Hemotology Flashcards
1
Q
Anemia
A
- Decrease in RBC production d/t iron deficiency, renal disease (decrease in erythropoietin that stimulates RBC production)
- RBC destruction (sickle cell, DIC, TTP, transfusion reaction)
- S/S: fatigue, weakness, SOB, exercise intolerance, hypotension, tachycardia
- Dx: CBC, hemoglobin (normal >12), hematocrit (normal 40%), serum iron, transferring, ferritin levels, WBC, platelet, reticulocyte count, peripheral blood smear
- Tx: Blood conservation (minimize waste and amount of blood draws, microtainers, pediatric phlebotomy tubes), Vitamin (folic acid, B12), Iron, hgb <7 = blood tx
2
Q
Heparin-induced thrombocytopenia (HIT)
A
- Within 5-10 days after heparin administration, the immune system forms antibodies against platelets causing both thrombocytopenia AND thrombosis
- Complications: DVT, limb gangrene, PE, storke, MI, anaphylaxis
- Dx: antibody testing (HIT panel), functional assay
- Tx: discontinue any/all form of Heparin, hold or reverse warfarin with Vitamin K via slow IV drip, non-heparin anticoagulation to prevent thrombosis (argatroban, Bivalirudin), restart maintenance warfarin once stable and platelet recover
3
Q
Immune Thrombocytopenia (ITP)
A
- Idiopathic or autoimmune thrombocytopenic (e.g., SLE)
- S/S: bleeding, petechia, purpura (flat, red, non-blancheable lesions usually found on lower extremities), splenomegaly, epistaxis
- Tx: platelet transfusion, IVIG, steroids, if bleeding still occurs despite platelet, Trasemic acid (anti-fibrinolytic) is administered
4
Q
Disseminated Intravascular Coagulopathy (DIC)
A
- Fibrinogen is made and secreted from the liver when there is vascular injury, fibrinogen is converted back to fibrin, which along with platelets forms blood clots. Blood clots then dissolved into fibrin degradation products via fibrinolysis.
- AKA Consumptive Coagulopathy: systemic clotting consumes platelets and fibrinogen and bleeding occurs in the absence of the clotting factors
- Can lead to MODS from vascular thrombosis, hemorrhage, and hypoperfusion
- Causes: Sepsis, trauma, OB complications, acute hemolytic transfusion reactions, release of procoagulant (bacterial endotoxins)
- Dx: decreased fibrinogen, decreased platelet <50k, prolonged PT/aPTT, increased FDP, increased D-dimer
- S/S: petechiae, ecchymosis, bleeding, renal/hepatic dysfunction, shock, MODS
- Tx: treat underlying cause first, transfuse, supportive measures
5
Q
HELLP
A
- Hemolysis, elevated liver enzymes, and low platelets
- Primarily during or after pregnancy, new onset HTN with SBP>160, proteinuria, preeclampsia, seizure = eclampsia
- A subtype of and most severe form of preeclampsia
- S/S: abdominal pain in RUQ (liver), protein uria, HTN with SBP>140, N/V, HA, visual changes
- Dx: schistocytes on peripheral smear - fragmented RBC that indicates hemolysis; elevated bilirubin >1/2 mg/dL (bilirubin is a breakdown product of RBC), elevated AST or ALT >2x normal; platelet <100k
- Tx: tx hypertension to reduce risk of stroke (IV labetalol, hydralazine, nicardipine), seizure prophylaxis (magnesium sulfate), deliver fetus and placenta ASAP
6
Q
Tumor Lysis Syndrome
A
- a large amount of tumor cells are killed off or lysed after treatment, and their contents spill into the bloodstream (K, phos, Ca, uric acid)
- Oncologic emergency resulting in AKI, seizures, cardiac arrhythmias
- Tx: prevention, IV hydration to improve renal perfusion prior to chemotherapy, allopurinol to reduce uric acid formation, close ICU monitoring, treat electrolyte imbalance
7
Q
Febrile non-hemolytic reaction
A
- The most common transfusion reaction commonly caused by donor leukocytes and cytokines that accumulate during the storage of blood
- Temperature increase of 1-2 degrees Celsius
- PRevention: transfuse leukoreduced cells
8
Q
Acute hemolytic reaction
A
- Usually d/t ABO incompatibility
- Causes rapid intravascular hemolysis –> AKI, DIC, hemodynamic collapse
- S/S: fever, chills, tachycardia, hypotension, back pain, hematuria
- Immediately stop transfusion, send blood back to the lab, and stabilize
9
Q
Anaphylactic blood reaction
A
- Allergic reaction to the donor blood
- Rapid onset of hypotension, angioedema, laryngeal edema wheezing, or respiratory distress within minutes of starting the transfusion
- Immediately stop the transfusion, give IM/SQ epinephrine, aggressive hydration, protect airway, pressor
- Prevent by ensuring blood product is washed of IgA/IgE antibodies and leukocytes prior to transfusion
10
Q
Transfusion-related acute lung injury (TRALI)
A
- Acute lung injury within 6 hours of transfusion caused by antibodies in the donor product reacting with antigens in the recipient
- Immune system responds and release mediators that cause pulmonary edema
- S/S: sudden respiratory distress, fever, hypotension, acute hypoxemia, and non-cardiogenic pulmonary edema during or after transfusion
- Abnormal CXR shows the clinical picture of ARDS
- Immediately stop the transfusion, supplemental O2, mechanical ventilation, fluids and pressors. ARDS protocol!
- Prevention: screen donors for HLA antibodies
11
Q
Transfusion-associated circulatory overload (TACO)
A
- Risk factors: pre-existing cardiac or renal dysfunction, elderly, small stature, multiple units transfused, faster rate of transfusion
- S/S: respiratory distress, no fever, hypertension, rales
- Abnormal CXR, elevated BNP
- Tx: supplemental O2, ventillatory support, diuresis
- Prevention: reduce number of transfusions, slower rate
