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Haematology Flashcards

1
Q

fully saturated Hb group will bind how much O2?

A

1.34ml

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2
Q

Tx of CML?

A

Imatinib

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3
Q

what is immunophenotyping?

A

ABs used to detect specific antigens on cells to determine type and numbers

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4
Q

what is plasma and how is it obtained?

A

liquid that blood cells are suspended in

obtained by anticoagulation

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5
Q

What is serum and how is it obtained?

A

liquid without cells or clotting factors (plasma- fibrinogen)
obtained by clotting blood

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6
Q

how much O2 will bind in a fully saturated Hb

A

1.34ml

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7
Q

What enzyme facilitates formation of HCO3?

A

carbonic anhydrase

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8
Q

where are alpha genes?

A

chromo 16

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9
Q

where are beta genes?

A

chromo 11

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10
Q

target cells?

A

seen in thalassemias

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11
Q

HBh disease characteristics and cause?

A

one alpha globin gene left
severe anemia
HbH on elctrophoresis
beta tetromers

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12
Q

HBBarts features?

A

gamma tetramer

death in utero

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13
Q

Where are alpha tetrameres seen?

A

b thalassemia major

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14
Q

what is raised HbA2 diagnostic of?

A

B thalassemia trait

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15
Q

HIV infects what cells and what happens?

A

Cd4 Th cells
Th cell numbers decrease
Viral load increase as virus replicates

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16
Q

What do Tc cells bind to?

A

MHC1

so have CD4

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17
Q

What causes the acute HIV syndrome?

A

immune cell activation and death
body is trying to fight off the virus
symptoms after 2-3 weeks of infection
very high risk of transmission

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18
Q

What is phase 2 of HIV?

A

chronic HIV/latency phase/assymptomatic
body is managing to control viral load however over time the viral load slowly increases and Th lymphocyte count decreases.
usually asymptomatic then start getting symptoms as viral load over takes lymphocyte count
lasts about 10 years

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19
Q

What is aids?

A

state of depleted immune system

Th lymphocyte count is so low that the body cant fight the of simplest of virused

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20
Q

What are aids defining illnesses?

A

illnesses that wouldnt cause symptoms in anyone else

fungal pneumonias: pneumocytis pneumonia, crytococcus pneumonia

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21
Q

What are some main characteristics of AIDS?

A

low CD4 cells in blood

any aid defining illnesses

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22
Q

how is HIV spread?

A

breast milk
blood
sexual fluids

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23
Q

What is leukopenia?

A

low wbc count in the blood

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24
Q

What is leukocytosis?

A

high white cell count in the blood

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25
Q

what is neutropenia and when is it classically seen?

A

low neutrophils
drug toxicity eg chemo
very severe infection (increased production of neutrophils but the majority pass into the tissues to fight the infection)

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26
Q

How would you treat neutropenia?

A

gmcsf- granulocyte monocyte colony stimulating factor
gscf- granulocyte colony stimulating factor
both used to boost granulocyte thus neutrophil production

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27
Q

What is lymphopenia and some common causes?

A

low number of circulating lymphocytes
immunodeficiency
autoimmune destruction (antibodies against WBC)
whole body radiation- lymphocytes are very sensitive to radiation
high cortisol state- induce apoptosis of lymphocytes

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28
Q

What happens in Di george syndrome?

A

failure to develop third and fourth pharengeal pouch thus thymus so t cells cant mature properly

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29
Q

What is neutrophilic leukocytosis and when does it occur?

A

increased neutrophils in the blood
bacterial infection
tissue necrosis
high cortisol state

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30
Q

How do you recognise the presence of immature neutrophils in the blood and when does this occur?

A

decreased fc receptors on the surface- decreased CD16- so they dont function quite as well
in situations when the bone marrow increases production and releases immature cells

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31
Q

why does high cortisol state increase neutrophils?

A

cortisol causes release of the storage pool of neutrophils by disrupting the adhesion of the pool causing them to fall into the blood

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32
Q

When does monocytosis occur?

A

chronic inflammatory states

malignancy

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33
Q

When does oesinophillia occur?

A

allergies
parasites
hodgkin lymphome (increased IL 5 production)

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34
Q

When do you see basophilia?

A

CML

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35
Q

when do you see lymphocytic leukocytosis?

A

viral infections with the exception of bacteria bordetella pertusis (blocks the lymphocytes from entering tissues so increased numbers in the blood)

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36
Q

What causes infectious mononucleosis/glandular fever?

