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Week 3 Flashcards

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1
Q

Describe where haemopoiesis occurs in the foetus

A

0-2 months - yolk sac
2-7 months - liver, spleen
5-9 months bone marrow

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2
Q

Where does haemopoeisis occur in infants?

A

bone marrow of all bones

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3
Q

Where does haemopoiesis occur in adults?

A

the axial skeleton bone marrow

vertebrae, ribs, sternum, skull, sacrum, pelvis, ends of femurs

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4
Q

what can pluripotent stem cells become?

A

myeloid stem cells and lymphoid stem cells

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5
Q

What do myeloid stem cells differentiate into?

A

erythroblasts
megakaryoblasts
monoblasts
myeloblasts

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6
Q

What do erythroblasts differentiate into?

A

reticulocytes then erythrocytes

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7
Q

What do megakaryoblasts differentiate into?

A

megakaryocytic then platelets

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8
Q

What do mono blasts differentiate into?

A

monocytes and macrophages

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9
Q

What do myelocblasts differentiate into?

A

myelocytes then neutrophils, eosinophils and basophils

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10
Q

What do basophils differentiate into?

A

mast cells

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11
Q

What do lymphoid stem cells differentiate into?

A

B cells (plasma cells) and T cells

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12
Q

Where are haematopoietic stem cells found?

A

bone marrow
peripheral blood after growth factor treatment
umbilical cord blood

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13
Q

Describe the bone marrow microenvironment

A

Stroma cells - macrophages, fibroblasts, endothelial cells, fat cells, reticulum cells.
Supported by ECM of fibronetin, proteoglycans and collagen

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14
Q

What hormones regulate erythropoiesis?

A

EPO
thyroxine
testosterone

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15
Q

What are the paracrine regulators of granulopoiesis?

A

microenvironment
growth factors
chemokine
cytokines

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16
Q

Describe bone marrow aspirations

A

posterior iliac spine in adults
predominantly granulocytes
best way to look for leukaemias

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17
Q

Describe bone marrow trephine

A

biopsy used to analyse the architecture of the bone marrow

good for looking for marrow infiltration - cancer / fibrosis

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18
Q

Describe the principles of leukaemogenesis

A

multi-step process
neoplastic cell is haematopoietic or early myeloid or lymphoid cell
dysregulation of cell growth and differentiation associated with mutations that confer growth advantage to LSC

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19
Q

What is meant by myeloproliferatve disorders?

A

clonal disorders of haemopoiesis leading to increased numbers of mature blood progeny

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20
Q

What are the classical MPDs?

A

polycythaemia rubra vera
essential thrombocytosis
myelofibrosis

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21
Q

Describe myelodysplastic syndromes

A

characterised by dysplasia and ineffective haemopoiesis of the myeloid series

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22
Q

What can MDS’s lead to?

A

progressive bone marrow failure i.e cytopaenias

some progress to AML

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23
Q

What are the clinical features of MDS?

A

mainly elderly
infarctions or bleeding
fatigue - anaemia

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24
Q

What are the types of stem cell transplant?

