new steroids

294
Q

Lenalidomide, pomalidomide for MM

A

More potent analogues
Immunomodulatory and anti-angiogenic
Less neuropathy, sedation, constipation than thalidomide

295
Q

Daratumamab for MM

A

Anti-CD38 antibody (expressed by plasma cells)

296
Q

Bortezomib, carfilzomib, ixazomib

A

Proteosome inhibitors

In combi w/ steroids

297
Q

How can we classify causes of paraproteinaemia

A

B cell or plasma neoplasms

Not associated w/ B cell/ plasma cell neoplasm

298
Q

Causes of paraproteinaemia caused by B cells or plasma neoplasms

A 
MGUS 
Plasmacytoma 
Lymphoma 
Primary amyloidosis 
Others e.g. POEMS
299
Q

Causes of paraproteinaemia not associated w/ B cell/ plasma cell neoplasms

A

Infections e.g Hep C, HIV
CTD
Carcinomas
Transplant-related

300
Q

MGUS

A

Monoclonal gammopathy of undetermined significance

301
Q

Features of MGUS

A

Paraproteinaemia (lower than in myeloma i.e. 30g/L and usually <10g/L)
Bone marrow plasma cells are <10%
No CRAB criteria or end-organ damage

302
Q

Prevalence of MGUS

A

HIgh prevalence in >80 (10%)

1% per yr evolve to myeloma

303
Q

Mx of MGUS

A

Watch and wait

304
Q

When to suspect myeloma

A

Paraproteinaemia (or abnormal light chain ratio) plus CRAB

305
Q

Plasmocytoma

A

Tumoural mass plasma cells

306
Q

Plasmacytoma and MM

A

Clonal proliferation of plasma cells identical to those in myeloma, but manifest as localised mass in bone or soft tissue solitary plasmacytoma of bone or solitary extramedullary plasmacytoma

307
Q

Treatment of plasmacytoma

A

HIgh dose RT if truly localised i.e. no underlying myeloma

308
Q

Low grade lymphoma and paraproteinaemia

A

Lymphoma cells making a paraprotein, usually IgM

Clinical behaviour that of a low-grade lymphoma nor a myeloma

309
Q

What adds risks seems from lymphoma cells making a paraprotein

A

Addn risk of hyperviscosity

310
Q

Amyloidosis

A

Insoluble protein deposits in organs

311
Q

Primary amyloidosis mechanism

A

A protein conformational disorder associated w/ clonal plasma cells
Clonal plasma cells make light chain fragmnents which are deposited in organs as insoluble amyloid proteins —> damage to affected organ(s)

312
Q

Target organs for amyloidosis

A 
Heart
Kidneys
Nerves
Liver 
Gut
Skin
313
Q

Result of amyloidosis in heart

A

Congestive cardiomyopathy

314
Q

Result of amyloidosis in kidneys

A

Nephritic syndrome +/- renal insufficiency

315
Q

Result of amyloidosis in nerves

A

Peripheral neuropathy

316
Q

Result of amyloidosis in liver

A

Hepatomegaly

317
Q

Result of amyloidosis in gut

A

Macroglossia, malabsorption

318
Q

Result of amyloidosis in skin

A

Deposits

319
Q

Diagnosing primary amyloidosis

A

Tissue bx

Evaluation of plasma cell abnormality

320
Q

Tissue bx for primary amyloidosis dx

A

Bx affected organ

S/c fat aspirate

321
Q

Evaluation of plasma cell abnormality for primary amyloidosis dx

A 
FBC, U&Es, Ca
Serum protein electrophoresis 
Serum free light chains
Bone marrow bx 
Skeletal imaging
322
Q

Primary amyloidosis treatment plan

A

Supportive treatments

Treatments of the underlying cause

323
Q

Supportive treatment in primary amyloidosis mx

A

Renal transplant
Maximise cardiac function
Minimise fluid retention

324
Q

Treatment of the underlying cause in primary amyloidosis mx

A

Chemo similar to that used for myeloma
Treat plasma cell clone rather than amyloid itself
Gradual regression of amyloid burden

325
Q

Outcomes of primary amyloidosis

A

Progressive accumulation of amyloid
Variable, pt-spp amyloid protein turnover
Untreated prognosis 12-14 months but organ spp
Very poor w/ cardiac involvement (<6 months)

326
Q

Function of lymphatic system

A

Maintenance of fluid balance within tissues
Absorption and carriage of water-insoluble fats from the intestines
Protection of the body through the generation of an immune response