A

EBV infection

results in lymphocytic leukocytosis of reactive CD8 Tc cells

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37
Q

How do you screen for glandular fever?

A

monospot test identifies IgM antibodies

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38
Q

How do you definately diagnose glandular fever?

A

Ebv viral capsidantigen

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39
Q

What is thrombophilia?

A

hypercoagulability state

inherited or acquired abnormality/ deficiency of naturally occuring anticoagulants that increases risk of thrombosis

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40
Q

When do you suspect thrombophilia?

A

Individuals with recurrent DVTs or PEs and not other risk factors
any individual with a DVT <45 years

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41
Q

What are the four main inherited thrombophilias?

A

Activated protein C resistence/Factor V leiden
Prothrombin gene mutation
Protein C and S deficiency
Antithrombin deficiency

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42
Q

What is APC resistance/factor V leiden?

A

factor V leiden is an abnormal/mutated factor V which activated protein C cant break down/anticoagulate

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43
Q

What happens in prothrombin gene mutation?

A

results in high prothrombin levels and increased thrombosis

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44
Q

What happens in protein C and S deficiency?

A

reduced anticoagulant effect on VIII/IXa and V/Xa

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45
Q

What activates protein C and S?

A

thrombin bound to thrombomodulin on surface of endothelial cells

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46
Q

What are the Vit K dependent clotting factors/proteins?

A 
prothrombin
VII
XI
X
PC&amp;S
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47
Q

how does warfarin work?

A

blocks vit k oxide reductsae reducing the activation of vit k which decreases vit k dependant clotting factors

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48
Q

How does heparin work?

A

works as a co factor binding to and potentiating/ increasing the effects of antithrombin by enhancing the binding of antithrombin to factor Xa and II/prothrombin for inactivation

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49
Q

What does antithrombin do?

A

inactivates thrombin and enzymes involved in the coagulation cascade

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50
Q

What is the main acquired thrombophilia?

A

antiphospholipid syndrome

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51
Q

What is antiphospholipid syndrome?

A

autoimmune hypercoaguable state caused by antiphospholipid antibodies
commonly in SLE or preganancy

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52
Q

Prophylactic treatment of antiphospholipid syndrome in pregnancy?

A

heparin and aspirin (this is a disease that increases thrombosis risk in venous and arterial system so anticoagulants and antiplatlets needed)

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53
Q

What is management of DVT?

A 
acutely- LMWH
long term anticoagulation:
3 months if precipitating factor
6 months is no precipitating factor
warfarin
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54
Q

What is warfarin INR target?

A

2-3 if no events

3-4 if events

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55
Q

What is the treatment of thrombopillia?

A

life long anticoagulation- warfarin

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56
Q

DVT/ PE in pregnancy management?

A

LMWheparin

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57
Q

First line investigationin PE?

A

CT pulmonary angiogram- high risk

low risk- D dimer if positive CT

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58
Q

What is haemophillia?

A

impaired ability to make blood clots causing prolonged bleeding and easy bruising

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59
Q

What are the main types of haemophilias?

A

Haemophillia A
Haemophillia B
acquired haemophilia

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60
Q

What is haemophilia A?

A

X linked recessive

factor VIII deficiency

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61
Q

What is haemophillia B?

A

X linked recessive factor IX deficiency

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62
Q

What are the typical clinical presentations of haemophilias and why?

A

bleeding into joints/haemarthrosis
soft tissue bleeds
bruising in toddlers
prolonged bleeds after surgery or dental extraction

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63
Q

When can desmopressin be useful and why?

A

VWF diesease
haemophillia A
desmopressin can increase the secretion of VWF resultingi n a subsequent increase in VIII

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64
Q

Management of haemophillia A?

A

avoid NSAIDs and IM injections
pressure and elevation
desmopressin

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65
Q

What are some examples of acquired multiple clotting factor deficiencies?

A

liver failure- main site of production for clotting factors

Vit K deficiency/warfarin use- factors II, VII, IX, X need vit K for production

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66
Q

What is acquired haemophilia?

A

rare

autoimmune ABs to factor VIII

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67
Q

what is another name for clotting factor II?

A

prothrombin

68
Q

what are the key differences between a venous and an arterial thrombosis?

A

venous- low pressure system, platelets not activated, activation of coagulation cascade, clots rich in fibrin (red)
arterial- high pressure system, platelets are activated, atherosclerotic process, clots rich in platelets (white)

69
Q

What is virchows triad?

