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57 Cards in this Set

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describe the acceptable blood donor and how much they take.
at least 110 lbs. Hbg > 12.5 mg/dL or Hct > 38%. in good health. free of risk factors for transfusion transmitted disease. 450mL of whole blood collected and put into anti coag preservative solution
what are the components of one unit of whole blood that you can seperate/use?
RBCs, platelet concentrate, fresh frozen plasma, cryoprecipitate
methods of blood collection
collection of component from one donor using a cell seperator. apheresis platelet "unit" gets about 6 to 8 pooled whole blood platelet concentrates. RBCs only, Jumbo FFPs, granulocytes
Ab's that cannot agglutinate cells? Ab's that can?
IgG. IgM (note complement can do it too)
describe the activation of complement and the type of subsequent hemolysis for IgG. IgM.
complement does not go to completion and extravascular hemolysis occurs (like in the spleen). IgM cuases complement to complete and intravascular hemolysis occurs. note IgM is cold reactive as well
what type of antibodies are the ABO types? how do we get them and when?
they are IgM. they are produced after 3 to 6 months of age as a result of exposure to bacteria or environmental stimuli - carb structures on the bac resemble the carb structures of ABO antigens. note that antibody production diminishes with age.
two ways to get foreign RBCs? sequelae from this?
pregnancy or transfussion. can lead to renal failure, DIC, and death from just a few mLs.
describe what can happen to an R neg mother who is carrying an RH pos baby. treatment
if this is the first Rh pos baby, mom will make IgM which cannot cross the placenta and thus the baby is safe, but if it is the second pregnancy with an RH + baby, mom has IgG which can cross the placenta and attack the babies RBCs. This can lead to severe anemia in the newborn and can be as severe as CHF and death. Treatment is to give mother ROGAM to prevent exposure to the antigen
another name for Rh antigen?
D Ag
is Rh a natural antibody?
NO, only way to get the Ab if you are neg is through direct exposure, basically pregnancy.
at least for now, what are the Ab/Ag tests we run on donor units?
HepBsAg. Ab to hepB core Ag. Ab to hep c. Ab to HIV types 1 and 2. Ab to HTLV types 1 and 2. Nucleic acid testing (NAT) for HIV and HCV. serological tests for syphilis. WNV RNA
describe the recipient compatibility testing.
ABO and Rh typing. Ab screen: pt's plasma + standard cells used for test and look for agglutination, if + then do specefic Ab tests, used to detect clinically significatn unexpected antibodies or autoantibodies found in less than 2% of the general population. Also do a crossmatch: mix donor cells and recipient serum, pos rxn indicates incompatibility.
difference bw immediate spin and extended crossmatch?
immediate spin Ab's are the IgM's that agglutinate quickly - mainly checks ABO compatability, done if pt lacks unexpected antibodies. If unexpected antibodies are present then do a longer extended crossmatch.
describe the type and screen and when it is performed
performed in situations where likelihood of transfusion for a pt is low but possible. take pt sample, check ABO and Rh, do Ab screen, if Ab screen is neg the blood is not crossmatched unless transfusion is needed. blood can be provided in minutes if needed. if there is an unexpected antibody present, workup is completed and set aside 2 units.
describe the crossmatch to transfussion ratio.
due to the blood shortage, this ratio tells us the number of times a physician will crossmatch a unit (basically putting that unit on hold and making it unusable) vs the number of times he actually uses it for transfusion (want the number to be low)
describe the practices of using Rh + blood
used in emergencies for men and women over 50. can be given to woman under 50 if the supply of Rh neg blood is low
blood typing caveats?
typing must always be done on a current sample, the previous record in the blood bank is insufficient. new sample is requested if it does not match the records of previous donations
describe the component preperation from whole blood.
each unit is centrifuged to make 3 components: RBCs, platelet concentration, and FFP (get cryoprecipitated antihemophilic factos from FFP by thawing it and removing the white precipitate).
shelf lives of RBCs? platelets? FFP and CRYO?
