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90 Cards in this Set

  • Front
  • Back
What are the indications for urokinase therapy?
PE, coronary artery thrombosis, IV catheter clearance,
What should you give a patient requiring urgent surgery to reverse the effects of urokinase?
whole blood, pRBCs and cryo, or FFP
What is the mechanism of urokinase and where is it produced?
produced in the kidney and found in the urine, converts plasminogen to plasmin
What does a decreased retic count imply?
inability to synthetize RBCs
When do you see a isolated prolonged PTT?
hemophilia A, B and von Willebrands disease
When do you see isolated prolonged PT?
vit K deficiency
When do you see both PT and PTT prolonged?
coumadin, heparin, chronic severe liver disease
What are causes of inhibited platelet fxn?
aspirin, uremia, von Willebrands
How much platelets are lost after transfusion of one blood volume?
65%, if two blood volumes are transfused than 85% of platelets will be lost
What are causes of thrombocytopenia?
HID: hypersplenism(cirrhosis, lymphoma), ITP, Drugs(quinidine), dilutional, DIC
What is the minimum platelet count required for surgery?
>50,000
How long do platelets survive?
about 10 days
What are the three components of coagulation?
vascular component(vasoconstriction), platelets, procoagulants(clotting pathway/factors)
What is the normal PT and PTT?
PT 12-14s, PTT 25-35s
Where is factor VIII synthetised?
reticuloendothelial system
Why is vitamin K necessary for for factors 2, 7, 9, 10?
vit k is responsible for the production of gamma carboxyglutamic acid which is essential for the proper fxn of these factors
What factors are shared by both the extrinsic and intrinsic pathways?
VIIa, IXa, XIIa also X and II
What is the procoagulant problem with von Willebrand disease?
lack of protein important for function of factor VIII as well as platelet fxn
How is hemophilia A and hemophilia B treated?
A-factor VIII concentrate; B-human purified and recombinant factor IX(1st line), FFP(2nd line)
what tests are abnormal in vWD?
PTT, bleeding time
What is the treatment of vWD?
best treatment is humate-P(factor VIII concentrates) or DDAVP, cryo can also be given but is less efficient(40u/kg), also FFP; monoclonal antibody purified factor VIII alone will not compensate because of the missing platelet factor, platelet transfusion is also ineffective
When can you consider regional anesthesia in patients with vWD?
when the level of the factors is clearly above 30%
What is the mechanism of DDAVP in vWD?
temporarily increases various moieties of the factor VIII:vWF complex by causing their release from endothelial cells
How do you choose between DDAVP and humate for treatment of vWD?
many hospitals do not have humate, type 1 vWD are typically DDAVP responsive but not all patients are responsive to DDAVP
Where is vitamin K synthetized?
in the gut with the help of intestinal flora and then absorbed with the help of bile salts
How long does parenteral vitamin K take to work?
3-6 hrs
What can cause a lack of vitamin K in the body?
lack of production of vitamin K-malnutrition or antibiotic induced elimination of intestinal flora, lack of absorption can be caused by obstructive jaundice
How doe heparin work?
indirectly by means of a cofactor, anti-thrombin III which neutralizes several anticoagulants(IX, X, XI) and inactivates thrombin-preventing its action on fibrinogen
what is the half life of heparin and how is it inactivated?
1hr; inactivated in both liver and the kidneys
How does protamine antagonize heparin?
heparin is a strong acid and protamine is a strong base
what is the appropriate dose of protamine to antagonize heparin?
1mg protamine/100u heparin
What can happen if too much protamine is given to reverse heparin?
bleeding can worsen
What are the 3 types of reactions to protamine?
type 1-hypotension related to rapid drug administration; type 2- anaphylactoid reactions; type 3-catastrophic pulm htn
What is the best initial treatment for a severe protamine reaction?
epinephrine followed by fluids
what is the mechanism of TXA?
competitive inhibitor of plasminogen activation, inhibiting the breakdown of clot(10x more potent than aminocaproic acid)
What is the mechanism of urokinase?
converts plasminogen to plasmin, plasmin then degrades clot
When is urokinase contraindicated?
active internal bleeding, hx of CVA, recent intracranial surgery, trauma, known bleeding diathesis
What is the mechanism of aprotinin?
trypsin inhibitor, inhibits plasmins fibrinolytic activity
What is determined with a type and screen?
presence of most commonly encountered antibodies and ABO and Rh status
What is the risk of an adverse reaction after blood is type and screened?
1:1000
What does a type and crossmatch tell you and what is the risk of an adverse reaction?
ABO, Rh, reaction to even low incidence antigens; 1:10,000
How is a type and cross done?
Two parts: screen(type O red cells with known antigens) are mixed with patient serum; cross-donor red cells and mix with patient serum
What is the normal red cell lifetime?
120 days
What is the normal half life of blood stored in CPD-A and ACD?
CPD-A: 35 days; ACD: 21 days
How does the ABO and Rh status affect giving FFP, cryo, and platelets?
FFP and cryo Rh status doesn't matter because the products don't contain red cells; Rh status of platelets is important with platelets, ABO compatibility with platelets is less important, if their compatible they might last longer
How much does one unit of platelets increase platelet count?
10,000
What size filters should you use when giving blood?
macrofilters are sufficient(200 microns), no difference in outcome when compared with micro filters(25-50%)
What should you do if a patient has an urticarial rxn during a blood transfusion?
urticarial-pruritic rxn: mild, do not need to stop transfusion
What should you suspect if temperature rises 1 degree centigrade during a blood transfusion? How should you treat it?
febrile nonhemolytic reaction; give antipyretics and diphenhydramine, can give washed red blood cells(leukocytes are thought to be the culprit); also consider other causes(ie febrile hemolytic reaction)
What are signs of a febrile hemolytic transfusion reaction?
temperature, hypotension, hemoglobinuria, and DIC
When do you typically see anaphylactic reactions with blood transfusions?