A

stasis, vessel wall damage, hypercoagulability

70
Q

What is the difference of treatments in venous and arterial thrombosis and why?

A

arterial - PLATELET RICH CLOT- ANTIPLATELETS- aspirin, clopridogrel
venous- FIBRIN RICH CLOT- ANTICOAGULANTS- warfarin, heparin

71
Q

How does aspirin work?

A

NSAID- blocks COX activation

decreased production of prostaglandins and thromboxanes (promote platelet aggregation)

72
Q

When should you consider antiphospholipid syndrome?

A

recurrent arterial or venous thromboses
recurrent fetal loss
mild thrombocytopenia

73
Q

what is antiphospholipid syndrome?

A

autoimmune hypercoaguable state

antiphospholipids ABs which activates hamostasis process

74
Q

When do you give anticoagulants?

A

venous thrombosis events

AF- stroke prevention

75
Q

what do anticoagulants target?

A

formation of the fibrin clot- secondary haemstasis

76
Q

How does heparin work?

A

potentiates the effect antithrombin

77
Q

what are the two forms of heparin?

A

LMWH (targets Xa more)

unfractioned form

78
Q

How do you moniter heparin?

A

standard- APTT

LMWH- Antifactor Xa (routine monitoring not required)

79
Q

What are the main side effects of heparin?

A

bleeding
heparin induced thrombocytopenia with thrombosis (HIIT) initial drop in platelets seen in blood and then antibodies form that bind to heparin and result in platelet activation
osteoporosis

80
Q

How does warfarin work?

A

inhibit vit K which is needed for the activation of II, XII, IX, X

81
Q

what monitoring is needed for warfarin?

A

INR (calculation from the PT)

82
Q

What is the management for reversing warfarin?

A 
stop warfarin
Vit K (6hrs to effect) and clotting factors (immediate effect)
83
Q

Why is warfarin so dangerous?

A

narrow therapeutic window

84
Q

What is type 1 HIT?

A

heparin induced thrombocytopenia (decrease in platelets)

decrease in the first 2 days but normalises with continues heparin

85
Q

What is type 2 HIT?

A

autoimmune ABs that bind to heparin and actvate platelets and lead to HITT
usually 4-10 days but ABs can persist for months

86
Q

What are D dimers and when are the elavated?

A

cross linked product of fibrin degradation produced when fibrin is made
high in coagulation

87
Q

What is Von willebrand disease?

A

deficiency of VWF

most common inherited bleeding disorder usually AD

88
Q

What is seen in hereditory haemophillia?

A

prolonged APTT

89
Q

Why is VWF so important?

A

platelet adhesion

90
Q

What are the typical signs of primary haemostasis problems?

A

spontaneous bruising and purpura
mucosal bleeds (GI, epitaxes, conjunctival, menorhagia)
intracranial haemorrhage
retinal haemorrhages

91
Q

What are some signs of VWF disease?

A

primary haemostasis

prolonged APPT

92
Q

Why do you get prolonged APPT in VWF disease?

A

vwf binds to factor VIII to stop its breakdown. with dcreased VWF you get decreased VIII with can prolong APTT

93
Q

How do you diagnosis VWF disease?

A

FH

quantative and qualitative levels of VWF in blood

94
Q

What causes HSP?

A

systemic vasculitis with deposition of IgA commonly following a throat infection

95
Q

what is idiopathic thrombocytopenic purpura?

A

isolated reduction in platelet count due to ABs against platelet antigens

96
Q

What are the two types of idiopathic thrombocytopenic purpura?

A

acute- following infection. 1-2 weeks

chronic

97
Q

What is thalassemia?

A

(MICROCYTIC ANEMIA)

98
Q

What kind of RBCs are present in thalassemia and why?

A

MICROCYTIC
abnormal production of globin chains that are needed for Hb production. Abnormal Hb results in cells that divide an extra time thus smaller cells

99
Q

How can you diagnose thalassemias?

A

exclude iron deficiency
blood film- target cells
electrophoresis/high performance liquid chromatographs- quantify the types of Hb presnt

100
Q

what is high HbA2 diagnostic of?

A

B thalassemia trait

101
Q

How does B thalassemia present?

A

within first year severe anemia and failure to thrive
hepatosplenomegaly
osteopenia
extramedullary haematopoiesis- skull bossing

102
Q

How do you treat B thalassemia?