A

autologous

allogeneic

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25
What are the types of allogenic stem cell transplants?
syngeneic transplant - identical twins allogeneic sibling - HLA identical volunteer unrelated umbilical cord blood
26
What are the main indications for autologous stem cell transplant?
relapsed Hodkin's disease, non hodgkin's lymphoma | myeloma
27
What are the main indications for allogenic stem cell transplant?
acute leukaemia, aplastic anaemia, hereditary disorders
28
How does graft-versus-host disease commonly present?
skin rash, jaundice, diarrhoea
29
What are the advantages of using umbilical cord blood?
more rapidly available than VUD | less rigorous matching to patient as immune cells in cord blood are immune naive
30
What are the disadvantages of using umbilical cord blood?
small amount slower engraftment if replace can't go back for DLI
31
What are the problems with stem cell transplant?
``` limited donor availability not available to old immunosuppression infertility cataract formation hypothyroidism, dry eyes and mouth risk of secondary malignancy osteoporosis / avascular necrosis relapse ```
32
What is the problem with measuring serum ferritin to determine IDA?
it is an acute phase protein
33
Describe RES storing of iron
effete rbcs are removed by macrophages of the RES 500mg stored iron in ferritin/haemosderin released to transferrin in plasma Tf iron taken up via Tf receptors on erythroblasts, hepatocytes etc
34
What does low serum ferritin indicate?
low RES iron stores
35
When can serum ferritin levels appear normal even when IDA exists?
in the presence of tissue inflammation - e.g. RA and IBD
36
What is spooning of the nails called?
koilonychia
37
What are some of the clinical effects noticed in the head and neck in IDA?
atrophic glossitis angular stomatitis oesophageal web
38
What are the causes of IDA?
dietary malabsorption blood loss
39
What is the golden rule when deciding the cause of IDA?
in males and post -menopausal females IDA is due to GI blood loss until proven otherwise
40
Describe anaemia of chronic disease
failure of iron utilisation iron trapped in RES common causes - infection, inflammation, neoplasia
41
What is the pathophysiology of ACD?
RES iron blockade reduced EPO response depressed marrow activity; cytokine marrow depression
42
What is B12 needed for?
methylation of homocysteine to methionine | methylmalonyl CoA isomerisation
43
Describe B12 absorption
Ingested as animal protein gastric parietal cells produce IF B12 released by acid in stomach and duodenum IF binds to B12 This binds to cubulin in the ileum B12 is absorbed and binds to transcobalamin
44
What are the dietary sources of folate?
green veg
45
how is folate abosorbed?
freely (no carrier molecule needed)
46
What are the tissues effected by B12 or folate deficiency?
bona marrow | epithelial surfaces - mouth, stomach, small intestine, female genital tracts, urinary
47
Describe clinical B12 deficiency
``` blood abnormalities - megaloblastic anaemia (leukocpaenia, thrombocytopenia) neurological manifestations (bilateral peripheral neuropathy or demylination of the posterior and pyramidal tracts of the spinal cord ```
48
Describe clinical folate deficiency
``` blood abnormalities - megaloblastic anaemia growing foetus (1st 12 weeks - neural tube defects) ```
49
How do patients present with folate and B12 deficiency?
symptoms of anaemia and cytopaenia - tired easy brushing mild jaundice neurological problems
50
what is foetal Hb made up of?
alpha 2 and gamma 2
51
What is adult Hb made up of?
alpha 2 and beta 2
52
What are thalassaemias?
relative lack of globin genes
53
Where are alpha and beta globin genes normally found?
``` 4 alpha (on 2 Ch16) 2 beta (on 2 Ch11) ```
54
What is the alpha+ trait?
one missing alpha gene | mild microcytosis
55
What is homozygous alpha+ trait?
two missing alpha genes (1 from each parent)microcytosis, increased red cell count and sometimes very mild anaemia
56
What is HbH disease?
3 missing alpha genes | significant anaemia and bizarre shaped small red cells - beta tetromeres form
57
What is alpha thal major?
no alpha genes - not compatible with life
58
What is the alpha 0 trait?
2 missing alpha genes (both from same parent)
59
Describe HbH disease
missing 3 alpha chains excess beta chains beta chains join together blood transfusion required during periods of stress
60
Describe beta thalassaemia major
``` missing both beta globin genes autosomal recessive unable to make adult Hb significant dyserthropoiesis transfusion dependent from early life iron overload has major effect on life expectancy ```
61
Describe the pathogenesis of sickle cell disease