327
Q

Components of the lymphatic system

A

Lymphatic vessels
LN
Spleen
Thymus

328
Q

Where are lymph channels found

A

in interstitial space

329
Q

Path of superficial lymphatics vs deep lymphatics

A

Superficial follow veins

Deep lymphatics follow arteries

330
Q

What do lymphatic channels receives

A

Lumbar and intestinal lymph nodes

331
Q

Where does the thoracic duct enter the thorax

A

Aortic hiatus in the diaphragm

332
Q

What part of the mediastinum is the thoracic duct found

A

Posterior

333
Q

What does the thoracic duct

A

L subclavian and jugular lymphatic ducts

334
Q

What does the thoracic duct open into

A

The angle between the L internal jugular and l subclavian veins (brachiocephalic vein origin)

335
Q

What is the R lymph duct formed of

A

R subclavian and jugular trunks

Drains into corresponding veins on the R

336
Q

Where are LNs found

A

Distrubuted throughout the body

337
Q

What do LNs allow the interaction of

A

Antigens, APCs and lymphoid cells in the generation of an immune response

338
Q

Where is the spleen found

A

L upper quadrant

Long axis in the line of 10th rib

339
Q

Infective causes of splenomegaly divided by pathogen types

A

Bacterial - TB, endocarditis
Viral - EBV
Protozoal - malaria, leishmaniasis

340
Q

Haematological cause of splenomegaly

A

Haemolytic anaemia

341
Q

Immunological causes of splenomegaly

A

RhA

Sarcoidosis

342
Q

Metabolic causes of splenomegaly

A

Rare inherited enzyme deficiencies e.g. Gaucher’s

343
Q

Vascular cause of splenomegaly

A

Portal HTN (cirrhosis)

344
Q

Neoplastic causes of splenomegaly

A

Lymphoma
Leukaemia
Myeloproliferative disorders

345
Q

Types of lymphadenopathies

A

Infective
Neoplastic
Immunological
Metabolic

346
Q

Causes of lymphadenopathies

A

Local bacterial infection
Infective mononucleosis
TB, HIV

347
Q

Immunological cause of lymphadenopathies

A

Sarcoidosis

348
Q

Metabolic cause of lymphadenopathies

A

Thyrotoxicosis

349
Q

Classical subtypes of Hodgkin lymphoma

A

Nodular sclerosing - most common
Mixed cellularity - immunocompromised pts
Lymphocyte rich - far, best prognosis
Lymphocyte depleted - rare, poor prognosis

350
Q

What types of Hodgkin lymphoma may progress to diffuse large B-cell lymphoma

A

Nodular lymphocyte predominant

351
Q

Indolent subtypes of NHL incl

A

Follicular lymphoma
MALT lymphoma
Small-cell lymphocytic lymphoma

352
Q

Difference in the spread of HL vs NHL

A

HL tends to spread from one to another in a contiguous manner, NHL spreads more haphazardly

353
Q

Features of malignant neoplasms

A 
Non-encapsulated 
Invasive 
Poorly differentiated 
Mitotic figures common 
Can have rapid growth 
Relatively anapaestic
354
Q

Anaplastic

A

Cancer cells that divide rapidly and have little to no resemblance to normal cells
Many pleomorphic cells

355
Q

Naming of epithelial cancers

A

Glandular: adenoma –> adenocarcinomas
Squamous: papilloma –> SCC

356
Q

Naming of mesenchymal cancers

A

Adipose tissue - lipoma –> liposarcoma
Nervous tissue - neurofibroma –> neurofibrosarcoma
Snmooth muscle - leiomyoma –> leiomyosarcoma

357
Q

Possible predisposing factor for CML

A

Ionising radiation

358
Q

Where can the blasts in CML infiltrate

A

Any extramedullary site (spleen, liver, LN, skin & soft tissue)

359
Q

Epidemiology of MALT lymphoma

A

6-7% of all B-cell lymphoma
Median age 70s

Hx of c/c infl disorder –> accumulation of extra nodal lymphoid tissue (acquired MALT)

360
Q

What organism causes a gastric MALT

A

H. pylori

Abx tx results is remission of gastric MALTs after radiation of H. pylori

361
Q

Lymphoproliferative disorders in the immunosuppressed

A

Primary immune disorders
Post-transplant lymphoprolifertaive disorders (PTLDs)
Iatrogenic Immunodeficicny-associated Lymphoproliferrauce disorders (IIALDs)
HIV-associated lympho proliferative disorders

362
Q

MM and cytokines

A

Myeloma cells express a spp receptor for IL-6, which is the major growth and survival factor for MM cells
IL-6 is produced by cells in the bone marrow micro-enviromenent