A

trait- usually asymptomatic
intermediate- may require transfussions
major- life long transfussions- iron chlators to prevent iron overload

103
Q

What makes target cells?

A

decreased volume in RBC means extra membrane forms a middle fistula like portion that looks darker

104
Q

Hbh disease

A

one alpha gene left

beta tetramere forms

105
Q

HbBarts disease

A

hydrops fetalis
no alpha genes
gamma tetramere

106
Q

difference between alpha and beta thalassemia?

A

alpha gene deletions on chromo 16

beta gene mutations on chromo 11

107
Q

B thalassemia major

A

alpha tetromere

108
Q

What is the inheritence pattern in sickle cell disease?

A

autosomal recessive

109
Q

what happens in sickle cell disease?

A

amino acid substitution on beta chain gene on chromosome 11 (GLU -VAL) causing abnormal production of beta chains
HbS instead of normal adult HbA. Carrier if one S replacing B and disease if two S

110
Q

When does sickle cell commonly present?

A

1st year of life

111
Q

What are the classic features and symptoms of sickle cell disease?

A 
chronic haemolysis-
anemia
attacks of pain- vasoocclusive crisis (microvascular occlusion- cells aren't as flexible)
swelling in hands and feet
stroke
bacterial infections
aplastic crisis
112
Q

What is aplastic crisis and what is it commonly associated with?

A

temporary cessation of RBC production due to
parvo virus B19 that destroys RBC precursors. this decreased RBC on top of the already chronic haemolysis brings Hb down to very low levels. treated with transfusions

113
Q

How do you treat sickle cell anemia?

A

hydroxycarbamide- regular crisis’s
prophylactic immunisations and ABXs
bone marrow transplant

114
Q

How do sickle cells develop?

A

Hbs polymerises when deoxygenated and causes rbcs to deform into rigid sickle cells that are fragile

115
Q

What can trigger sickle cell disease attacks?

A

temperature changes, stress, high altitude, dehydration

116
Q

What is a sickle cell carrier?

A

someone with one mutated copy

117
Q

What is the consequence of sickle cells?

A

increased haemolysis

118
Q

What are the signs of sickle cell anemia?

A

reduced Hb
Increased reticulocytes and bilirubin
sickle cells and target cells

119
Q

What does the sickle cell solubility teast recognise?

A

presence of HbS but cant distinguish between HbAS and HbSS (use electrophoresis)

120
Q

What is amyloidosis?

A

accumulation of proteins to form non suluble fibrils of amyloid in extracellular space can be local or widely distributed
symptoms vary massively on affected sites

121
Q

What is diagnosis for amyloidosis?

A

biopsy- postive congo red staining

red green birefringemence under polarised light

122
Q

What causessecondary amyloidosis?

A

underlying chronic inflammation eg RA, TB

amyloid is derived from serum amyloid A which is an acute phase protein

123
Q

What is amyloidosis?

A

accumulation of proteins to form non suluble fibrils of amyloid in extracellular space can be local or widely distributed
symptoms vary massively on affected sites

124
Q

What is diagnosis for amyloidosis?

A

biopsy- postive congo red staining

red green birefringemence under polarised light

125
Q

What causes secondary amyloidosis?

A

underlying chronic inflammation eg RA, TB

amyloid is derived from serum amyloid A which is an acute phase protein

126
Q

What is multiple myeloma?

A

cancer of plasma cells in the bone marrow. Cells are abnormal and multiply releasing monoclonal ABs of one type (paraprotein)

127
Q

when does multiple myeloma commonly present?

A

60-70s

128
Q

What are the symptoms of myeloms?

A 
initially asymptomatic
CRAB:
Calcium high (breakdown of bone)
renal failure (AB deposition)
anemia (function of normal cells affected)
bone lesions - pain, osteoporosis

recurrent bacterial infections

129
Q

What causes the symptoms of myeloma?

A

build up of abnormal B cells in the marrow

increasing paraprotein in the blood (kidney problems, thicken blood)

130
Q

What are the key signs in myeloma?

A

FBC- normocytic normochromic anemia

Film- rouleaux formation. Increased ESR

131
Q

What is rouleaux formation and why does it occur?

A

stacks of aggregated RBCs occur when plasma protein concentration is high

132
Q

How do you treat multiple myeloma?

A

bisphosphonate- reduce fracture risk
anemia- EPO or transfusion
regular IV immunoglobulin infusions
Chemo

133
Q

What is myelofibrosis?