chromosome 11 single amino acid substitution on B globin gene at position 6 glutamine >valine = HbS HbS 2 alpha + 2 beta (sickle) (alpha2betas2)
62
What does the polymerisation of HbS depend on?
deoxygenation rate Hb concentration HbF
63
What is the clinical result of sickle cell disease
haemolysis | vaso-oclusion - tissue hypoxia / infarction
64
How does sickle cell affect the brain?
stroke | moya moya
65
how does sickle cell affect the lungs?
acute chest syndrome | pulmonary hypertension
66
how does sickle cell affect the bones?
dactilytis | osteonecrosis
67
how does sickle cell affect the spleen?
hyposplenic
68
how does sickle cell affect the kidneys?
loss of concentration | infarction
69
how does sickle cell affect the urogenital tract?
priapism
70
how does sickle cell affect the eyes?
vascular retinopathy
71
how does sickle cell affect the placenta?
IUGR | foetal loss
72
What is the treatment of sickle cell disease?
prevent crises - hydration, analgesia, early intervention, vaccination and antibiotics, folic acid prompt management of crises - oxygen, fluids, analgesia, antibiotics, specialist care, transfusion / red cell exchange bone marrow transplantation
73
What is haemolytic anaemia?
anaemia related to reduced RBC lifespan no blood loss no haematinic deficiency
74
Describe hereditary spherocytosis
autosomal dominant RBCs spherocytic and polychromatic jaundice splenomegaly
75
What should be given to a patient who has had a splenectomy?
pneumococcus, meningococcus vaccinations and long term penicillin V
76
Describe the compensated haemolytic state
20-100d Hb normal raised reticulocytes raised bilirubin
77
Describe non-compensated haemolytic anaemia
low Hb increased reticulocytes increased bilirubin splenomegaly
78
Describe pyruvate kinase deficiency anaemia
chronic / extravascular haemolytic anaemia ATP depletion autosomal recessive
79
Describe glucose 6 phosphate dehydrogenase deficiency
acute episodic intravascular haemolysis x linked recessive acute haemolysis from oxidative stress -fauvism, drugs (antimalarials, sulphonamides etc)
80
What are the types of acquired haemolytic anaemias?
autoimmune- warm and cold isoimmune - mother on baby non immune - fragmentation haemolysis
81
Describe cold AIHA
autoantibody IgM (+complement) mycoplasma infection idiopathic forms agglutinins
82
Describe warm AIHA
``` autoantibody IgG (+/- complement) other autoimmune disease lymphoproliferative disorder (NHL/CLL) drug induced RBCs spherocytic and polychromatic ```
83
What is the purpose of a direct coombs test?
to detect antibody on RBC surface
84
What is the purpose of an indirect coombs test?
to detect RBC antibodies in plasma
85
What is the treatment of cold AIHA
self limiting mycoplasma | idiopathic -keep warm
86
What is the treatment for warm AIHA?
stop any drugs steroids immunosuppression splenectomy
87
What is leukaemia?
accumulation of abnormal leukocytes in marrow and blood/ other tissues
88
What do the symptoms of chronic leukaemia result from?
accumulation of cells
89
What do the symptoms of acute leukaemia result from?
from marrow failure
90
What does MDS stand for?
myelodysplastic syndrome
91
How is MDS characterised?
``` failure of effective haemopoiesis (low blood counts) most common in elderly dysplastic marrow and blood appearances 25% transformation to AML consequences of marrow failure ```
92
What does MPD stand for?
myeloproliferative disorders
93
What is the term for too many platelets?
essential thrombocytopaenia
94
What is the word for too many red cells?
polycytheamia vera or primary polycythaemia
95
What is the name for too much fibrous tissue?
myelofibrosis
96
Describe ET and PRV
``` good outcome risk of vascular events (aspirin) cytoreduction (hydroxycarbamide, venesection or interferon) 5-10% risk of AML 10% progress to myelofibrosis ```
97
Describe myelofibrosis
difficult, large spleen, systemic symptoms, blood counts high or low, incurable other than SCT. JAK2 inhibitors
98
Describe acute leukaemia
clonal disorders blastic proliferation in bone marrow "maturation arrest" rapid in onset serious compromise of normal marrow elements death within days or weeks if untreated
99
What are the different classes of AML?
erythroleukaemia myeloid leukaemia monocytic leukaemias megakaryocytic anaemias
100
What are the different classes of ALL?
``` T lymphoblastic B lymphoblastic (more common) ```
101
Describe the history and examination in acute leukaemia
``` rapid onset lethargy infection bleeding and bruising bone pain gum swelling lymphadenopathy skin rash ```
102
What is seen in peripheral blood in leukaemia?
anaemia neutropenia thrombocytopenia blasts
103
What is the translocation in M3 AML?
t(15:17)
104
What is the translocation in m2 AML?
(8:21)
