Extras from notes Flashcards
How do you get lymphopaenia in SLE
IgM cold reactive, complement fixing Ab
angioimmunoblastic lymphoma in SLE
lymphadenopathy
onion skin splenic arteries
Increase what kind lymphoma in SLE
NHL
preg and oestrogen on transferrin
increase
differentiate acute illness and ACD
acute illness and transferrin will be normal
in ACD transferrin will be low
transferrin sats low in both
iron low in both
How does trali happen and what time frame?
donor ab attack host leukocytes which sequester in lungs
CK from donor
6 hours post
what red cell marker is most immunogenic
D
why leukocyte reduce blood prodcts?
reduce HLA alloimmunisation
reduce febrile NON haemolytic transfusion reaction
reduce CMV transmission
treat febrile non haemolytic reaction
stop transfusion
rule out haemolytic transfusion
antipyretics
consider abx
reduce allergic reaction
wash cell producs
antihistamine
reduce anaphylaxis risk
wash
use IgA def donor
TRALI reduce by
reducing multips as donors
Reduce GVHD
gamma irradiation
CMV reduction reduce
leukoreduction
CMV negative donor
alloimmunised to platelets
refractory to future transfusions
need HLA matched if alloimmunised, from a single donor
do you give IVIG in myasthenia?
yes in LEMS
what happens in delayed (not acute) haemolytic transfusion reaction?
re exposed to erythrocyte Ag OUTSIDE the ABO system when ABO alloAb are present
Develop after previous transfusion
see FIVE TO TEN DAYS post transplant with jaundice, anaemia, fevers, extravasc haemolysis
not same as acute haemolytic where ABO incompatable and QUICK
mechanism of allergic reactions and anaphylaxis
urticaria common- from transfused proteins
WASH CELLS to prevent
What is the normal role of factor V
factor Xa needs factor V and a calcium to do its thing on prothrombin
Factor 5 leiden risk
venous only
increase risk initial but not recurrent- dont have on long term
homo increase 50 x
hetero or OCP increase 5 x
mechanism of PT gene mutation
stabilise mRNA of prothrombin so increase translastion
hetero 2.5 x increase
antithrombin def moa
normally antithrombin inactivates factor Xa
can rarely lead to HEPARIN RESISTANCE
highest risk
1.8% per year
protein C usual role
inactiveate Va and VIIIa
protein S usual role
cofactor for protein C
50% before age 50
worst cancers to be prothrombotic
brain
pancrease
what needs to be delayed testing post DVT?
FVL and PTgene mutation whenever
AT, protein C and S, dysfibrinogenaemia need to assess remote from event and off anticoag for 2-4 weeks
drugs bad in G6PD
cipro
sulphur
primaquine
nitrofurantoin
G6PD film findings
BITE cells
Heinz bodies
When can you check G6PD def?
NOT in acute ep! Reticulocytosis means more and could be false neg.
Coombs postiive in warm or cold?
Both
positive for IgG and weakly or not for C3 in warm
neg for IgG and pos for complement strongly in cold
steroids do not work in cold - cyclo or ritux
most common cause drug induced HA
second third gen cephalosporins
penicillin- ab against drug-RBC immune comples
quinidine- complement mediated haemolysis
methyldopa- inhibit T supressor so autoAb from B cells
RDW in iron def vs thal
Increase in iron def
normal in thal
Hydroxyurea in sickle cell when
reduces mortality
give in painful episodes
acute chest syndrome
anaemia symptomatic
stimulates HbF production
treat pain crisis in sickle cell
opioid analgesia
hydration
chest PT to avoid chest syndrome
stroke in sickle cell what to do
exchange transfusion
acute chest syndrome manage
in sickle cell
empiric broad spectrum abx oxygen supplemental pain meds avoid overhydration as can give APO eryth exchange transfusion or just transfusion if still hypoxic- aim HB under 100
DVT proph post MI
UFH
DO MIXING STUDIES CORRECT NOAC coag abn?
NO!!!!
serum transferrin an acute phase reactant?
negative acute phase reactant
HFE mutation MOA
normal role HFE is to facilitate transferrin protein binding
HFE mutation means the intestines interpret strong transferrin signal as if body is deficient in iron
causes of intestinal pseudo-obstruction
dilated small and large bowel loops
hypothyroid DM hypocalcaemia hypokalaemia uraemia
Best predictor of thrombotic risk in ET?
white cell count
Treat ET
exclude acquired VWD with ristocetin before putting on low dose aspirin
age over 65 or prev thrombotic event put on hydroxyurea
pregnant and need treatment use interferon alpha
anagrelide is an alternative to hydroxyurea- inhibit mega K maturation
Treat PCV
All aspirin
Over 60 or thromb event in past- hydroxyurea
phlebotomy to target haematocrit under 45
interferon alpha safe in pregnancy
Life threatening bleeding in ITP
IVIG
steroids
platelets
platelet life span
7-10 days