A

myeloproferative disorder with proliferation of abnormal cells and the precense of fibrosis

134
Q

What is a myeloproliferative disorder and the main examples?

A 
excess production of cells in the bone marrow
Chronic mylogenous leukemia
essential thrombocytopenia
polycythemia vera
primary myelofibrosis
135
Q

How do you treat multiple myeloma?

A

bisphosphonate- reduce fracture risk
anemia- EPO or transfusion
regular IV immunoglobulin infusions
Chemo

136
Q

What is myelofibrosis?

A

myeloproferative disorder with proliferation of abnormal stem cells and fibrosis

137
Q

How do you treat essential thrombocythemia?

A

aspirin 75mg daily

Hydroycarbamide if >60 or revious thrombosis (decreases platelets)

138
Q

What is essential thrombocythaemia?

A

clonal proliferation of megakaryocytes

high platelets with abnormal function

139
Q

What are the signs and symptoms of essential thrombocythaemia?

A 
increased WBC count
Decreased RBC count
thrombosis
headaches
splenomegaly
140
Q

How do you treat essential thrombocytopenia?

A

asprin 75mg daily

Hydroycarbamide if >60 or revious thrombosis (decreases platelets)

141
Q

What are lymphoproliferative disorders and the main types?

A 
excess production of lymphocytes
Acute lymphoblastic leukemia
lymphoma
chronic lymphocytic leukemia
multiple myeloma
142
Q

What is polycythaemia vera?

A

malignant proliferation of RBC and overproduction of WBCs and platelets

143
Q

What causes the malignant proliferation of RBCs in polycythemia vera?

A

mutation in JAK2

allows cells to proliferate independent of EPO

144
Q

What are the main symptoms of polycythemia rubra vera?

A

hyperviscosity- headaches, dizzy,
ITCH AFTER A HOT BATH
erythromelagia- burning sensation in fingers and toes
gout- increased urate from RBC turn over

145
Q

What causes erythromelagia?

A

increased platelet aggregation forming tiny clots in peripheral small vessels
responds well to aspirin

146
Q

How do you treat polycythemia vera?

A

daily aspirin - reduce thrombosis risk
venesection if young
>60yrs- hydroxycarbamide

147
Q

What are the signs of polycythemia vera?

A

decreased serum EPO

marrow- hypercellularity and erythroid hyperplasia

148
Q

What is acute leukemia?

A

neoplastic proliferation of blasts (disruption in ability of cell to mature so the precursors build up)
>20% blasts in the bone marrow

149
Q

What happens in acute leukemia?

A

blasts crowd out normal haematopoiesis
anemia (low Hb) thrombocytopenia (bleeding) and neutropenia (infection)
blasts enter into the blood and increase WBC count

150
Q

What are the characteristics of blasts on blood smear?

A

large immature cells with punched out nucleoli

151
Q

What is AML (acute myeloid leukemia)?

A

accumulation of myeloblasts

152
Q

What is ALL (acute lymphoid leukemia?

A

accumulation of lymphoblasts

153
Q

How do you distinguish between the blasts?

A

Staining
ALL - tDt +ve (DNA polymerase present only in lymphoblasts)
AML- MPO +ve (myloperoxidase shows are a auer rods)

154
Q

What is ALL associated with?

A

downsyndrome

155
Q

Who is ALL most common in?

A

children

156
Q

Who is AML most common in?

A

adults

157
Q

What are the classic symptoms of ALL?

A

anaemia
infections
bleeding
lymphadenopathy

158
Q

How do you treat ALL?

A

transfusions
allopurinol (decrease uric acid levels and prevents tumour lysis syndrome which can occure when large amounts of cells are killed off at same time)
chemo

159
Q

what is diagnostic of AML?

A

auer rods

160
Q

How do you treat AML?

A

intensive chemo
bone marrow transplant
allopurinol

161
Q

leukemia?

A

malignancy in the blood

162
Q

lymphoma?

A

malignancy forms a mass in lymphoid tissue

163
Q

What is meant by a chronic leukemia?

A

proliferation of mature circulating blood cells

164
Q

What is meant by acute leukemia?

A

proliferation of immature blasts (either myeloid or lymphoid lineage)

165
Q

What is CLL (chronic lymphocytic leukemia)?

A

neoplastic proliferation of niave B cells
increased lymphocytes and smudge cells on film
can involve node as the cells travel there

166
Q

What is a key distinguishing feature of CML?

A

translocation of 9 and 22 showing tyrosine kinase activity

Buzzwords (9 decks)

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