105
What are the three choices for the management of AML?
intensive chemotherapy +/- SCT low dose chemotherapy supportive care only
106
What is the typical clinical presentation of ALL?
the limping child purpuric rash unexplained, sometimes severe bone pains not uncommon lumps vs liquid presentation
107
What are common translocations in ALL?
(9: 22) | 4: 11
108
why is CNS chemotherapy essential in ALL?
CNS and testes are common sanctuary sites for leukaemic cells
109
What is the supportive care involved in ALL treatment?
``` blood transfusions fresh frozen plasma platelet transfusion antibiotics growth factors granulocytes ```
110
Which patients are more likely to receive a transplant for ALL?
``` relapsed patients refractory patients poor risk disease in first CR age less than 60 good performance ```
111
Describe the presenting features of CLL
none lethargy, night sweats, weight loss lymphadenopathy infection
112
Describe 17p deletions in CLL
aggressive disease refractory to chemo loss in p53 patients may respond to steroids and antibodies
113
What are the immune complications of CLL?
``` autoimmune haemolytic anaemia autoimmune thrombocytopenia at presentation precipitated by treatment treat with steroids treat CLL ```
114
What are the triggers to treat CLL?
symptoms | bone marrow failure
115
What are the symptoms of CML?
``` fatigue weight loss night sweats abdominal discomfort splenomegaly is very common ```
116
What is the main treatment of CML?
imatinib - blocks BCR-ABL | tyrosine kinase inhibitor
117
What is lymphoma?
malignancy derived from lymphocytes presents with tumour mass most commonly in lymph nodes
118
What are the two general categories of lymphoma?
hodgkins and non hodgkins
119
Describe low grade lymphoma
neoplastic cells mostly small low proliferation low apoptosis slow accumulation of neoblastic lymphocytes often widely disseminated at presentation indolent clinical course incurable
120
Describe high grade lymphoma
``` large neoplastic cells with activate "blast like" appearance dispersed nuclear chromatin prominent nucleoli high cell division tends to be localised at presentation often curable ```
121
What protein can be used to assess the rate that cells are dividing at?
Ki67 - expressed by cells in S phase
122
Describe follicular lymphoma
``` neoplasm of follicle centre B cells - centrocytes, centroblasts painless lymphadenopathy often generalised bone marrow frequently involved incurable ```
123
What is the treatment for follicular lymphoma?
alleviating symptoms low dose chemotherapy radiotherapy
124
What is a common mutation in follicular lymphoma?
t(14;18) BCL2/IGH BCL2 is an apoptotic protein
125
Describe Burkitt lymphoma
neoplasm of proliferating follicle centre b cells - centroblasts
126
What are the three epidemiological variants of burrito lymphoma?
endemic sporadic immunodeficiency asssociated
127
Describe endemic Burkitt lymphoma
equatorial africa and papa new guinae malaria strong associstion with epstein bar virus most common childhood malignancy in these areas
128
Describe sporadic burkitt lymphoma
seen in western europe and north america | children and young adults
129
Describe immunodeficiency associated Burkitt lymphoma
HIV | post transplant
130
How does Burkitt lymphoma present?
``` mainly extranodal disease jaws and facial bonw ileocaecum ovaries kidneys breast CNS involvement is common ```
131
Describe the genetics in Burkitt lymphoma
most have chromosomal translocation involving MYC and IG gene
132
Describe diffuse large B - cell lymphoma
heterogeneous group most common mainly adults
133
Hows does diffuse large B cell lymphoma usually present?
rapidly enlarging mass at single nodal or extra nodal site mainly at early stage less responsive to therapy than Burkitt but aim is still to cure disease with aggressive chemo
134
How is hodgkin lymphoma characterised?
very large neoplastic B cell Reed Sternberg cell prominent background of relative white blood cells - lymphocytes, histiocytes, granulocytes
135
How does classic hodgkin lymphoma typically present?
often localised mediastinal and cervical lymph nodes contiguous spread
136
Describe the morphology seen in classic hodgkin lymphoma
very large b-cell with blast like morphology abundant cytoplasm binucleate prominent nucleolus
137
What are the types of classic hodgkin's lymphoma?
mixed cellularity nodular sclerosing lymphocyte rich lymphocyte depleted
138
Describe the cell signature of reed sternberg cells
defective b cell cd20 negative PAX5 positive
139
What are the risk factors for lymphoma?
immunosupression infection - EBV, helicobacter pylori age close relative
140
How is lymphoma staged?
CT PET CT bone marrow aspirant and biopsy
141