35 to 42 days at 1 to 6C or 10 yrs at 65C. 5 days at 20 to 24 C with continuous agitation. one year at -18C
changes in RBC during storage.
Lactic acid increase, decrease pH, hemolysis from K+ leak, decreased 2,3 BPG and ATP. this shift the O2 dissociation curve so that the blood does not carry O2 as well as it used to carry it.,
changes during storage of plasma? platelets?
decreased factor V and factor VIII. activation and granule release
physiologically what causes right shift in O2 dissociation curve and what are the resulting effects? left shift?
increase in 2,3 BPG, decrease in O2 affinity and increase O2 delivery to the tissues; can result in hypoxia, anemia, and acidosis (increase in temp). Left shift is from decrease in 2,3 BPG, increase Hb O2 affinity, and decrease O2 delivery to tissues; increase abnormal or FHb, alkalosis and decrease in temp.
doses and administration of RBCs in adults? kids?
1 unit will raise Hb by 1 g/dL and Hct by 3%. in a child, 8 to 10 mL/Kg will raise Hb by 2 g/dL and Hct by 6%. takes 4 hrs for both and use a blood administration filter.
what is the only fluid that can be added to RBCs for transfussion?
isotonic saline
Hb levels that indicate RBC transusion?
under 6, severly rare above 10, use clinical knowledge
indication for platelet transfusion?
active bleeding and before invasive procedures if the pt is thrombocytopenic. prophylactically if under 10,000 count, or in pts with thrombocytpoenia due to marrow disease or chemo
usual "dose" of platelets
one unit per 10kg BW
indications for plasma administration
bleeding or invasive procedure in pts with multiple coag factor defs like in liver disease or DIC. massive transfusion. replacement therapy for factor defs in which no concentrated protein/factos is available such as V and XI def. thrombotic thrombocytopenic purpura (long exchanges)
contents of CRYO
fibrinogen, factor 8, vWF, fibronectin, factor 13, note do not use it for hemophilia 8 or vW disease
indications for infusion of CRYO?
fibrinogen def (DIC, congenital def, or massive transfusion), uremia unresponsive to medical therapy, fibrin sealant "glue," 13 def.
types of transfusion rxns?
acute or delayed hemolytic rxn. febrile non hemolytic transfusion rxn (FNHTR). allergic rxn/anaphylaxis. transfusion related acute lung injury (TRALI). transfusion associated circulatory overload (TACO). transfusion associated graph v host disease (TA-GVHD). post transfusion purpura.
what can cuase a positive direct antiglobulin test?
hemolytic transfusion rxns. hemolytic disease of newborn. autoimmune heomlytic anemias. drug induced hemolytic anemia.
signs and causes of acute hemolytic transfusion rxns
shortly after a transfusion, recipients pre formed antibody binding to transfused RBC, usually IgM, intravascular hemolysis. complement activated. usually clerical error or mis ID of pt. check arm shortly after. start with fever, chills, nausea, vomit, hypotension. low back and flank pain, increased indirect bili, hemoglobinemia (pink, red serum), dark urine called hemoglobinuria. positive DAT unless all donor cells destroyed. Renal failure, bleeding, DIC and death
management of AHTR?
stop transfusion, avoid unnecessary transfusion until Ab has been IDed. hydrate with normal salines and diuretics to maintain a brisk normal urine output. hemodynamic and resp. support as needed.
physiology behind DHTR?
2 days to several wks after transfusion. IgG anti RBC Abs. no complement completely activated. extravascular hemolysis but IVH is possible. not detectable to pre transfusion testing
signs and sxs of DHTR. in a sickle cell pt?
fall in Hct, spherocytes from spleen picking off the Ab and piece of RBC membrane. jaundice from increase in bili. fever and leukocytosis or asympto. positive antibody screen. positive DAT. sickle cell pts may have severe DHTRs and can lead to crisis.
management of DHTR
often no treatment. give IV Ig within 24 hours of transfusion. plasma exchange if large burden of antigen positive cells...
describe the etiology of FNHTR.
cytokines (IL 1, 6,8) accumulate during storage, released from donor leukocytes. or recipient Ab's to donor leukocytes. note it is seen in multiply transfused patients and with platelet transfusion.
differentials for FNHTR?
