Flashcards in Hematology #2 Deck (30):
DIC excessive clotting cascade and lysis cascade results in:
-Exhausted factors and co-factors
-partially developed and broken down clots
-micro emboli caught in capillaries
Organs with most capillaries
Heart, liver, spleen, brain, lungs,
MODS and death result from DIC why?
Entire system losing blood due to mass micro emboli occlusion
DIC lab values
1. Positive D-Dimer (fibrin degradation products)
2. Low fibrinogen and platelets (clotting factors)
3. Hg PT, aPTT, INR, FSP
-measurement of intrinsic coagulation
Activated partial thromboplastin time
-measurement of extrinsic coagulation
International Normalized Ratio
-universalized rabbit serum to measure PT
-high INR suggest it is taking longer to clot
FSP or FDP
Fibrin Split / Degradation Product
-clot break down
DIC treatment #1 goal
Treat precipitating cause
DIC traditional treatment
Give FFP, Cryo, platelets to create clots
-May add to the problem
DIC and heparin treatment
Only studies to be beneficial when secondary yo neoplasms and CA
Antithrombin III (ATIII) therapy
Interferes with fibrinogen converting to fibrin (normal process in body)
-primarily inhibits factors IIa (thrombin) and X (Stuart factor)
Chronic heparin therapy can cause what deficiency?
-body processes out heparin bound w/ ATIII
- can cause DIC, tx w/ FFP
Increase O2 carry capacity of blood
-volume expander only secondary to this qualification
PRBC HgB indications
RBC antigen that can cause a reaction
Can reach sensitization with Rh (+) blood.
-Rh (+) fetus can be aborted (rogan can prevent this)
Rh(+) / Rh(-) blood to male or females
Males: Rh (+)
-can be sensitized, but does not have fetal complication for future.
How many ml are in one unit of PRBCs?
PRBC pediatric dose
Citrate toxicity considerations
Multiple units: 4 units in less than 20 minutes
-citrate chelates ionized Ca- renders it useless in clotting cascade
Administer Ca if giving PRBCs at what rate
One unit in less than 5 minutes or 1 ml/kg/min
General rule: 1 amp of Ca q 4 units PRBCs.
Liver considerations with citrate
Liver processes citrate. Liver dysfunction can lead to citrate toxicity despite PRBC admin at slower rates.
Can take A, B, AB
1 unit of PRBCs increases the H&H by what?
Q unit of PRBCs at storage temp will decrease core temp by?
PRBC and acidosis considerations
Store blood continued metabolism = lactate = acidotic
-citrate converts to HCO3 = self correcting
PRBC and hyperkalemia considerations
RBCs die and release K in storage. Stored blood K levels can reach 17-24.
-administration rates greater than 90-120 ml/min can result in hyperkalemia. Watch ECG for changes.