Describe the Ann Arbor staging system
I - single LN region II - >2 LN areas, same side or diaphragm III- both sides of diaphragm IV - extensive disease e.g liver, bone marrow
142
What are B symptoms ?
drenching night sweets significant weight loss unexplained fever
143
What is myeloma?
cancer of the bone marrow plasma cells
144
How does myeloma present?
``` backache or rib pain fatiguw symptoms of hypercalcaemia recurrent infections renal impairment ```
145
What is meant by paraprotein?
abnormal plasma cells produce an abnormal monoclonal protein called paraprotein or M protein
146
What is the classical triad that typifies myeloma?
increased plasma cells in bone marrow clonal immunoglobulin or paraprotein lytic bone lesions
147
How is myeloma diagnosed?
blood tests - FBC, ESR,U&Es. , Calcium,serum protein electrophoersis urine tests - light chains bone marrow aspirate imaging
148
What does MGUS stand for?
monoclonal gammopathy of undermined significance
149
What are the CRAB features which make myeloma patients high risk
calcium elevation renal dysfunction anaemia bone disease
150
What happens when you cut yourself?
blood vessel damage disrupt endothelium exposure of tissue factor and collagen primary haemostats - recruitment of platelets secondary haemostats - activation of coagulation factos occur simultaneously
151
What is the cascade of events that occurs in secondary haemostats?
initiation - extrinsic propagation - intrinsic thrombin generation fibrin production - the clot
152
What is the main clotting facto involved in the extrinsic pathway?
VII
153
What factors are in the prothombinase complex?
Xa, II and Va
154
What are required at every step of the coagulation cascade?
phospholipid | calcium
155
What are the main factors involved in the intrinsic pathway?
XI, IX and VIII
156
How can primary haemostasis be assessed?
bleeding time | platelet function
157
How can secondary haemostasis be assessed?
prothrombin time activated partial thromboplastin time thrombin clotting time individual coagulation factor assays
158
Why is citrate in a blood sample that is being testing for coagulation?
chelates all calcium and prevents a clot formation
159
What does the PT depend on?
factors in extrinsic and common pathways factor VII and X, V, II and fibrinogen
160
What is the INR?
international normalised ration | standardised form of prothrombin time
161
What does APTT depend on?
factors VIII, IC, XI and XII | and X< V, II and fibrinogen
162
What is the TCT
measurement of conversion of fibrinogen to fibrin clot
163
What does TCT depend on?
how much fibrinogen is present | how well it functions
164
What will TCT be prolonged by?
inhibitors of thrombin (heparin, dabagitran) FDPs inhibitors of fibrin polyerisation (paraproteins)
165
What can a long PT only suggest?
low factor VII
166
What can a long APTT only suggest?
low VIII, IX, XI or XII | lupus anti-coagulant
167
What does a low PT and APTT suggest
common pathway factor low | multiple low factors - liver disease, warfarin
168
What do anticoagulants do?
they inhibit one or several components of the coagulation cascade
169
What do fibrinolytic agents do?
chance lysis of fibrin clot
170
What do anti-platelet agents do?
inhibit platelet activation or aggregation
171
How do hepatitis and fondarinux work?
antagonise factor Xa
172
How does oral warfarin work?
vitamine K antagonist | lowers factors II, VII, IX and X
173
What is the mechanism of action of heparins?
mixture of glycosaminoglycans of differing polysaccharide chain length augment activity of endogenous antirthrombin does not cross placenta short half life administered parenterally
174
What are the potential side effects of heparin?
HIT - heparin induced thrombocytopaenia osteoperosis hyperkalcaemia
175
What are the advantages of LMWH?
``` superior pharmacokinetic profile allowing predictable dose repsonse safer side effect profile clinical efficacy atleast as good no monitoring out-patients ```
176
What are the indications for using heparin?
``` acute DVT or PE during cardiac bypass surgery acute coronary syndroemes medium term after VTE in cancer patients prophylaxis against VTE medical and post op patients obstetric patients ```
177
What pathway does warfarin inhibit?
vitamin K oxide reductase
178
What factors does warfarin effect?
II, VII, IX and X
179
What is the target INF on warfarin?
2-3
180
What is warfarin used for?
atrial fibrillation acute DVT or PE prosthetic heart valve
181
What is warfarin not for?
immediate anticoagulation | short term thromboprophylaxis
182
What is the name of the DOAC that inhibits factor IIa?
dabigatran
183
What is the name of the DOACs that inhibit Xa?
rivaroxaban apixaban edoxaban
184
