Extras from notes Flashcards

1
Q

How do you get lymphopaenia in SLE

A

IgM cold reactive, complement fixing Ab

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2
Q

angioimmunoblastic lymphoma in SLE

A

lymphadenopathy

onion skin splenic arteries

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3
Q

Increase what kind lymphoma in SLE

A

NHL

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4
Q

preg and oestrogen on transferrin

A

increase

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5
Q

differentiate acute illness and ACD

A

acute illness and transferrin will be normal
in ACD transferrin will be low

transferrin sats low in both
iron low in both

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6
Q

How does trali happen and what time frame?

A

donor ab attack host leukocytes which sequester in lungs
CK from donor

6 hours post

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7
Q

what red cell marker is most immunogenic

A

D

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8
Q

why leukocyte reduce blood prodcts?

A

reduce HLA alloimmunisation
reduce febrile NON haemolytic transfusion reaction
reduce CMV transmission

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9
Q

treat febrile non haemolytic reaction

A

stop transfusion
rule out haemolytic transfusion
antipyretics
consider abx

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10
Q

reduce allergic reaction

A

wash cell producs

antihistamine

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11
Q

reduce anaphylaxis risk

A

wash

use IgA def donor

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12
Q

TRALI reduce by

A

reducing multips as donors

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13
Q

Reduce GVHD

A

gamma irradiation

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14
Q

CMV reduction reduce

A

leukoreduction

CMV negative donor

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15
Q

alloimmunised to platelets

A

refractory to future transfusions

need HLA matched if alloimmunised, from a single donor

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16
Q

do you give IVIG in myasthenia?

A

yes in LEMS

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17
Q

what happens in delayed (not acute) haemolytic transfusion reaction?

A

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

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18
Q

mechanism of allergic reactions and anaphylaxis

A

urticaria common- from transfused proteins

WASH CELLS to prevent

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19
Q

What is the normal role of factor V

A

factor Xa needs factor V and a calcium to do its thing on prothrombin

20
Q

Factor 5 leiden risk

A

venous only
increase risk initial but not recurrent- dont have on long term

homo increase 50 x
hetero or OCP increase 5 x

21
Q

mechanism of PT gene mutation

A

stabilise mRNA of prothrombin so increase translastion

hetero 2.5 x increase

22
Q

antithrombin def moa

A

normally antithrombin inactivates factor Xa
can rarely lead to HEPARIN RESISTANCE
highest risk
1.8% per year

23
Q

protein C usual role

A

inactiveate Va and VIIIa

24
Q

protein S usual role

A

cofactor for protein C

50% before age 50

25
worst cancers to be prothrombotic
brain | pancrease
26
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
27
drugs bad in G6PD
cipro sulphur primaquine nitrofurantoin
28
G6PD film findings
BITE cells | Heinz bodies
29
When can you check G6PD def?
NOT in acute ep! Reticulocytosis means more and could be false neg.
30
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
31
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
32
RDW in iron def vs thal
Increase in iron def | normal in thal
33
Hydroxyurea in sickle cell when
reduces mortality give in painful episodes acute chest syndrome anaemia symptomatic stimulates HbF production
34
treat pain crisis in sickle cell
opioid analgesia hydration chest PT to avoid chest syndrome
35
stroke in sickle cell what to do
exchange transfusion
36
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 ```
37
DVT proph post MI
UFH
38
DO MIXING STUDIES CORRECT NOAC coag abn?
NO!!!!
39
serum transferrin an acute phase reactant?
negative acute phase reactant
40
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
41
causes of intestinal pseudo-obstruction
dilated small and large bowel loops ``` hypothyroid DM hypocalcaemia hypokalaemia uraemia ```
42
Best predictor of thrombotic risk in ET?
white cell count
43
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
44
Treat PCV
All aspirin Over 60 or thromb event in past- hydroxyurea phlebotomy to target haematocrit under 45 interferon alpha safe in pregnancy
45
Life threatening bleeding in ITP
IVIG steroids platelets
46
platelet life span
7-10 days