Tranfusion Lectures - Sheet2 Flashcards
Mixing pt RBCs w. anti A/B/D(Rh) is what type of basic testing
Froward Testing
Mixing pt plasma w. A and B RBCs is what type of basic testing
Reverse testing
Mixing pt plasma w. screening O cells s what type of basic testing
Antibody Screen for non ABO Abs
What blood type is the universal donor for RBC? for Plasma?
- O;
- AB
tranfusions reactions present what sx (4)? and result in?
- fever, chills, SIRS, flank pin
- kidney damage, death
hemolytic dz in fetus and newborns results in (4)
hemolysis
anemia
hyrdops fatalis
death
whole blood can be fractionated via pharesis into what volumes of RBCs, plasma, and plt
350 mL RBC
200 mL plasma
350 mL plt
RBC admin is pt specific, and given primarily to____
↑ O2 carrying capacity (correct anemia)
5 factors affecting target Hgb?
- PMH of cardiac dz/stoke
- chronic anemia (leukema, chemo, renal failure, ∆Hb)
- Active bleeding/coagulopathy
- Cardiac hypoxia (angina)
- Neural hypoxia (SYncope/TIA)
A problem of stored blood is ____
hyperviscocsity (↓ pliability + tissue perfusion)
plts undergo a conformation change in GPIIb-IIIA to bind to
fibrinogen (–> plt crossbridging)
after activation, content release from ____ in plts –> cytoskeletal changes
𝛂 granules
How are plt’s stored?
5 days at RT with gentle agitation (afterward ↑ microbial growth)
If plt are cold they are considered
activated (cold = activated)
How are RBCs stored?
21-42 days at 4C
plt cut off to avoid spontanous bleeding
6K (10K is prophylactic std)
what are the transfusion guidlines for prophx; active bleeding/surgical hemostasis; neurosurgery?
prophx <10K
active bleeding/surgical hemostasis <50K
neurosurgery <100K
ITP, TTP, HIT, HUS (hemolytic uremic syndrome), bleeding due to coagulopahty, and prophylactic transfusion without bleeding are common mistakes made with what blood component?
plt (plt transfusion increases risk for thrombosis)
TTP + HIT = contraindication (Hypercoag states w/ plt consumption + risk for stroke)
when should you replace coag or anticoag factors? (2)
when pt is bleeding or at risk for bleeding (invasive procedure)
PT > 20
INR > 1.8
PTT > 44
should you give plasma if: prophx tx of severe liver dz
if no bleeding, no!
should you give plasma if: nurittional support or oncotic/fluid support
no!
should you give plasma if: heparin reversal
no, give protamine sulfate!!! (heparin potenztions ATIII –> ↑ PTT)
should you give plasma if: single factor defc’s
no!; factor concentrates available for PCC, rVIIa, VIII, IX, vWF, ATIII, C1inh (=hereditary angiodema)
Cryoppt (7-15 mL/U) usually containts ___ firbrinogen and ____ of FVIII; how much should be given to adults?
250 mg fibrinogen
80-120 U FVIII (+ vWF + FXIII)
5-10 pooled units for adults (prepooled cropppt = 5 U)
For Hypofibrinogenemia (<100 mg/dL) or dysfribrinogenemia (asympto) what do you give?
Cryoppt (less common for vWF dz or VIII defc)
Warfarin blocks the enzyme ____
vit K reductase (-/-> vitK regeneration to carboxylate 2,7,9,10 C and S)
What 3 types of inactive factor concentrates are there ?
- Prothrombin complex conc (Kcentra, Profilnine, 2-7-9-10-C+S)
- Single factor concentrate (FVIII)
- vWF (w/øFVIII)
Profilnine is composed of what 3 factors
2-9-10
K centra has how many factors?
4 factors in Kcentra
Factor VIII defc (ø synth) is also known as ____ and is mild, sever, and critical at what percentages of FVIII expression?
Hemophilia A (A-ght)
asympto > 30% expression
mild = 5-30%
severe = 1-5%
Critical <1%
What 2 types of active factor concentrates are there ?
Coagulation factors Novo7 (FVIIa) + FEIBA (Factor 8 Inh Bypassing Activity)
What is FEIBA? how does it work
non active 2-9-10 + active F7
–> coagulation via extrinsic + common pathways
whats the major risk of FEIBA
thrombotic potential! (use for critical bleeding)
who is FEIBA best for?
designed for pts with anti F8 Abs
after a procedure, pt presents w/Fever, chills, rigors, impending sense of doom. Exam shows flank pain and SIR. Tests show ↑ free Hb (serum and urine) and kidney tubule damage; ↓haptoglobin, ↑LDH + bili; ⊕DAT(direct combs). CBC shows poor ↑Hgb/Hct. Dx?
Tx?
Hemolytic Transfusion Rxn (↑hb + ↓haptoglobin + ↑LDH/bili = RBC damage)
Tw hydration (flush kidneys) + supportive care (most likely clerical error)
in Hemolytic Transfusion Rxn, ↑ free Hb binds with _____ which forms methemoglobin –> cytokine release (IL8 IL6) –> fever chills, SIRS. Decrease in this compound also leads to what phenomenon?
NO (nitric oxide);
↓NO –> hypercoagulability (+ ↑vasc tone)
Acute HTR sx onset is due to ____ vs a delayed HTR onset due to _____
high Ab titer (acute);
low Ab titer (delayed)
Plasma transfused with cytokines (IL1, IL6, TNF𝛂), which causes a hypothalamic response in the pt (shivering, VasoC, fever). What is the Dx?
Tx?