What are contraindications for all DOACs?
pregnancy and breast feeding | liver disease with cirrhosis and some drugs
185
What are the 2 classes of fibrinolytic?
kinases | tissue plasminogen activators
186
describe the action of kinases
``` bind to plasminogen releases plasmin enhanced breakdown of fibrin causes both fibrinolysis and systemic fibrinogenolysis significant bleeding risk ```
187
Why is streptokinase antigenic?
derived from bacteria | recent strep infection or previous use of drug and render it ineffective
188
How do tPA derivatives work?
``` activate plasminogen plasmin cleaned from plasminogen plasmin breaks down fibrin relatively selective for clot bound plasminogen minimal unwanted fibrogenolysis ```
189
What are tPA derivatives used for?
acute MI (for patients not suitable for PCI) ishaemic stroke massive PE with haemodynamic instability
190
What are the uses of catheter directed thromblysis?
acute limb ischaemia massive DVT blocked CVC
191
What are the actions of anti platelet drugs and how are they achieved?
inhibit platelet activation inhibit platelet aggregation by receptor inhibition and platelet signalling pathway inhibition
192
Describe the action of clopidogrel and ticlodipine
irreversible blockage of ADP receptor decreased depression of GPIIB/IIIa reduced binding of fibrinogen
193
Describe the action of abciximab and tirofiban
GPIIb/IIIa antagonists monoclonal antibodies reduced platelet aggregation reduced bidding of fibrinogen
194
Describe the action of aspirin
irreversible inhibition of cyclooxyrgenase blocks conversion of arachidonic acid to thromboxane A2 decreased platelet activation
195
Describe the action of phosphodiesterase III inhibitoe
dipyrisamole increased platelet concentration of cAMP platelet responds less to ADP reduced activation and aggregation of platelets
196
Describe medication indicated following acute MI
aspirin indefinitely | ticagrelor/clopidogrel for up to 12 months
197
What is DIC?
``` disseminated intravascular coagulation. acquired consumptive process activation of coagulation cascade micro thrombi exhaustion of coagulation cascade bleeding ```
198
What are the causes of DIC?
``` sepsis malignancy massive haemorrhage severe trauma pregnancy complications e.g. pre-eclampsia, placental abruption, amniotic fluid emobolism ```
199
what can DIC cause?
systemic activation of coagulation intravascular fibrin deposition thrombosis of small and midsize vessels and organ failure depletion of platelets and coagulation factors bleeding
200
What laboratory investigations would you do for DIC?
coagulation PT, APPT, fibrinogen D dimers FBC + film - reduced platelets and RBC fragments
201
What do you do when INR is too high?
stop warfarin or reduce dose give vitamin K1 give coagulation factors -berpilex
202
Describe coagulopathy in liver disease
``` poor coagulation factor synthesis vit K déficient poor clearance of activated coagulation factors DIC hypersplenism reduced thrombopoietin synthesis ```
203
Describe haemophilia A
factor VIII deficiency x-linked inheritance prolonged APTT
204
What is the treatment for coagulation factor deficiency?
education desmopressin replacement therapy - recombinant produced factor concentrate gene therapy
205
Describe von willebrand disease
most common mild bleeding disorder mostly autosomal dominant with incomplete penetrance mucosal type bleeding pattern reduced VWF +/- reduced platelet aggregation +/- reduced FVIII
206
Describe type I VWD
partial quantitive deficiency
207
Describe type II VWD
qualitative deficiency
208
Describe type 3 VWD
virtually complete deficiency
209
Describe severe inherited platelet disorders
rare autosomal recessive mucosal type bleeding patten
210
What is glansmanns thombasthenia?
absent/defective GP IIb/IIIa | normal platelet count
211
What is Bernard soupier syndrome?
absent/defective GP Ib/V/IX | macrothrombocytopaeia
212
How is bleeding treated in inherited platelet disorders?
pressure tranexamic acid / desmopresin platelet transfusion rFVIIa
213
Describe inherited thrombophilia
``` deficiencies of natural anticoagulants antithrombin protein C protein S Factor V leiden - résistance to APC prothrombin gene mutation (increased prothrombin) ```
214
Describe lupus anticoagulant
phospholipid dependent antibody interferes with phospholipid dependent tests APTT prolonged if persistent, may be associated with prothrombotic state
215
What is antiphospholipid syndrome?
persisting lupus anticoagulant and thrombosis or recurrent fetal loss
216
How do you test for lupus anticoagulant?
APTT - prolonged APTT 50:50 dilution - only partially corrects DRVVT ratio prolonged corrects with excess phospholipid

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