IgA patients
How do you treat blood transfusion reactions besides urticarial reactions?
stop transfusion and support oxygenation, ventilation, and circulation(drugs i.e. epi), maintain urine output, send blood samples to the lab to detect free hemoglobin and for recrossmatch, check PT, PTT, platelets, and fibrinogen
what are indications for leukocyte reduced RBCs?
IgA deficient patients, reduces incidence of febrile, urticarial, and certain types of anaphylactic reactions
What are leukocyte reduced RBCs?
washing process removes plasma proteins, microaggregates, platelets, and leukocytes
what blood should you give in emergency situations when a full cross match isn't practical(45min)?
type specific partial cross match>type specific uncross matched>O-
why should you not dilute blood with LR?
ca in LR when combined with blood can form microclots(binding citrate)
What can happen with citrate intoxication?
hypocalcemia with its associated problems of seizures, tetany, and laryngospasm, hypotension, narrow pulse pressure, QT prolongation, elevated end diastolic pressure and CVP
What are the indications for giving FFP?
replacement of isolated factor deficiencies or replacement of antithrombin III deficiency, TTP, documented deficiencies of factors V or VIII(less than25%)
What are signs of a transfusion reaction under anesthesia?
hemoglobinuria, hypotension, bleeding
What are consumed in DIC?
fibrinogen, factors V and VIII, platelets
What are lab findings suggestive of DIC?
PT>15s, fibrinogen <150(nml fibrinogen 150-200, in pregnant patients it should be >300), platelet count <150,000
What are causes of DIC?
SATT: sepsis, amniotic fluid embolism, trauma, transfusion reaction
what is cryo used for?
replace factor VIII, fibrinogen, fibronectin, and von willebrands factor
what is the problem with commercially prepared fibrinogen?
high incidence of associated hepatitis
What are problems with massive blood transfusion?
PATCH: Platelets(thrombocytopenia), Potassium(hyperkalemia), ARDS, Acid base changes(usually acidosis), temperature decreased, Citrate intoxication leading to hypocalcemia(prolonged QT and hypotension), Hepatitis and other infections
why can you hold off on giving calcium to a patient with hypocalcemia after blood transfusion?
serum ca often returns to normal rapidly after transfusion because citrate is metabolized by the liver and calcium is mobilized from endogenous source
How does aspirin affect platelet aggregation?
inhibits COX(arachadonic acid to protaglandin 2), prevents the formation of thromboxane(potent platelet aggregator)
What does ADP and fibrin do for platelet aggregation?
ADP is the most potent platelet aggregator, fibrin stabilizes occlusive platelet plug
What are the advantages of preop transfusion?
increasing 2,3-DPG, and increased O2 carrying capacity
How do you treat DIC?
treat cause, also platelets, FFP, and cryo
What factors does PTT screen for?
levels of V and VIII
If PTT >1.5 x control what should you give?
FFP
How is the diagnosis of a hemolytic transfusion reaction confirmed?
presence of free hemoglobin in spun plasma with a direct coombs test
In a patient that required an O- emergency transfusion what should you do after giving 4 units of uncrossmatch blood?
continue giving uncrossmatch blood or imcompatabilities with the new blood will develop
How often can patient's give autologous blood?
1 unit per week for 4 weeks
How does blood change as it sits on a shelf?
PaCO2 increases leading to acidosis, 2-3 DPG decreases, platelets decreases, factors deteriorate especially V and VIII, potassium increases from hemolysis
Why can cigarette smokers have an effective anemia?
binding of hemoglobin by carbon monoxide creates carboxyhemoglobin
Why do patients with poor LV function or ischemic heart disease require higher hematocrits?
it optimizes O2 delivery and does not predispose to compensatory cardiovascular changes like tachycardia, which increases oxygen consumption
What is fluosol-DA?
in combination with 100% oxygen fluosol(20mg/kg) increases oxygen content and improves mixed venous oxygen saturation(has a very short half life and may predispose to coagulopathies)
When are cells savers likely to be used?
when there is expected to be at least 1500mL of blood loss; in the setting of difficult cross match problems when availability of enough cross matched blood is in doubt
When should cell savers not be used?
risk of contaminated blood is high(infection, gut perforation, malignancy-risk of systemic spread)
What is contained in blood salvaged by a cell saver?
red blood cells and saline
What are benefits and risks of acute normovolemic hemodilution?
benefits: reduce the need for allogenic blood, improve blood viscosity and thus increased tissue perfusion, reduced intraop red cell loss
risks:decreased arterial O2 content, increased HR and CO can lead to myocardial ischemia
How much blood loss should be expected for considering ANH?
1500 mL or 30% of blood volume
How do you know how much blood to withdraw for acute normovolemic hemodilution?
volume to be removed=EBV x ((Ho-Hf)/Ha), Ho is initial hematocrit, final hemoglobin, Ha is average of initial and final hemoglobin
How is blood that was withdrawn from a patient during acute normovolemic hemodiluation retransfused?
blood should be transfused in the reverse order of removal(1st unit has the highest hematocrit and should be given last)
How long can you keep blood that was removed during acute normovolemic hemodilution at room temperature?
8 hours
What is more often transmitted in blood transfusion, hep B or C?
hep B
Where are the A and B antibodies located?
in the serum and not in the plasma
When a patient receiving uncrossmatched O- blood receives multiple units of O- uncrossmatch blood can you switch back to their actual type specific blood?
they can be switched back to their type specific blood after further testing by the blood bank indicates that it is safe to do so