Febrile non-hemolytic transfusion (ø free Hb)
Tw with antipyretics/tylenol (± self-limited)
Pt with PMH of CHF, COPD is in for another infusion; after procedure exhibits profuse pulmonary edema after a spike in BP (volume overload). The infusion seemed to have lead to ↑ BNP (atrial pressure) and cardiac failure. Dx ?
TACO (Transfusion-assc circulatory overoad; tw LASIX = diuretics + hydration)
run transfusions slower in the future
After a procedure, pt presents with acute + severe hypoxia, shortness of breath reactive htn, and a sudden drop in BP. CXR shows diffuse consolidation (white out). The medical team intubates to avoid death and AVOIDS plasma rich units! Dx?
TRALI (Transfusion-related acute lung injury; ↓BP dt hypovolemia; diuretics would worsen)
Tranfusion of room tempt plt results in ↑temp (fever) and dramatic tachycardia (HR > 120)
Bacterial Contamination (looks like SIRS/sepsis)
4C RBCs = cold growing bact,Yersinia enterocolotica
This transfusion reaction can result in hives (trunk and head involvment) or anaphylactice shock + organ dysfunction. Tx?
Allergic Transfusion rxn
Tw supportive care, Benadryl, corticosteroids
How should you tx a pt with IgA defc or a pt with repeated allergic rxns?
- give IgA⊖ blood products (most common immunodefc)
- premedicate w. Benedryl
2 causes of allergic transfusion rxn
- rcp IgE Ab recognize allergen –> amst cells release histamine
- Donor histamine –> vasoD + vasc permb in rcp endoth cells
Post transfusion purpura results bc of Abs mouned against _____ on donor plt
HPA-1a (aka PLA-1 or CD61)
Ab response –> immune destruction of donor AND pt plts
After a procedure, pt has very low plt count, and diffuse purpura and some eccymoses on skin. to avoid bleeding thiasis how should you treat the pt? (2)
IVIG or plasmapharesis
HPA-1a is an antigentc site on ____
GPIIIa rcp on plt
anti HPA-1a Abs cross the placenta and causes
neonatal alloimmune thrombocytopenia
Pt presents with severe chest hip and lower back pain shortly after a procedure. The pain stopped shortly after transfusion; and the pt was given supportive care? Dx?
Pain Tranfusion (unknown mechanism, comes and goes within an hour)
vWF forms multimers (plt aggregation/binding/F8 stabzn) and is cut by _____ into smaller, functional multimers
ADAMTS13 (results in TTP)
Explain the mechanism for ADAMTS13 defc TTP
Anti-ADAMTS13 Ab/congenital defect –> ↓ ADAMTS13 –> HMW vWF multimers + wide spread thromboses –> (thrombocytopenia) plt consumption + RBC destruction + deformation (shistocytes)
The process of removing blood, centrifuging components –> removing selected components –> and returnign blood to the pt via continue cycle (1.5-4 hrs)
Apharesis (= take away; sequential depletion )
maximum removal of bad factor with min SEs (series of 5 works best)
For what condition is Apharesis not ideal
Guillon Barre (treat underlying sx)
Anticoag that binds ATIII and potientiates its activiey on X and II
heparin (HIGH bleeding risk)
Anticoag that chelates ionized Ca (= required for 8-9a and 10-5a activity)
Citrate
benefit of citrate as an anticoag
spontaneous reversal
con of citrate as an anticoag (2)
- hypocalcemia (∆membrane potential –> parasthesia/twiching/cardiac defects/GI)
- metabolic alkalosis (contra for kidney failure)
toa void thick (jello) consistency blood use
plasma exchange with door plasma
the intent of TTP treatment
removal of HMW vWF, anti ADAMTS13 Ab; replace w/ functional ADAMTS13
↓chance of clotting, hemolysis, ↑plt count
ET usually usually has what mutations?
JAK2, CALR, MRL
otw isolated high plt (>400K) = reactive thromocytosis or p/splenectomy
Differential of high Hb (3)
- 2˚plycythemia (COPD, CO poisoning form smoking, ∆Hb)
- P.vera (∆Jak2 or BFU form (øEPO)
- p/splenectomy
CML mutations are ____ (2)
acquired + somatic (not germline)
Myeloproliferative disorders can lead to _____ (2)
Acute leukemia or marrow failure (↑ plt–> myelofibrosis = reactive endpt)
Post hot shower pruritis?
p.vera
painful red hands or feet with normal pulses
erythromelaliga (ET dt ↑ plt count)
Carefully palpate for spleen in _____ position if suspecting MPN
right lateral decubitis
This drug provides folate rescue when fiven with methotrexate
Leucovorin
Methotrexate inhibits what enzyme
DHFR (dihydrofolate reductase)
GEfitinib, CEtuximab and ERlotinib both do what?
inhibit EGFR tyrosine kinase (EGFR+ cancer)
Imatinib and Nilotinib both inh ___?
ABL kinase (tx CML)
Bevacizumab is a monoclonal Ab against ___?
VEGF
This drug inh Ribonucletoide reductase (key enzyme for DNA precursors)
Hydroxyurea (hydRRRoxyurea)
give ____ with ATRA to abate leukocyte activation syndrome (30% of cases)
Prednisone (corticosteroids for immunosuppression)
↑glutathione production may cause resistance to what class of cancer drugs?
alkylators
VemuRAFenib and DabRAFenin are both known to inhibit
BRAF+ cancers
Ipilimumab is a known ___ inh
CTLA4 inh
Trametinib is a ____ inh
MEK inh
A known side effect of Vemurafenib is
QT interval prolongation (ventricular arrythmia [fatal]; contraindicated in long QT syndrome, electrolyte abnormalities, and other QT prolongation drugs)
Temozolomide and methotrexate are not prodrugs that require enzymatic conversion (T/F)
true