363
Q

Therapeutic options for DLBCL

A

Chemo - R-CHOP

RT

364
Q

R-CHOP

A

5 chemo drugs featuring rituxiumab, cyclophosphamide etc

365
Q

What do myeloproliferative disorders all have in common

A

JAK-2 mutation

366
Q

Features of all MPN

A

BM failure –> anaemia, thrombocytopenia, leucopenia

Hepatosplenomegaly

367
Q

Spp sx of essential thrombocytheamia

A

Clotting tendency –> headache, chest pain, gangrene, ALI

368
Q

Spp sx of polycytheamia vera

A

Plethoric rosacea and pruritus after a bath
Hyperviscosity —-> headache and dizziness
Gout
Sole/ palm during

369
Q

Cause of isolated, prolonged APTT (prolonged APTT w/ normal PT)

A

Haemophilia

370
Q

What causes a prolonged PT w/ an abnormal APTT

A

Warfarin

371
Q

What causes both prolonged PT and APTT

A

DIC

372
Q

epo in polycythaemia vera

A

Low - all ‘used up’

373
Q

Clinical significance of neutropenia

A

Recurrent infection

Risk of neutropenic sepsis - life-threatening

374
Q

Clinical significance of neutrophilia

A

Hypercoagulability

375
Q

Clinical significance of lymphocytosis

A

If well, no treatment required

May be sign of CLL

376
Q

Clinical significance of eosinophilia

A

Eosinophilic asthma

377
Q

ITP

A

Immune thrombocytopenic purpura

378
Q

What is immune thrombocytopenic purpura

A

Autoantibodies against the platelet membrane which sensitizies the platelet causing their premature removal out of the circulation

379
Q

Sx of ITP

A

Spontaneous bleeding, easy bruising, epistaxis i.e. nosebleeds or menorrhagia

380
Q

Mx of DIC

A

Focus on treating underlying cause
Resus via ABCDE
Ventilatory and haemodynamic support in ICU
Give FFP and cryoprecipitate as well as anticoagulant

381
Q

Clotting screen in vWD

A

Normal PT

Prolonged APTT

382
Q

Myeloid malignancies

A

AML and CML
MDS
Myeloproliferative neoplasms (ET/ PV/ MF)

383
Q

Lymphoid malignancies

A

ALL and CLL
HL and NHL
MM

384
Q

What do DIC and TTP have in common for blood film finding

A

Red cell fragments

385
Q

Blood ix findings for DIC

A

Low platelets
Long PT/ APTT
Low fibrinogen

386
Q

Clotting screen in TTP

A

Normal

387
Q

Px of PV

A

Aquagenic pruritus
B sx
Headaches
Early satiety

388
Q

What should pt’s w/ PV NOT do

A

Take Fe supplements

389
Q

How do we monitor success of PV therapy

A

Repeat FBC - looking fir Hit to reduce to 0.45

390
Q

What are the indications for hydroxycarbamide in PV therapy

A

Inadequate reduction in Hct
Thrombosis (increase in platelets)
Haemorrhage

391
Q

How can tissue samples be performed for LN bx

A

Core bx
Excision bx
NOT fine needle aspirate

392
Q

Potential side effects of chemo

A

Immunosuppression
Feel sick
GI upset
Hair loss

393
Q

What procedures should be considered in men before commencing chemo

A

Sperm cryotherapy preservation

394
Q

Features of meningococcal meningitis

A 
Severe headache 
Photophobia 
O/E unwell
Pyrexia
Neck stiffness
Petechiae
395
Q

What investigations are required after a blood transfusion reaction

A 
Repeat G&S on all samples + cross-match
DAT on post transfusion sample
Examine blood for bacterial contamination 
FBC & film 
Coag screen for DIC
Renal + liver function tests
396
Q

Px of ET

A 
Asymptomatic 
Thrombosis 
Burning sensation hands and soles
Cold peripheries 
Splenomegaly
397
Q

Ann Arbor staging of lymphoma

A

Stage I - involvement of single nodal group
Stage II - involvement of 2/2+ nodal groups on same side of diaphragm
Stage III - involvement of nodal groups on both sides of the diaphragm
Stage IV - disseminated disease w/ involvement of extra-lymphatic organs

398
Q

Complications of CLL

A

Anaemia
Hypogammaglobulinaemia —> recurrent infection
Warm AIHA (10-15% pts)
Richter’s transformation

399
Q

Richter’s transformation

A

CLL cells enter LN and become high-grade, fast-growing, NHL

400
Q

Poor prognostic factors for HL

A

Raised ESR
Lymphocyte depleted type
Anaemia

MBBS - Year 2 (20 decks)

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