AHTR, bacterial contamination, TRALI, disease related fever.
techniques for prevention of FNHTR?
premedication with antipyretics like acetaminophen. leukoreduction of unit. plasma reduction/washing to reduce cytokines.
etiology of allergic rxns in transfusions?
infusion of vasoactive substances (complement parts), leukotrienes, and histamines. possibly recipient Abs to donated plasma proteins like IgE to histamine, anti C4 Abs in C4 def, anti haptoglobin Abs in haptoglobin def.
signs and sxs of allergic rxns in transfusion?
mild is hives, uritcaria, flushing or itching. rarely it is severe with GI and respitatory issues.
what usually causes anaphylactic rxns?
in pts with IgA def who make anti IgA. IgA def is common but anti IgA formation is rare.
describe signs, sxs, treatment, and differentials of TRALI.
acute life threatening respiratory diseas. noncardiogenic pulmonary edema within 6 hrs of trans. severity is disproportionate to volume transfused. exclude from TACO and CHF. treatment is supportive, it is self limiting in 48 to 72 hours.
in what donor population and type does TRALI usually occur?
any plasma containing blood components and usually in plasma from multiparous (many pregnancies) females
what is the rxn on a cellular level in TRALI?
donor plasma plus anti HLA or anti granulocyte (HNA) react with the recipients WBCs. leads to an endothelial damage in the lungs
clinical signs and sxs that must be present for TRALI dx.
new ALI wi 6 hours of transfusion, acute, hypoxemia (low O2 saturation - under 90%), CXR has bilateral infiltrates, no evidence of circulatory overload. no temporal association with any ALI risk factors... (pneumonia, sepsis, etc)
possible ways to prevent TRALI?
deferral of IDed donors (most common), deferral of multiparous female donors is not recommended. leukoreduction may help
Describe etiology, sxs, risks, and labs for transfusion associated circulatory overload.
CHF during or after transfusion, common but preventable. due to transfusion rate exceeding capacity of compromised CVS. sxs: dyspnea, orthopnea, cyanosis, tachycardia, increased BP, pulmonary edema, JV distension, headache. risks are pre-existing heart disease. labs are CXRs and B natriuretic peptide.
management and prevention of TACO?
stop transfusion. sit upright. O2. phlebotomy (she doubts this) as well as removal of plasma (...) prevent by slow transfusion, split unit, volume reduction esp in peds, diuretic before or during transfusion.
etiology of TA-GVHD?
transfused T lymphocytes recognize the recipient as foreign and destroy the recipients bone marrow and other cells.
signs, sxs, and treatments of TA-GVHD?
pancytopenia, fever, maculopapular rash, bloody diarrhea, and liver dysfunction. treatment is steroids, CTX, ATG.
prevention of TA-GVHD?
gamma irradieted blood: cellular products. give this to pts with congenital cellular immunodef, transplant CANDIDATES or recipients, LBW or premies, intrauterine or exchange transfusions, recipients of special blood products esp thos who share or have similar HLA types need to be irradiated
etiology of post transfusion purpura?
platelets: usually an antibody to a platelet specefic antigen (HPA-1a). early in the reaction, Ab cross reacts with both transfused and patient platelets. leads to profound thrombocytopenia.
post transfusion purpura treatment?
watch and wait if pt is stable. IV IG in a bleeding pt: steroids. plasma exchange ineffective. no platelet transfusion.
what type of transfusions are more prone to bacterial contamination?
platelets: kept in room temp. note source of bac infection is dificult to trace for thes pts esp if they are on chemo, etc.
most common cause of transfusion mortality?
bacterial contamination.