HEMATOLOGY Flashcards

1
Q

intrinsic coagulation pathway is stimulated by vascular endothelium injury such as:

A
  • cell trauma (valve, IABP)
  • sepsis
  • shock
  • ARDS
  • hypoxemia, acidemia
  • cardiopulmonary arrest
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2
Q

extrinsic coagulation pathway is stimulated by tissue injury, releases “tissue thromboplastin”

A
  • extensive trauma
  • OB emergencies
  • mallignancies
  • dissecting aortic aneurysm
  • extensive MI
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3
Q

what does Coumadin do? how is it reversed?

A

inhibits conversion of prothrombin; vitamin K

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4
Q

what does heparin do? how is it reversed?

A

inhibits thrombin; protamine

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5
Q

what happens in disseminated intravascular coagulopathy (DIC)?

A
  • activation of clotting (microembolism) with resultant consumption of clotting factors (hemorrhage)
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6
Q

is DIC more of a clotting/bleeding problem?

A

clotting

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7
Q

what causes DIC?

A
  • endothelial damage - sepsis, hypoxemia, shock, ARDS, AAA, acidemia, cardiopulmonary arrest
  • release of tissue thromboplastin - extensive trauma, malignancies, OB emergencies, dissecting aortic aneurysm
  • factor X activation - acute pancreatitis, liver disease
  • miscellaneous - massive transfusions, PE, hemolytic anemia, fresh H2O drowning, ASA poisoning
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8
Q

what labs can be seen with DIC?

A
  • primary - **ELEVATED FSP (increased fibrinolysis), PT/PTT/INR; decreased platelets, fibrinogen, hct
  • secondary - INCREASED D-DIMER, increased antithrombin III
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9
Q

what are normal fibrin split products (FSP) and fibrinogen levels?

A

FSP <10mcg/mL

fibrinogen 200-400mg/dL

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10
Q

how is DIC treated?

A
  • treat cause
  • vitamin K
  • FFP, cryo, platelets
  • low dose heparin
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11
Q

what causes heparin-induced thrombocytopenia (HIT)?

A
  • immune (IgG) response

- results in thrombosis (white clots) that consumes platelets

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12
Q

what are some S/S of HIT?

A
  • platelets <150K or drop 30-50%
  • petechiae - early sign
  • clots leading to PE, MI, stroke, amputation
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13
Q

how is HIT treated?

A
  • stop heparin
  • ELISA (enzyme-linked immunosorbent assay) test for heparin antibody presence
  • start direct thrombin inhibitor and continue until platelets stabilize, monitor PTTs, argatroban
  • warfarin
  • platelets <10K, monitor for changes in LOC (intracranial bleed)
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14
Q

how is idiopathic thrombocytopenia purpura (ITP) diagnosed?

A
  • only decreased platelets, rest of CBC normal
  • drugs that lead to thrombocytopenia and other clinical conditions (lupus, chronic lymphocytic leukemia) are not present
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15
Q

what are S/S of ITP?

A
  • expected: petechiae, purpura, easy bruising
  • common: epistaxis, gingival bleeding, menorrhagia
  • rare: GI bleeding, hematuria, ICH
  • numerous differential diagnoses need to be r/o
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16
Q

what is plasmapheresis and what is it indicated for?

A
  • filtering and separation of plasma from whole blood via semipermeable membranes; done via central line similar to catheters used for HD
  • Guillain-Barre syndrome, myasthenia gravis, thrombotic thrombocytopenic purpura
17
Q

what are contraindications for plasmapheresis?

A
  • pt’s who can’t tolerate central line placement
  • actively septic or hemodynamically unstable
  • allergies to FFP or albumin
  • heparin allergies; used as an anticoagulant during plasmapheresis
  • hypocalcemia pos at risk for worsening b/c citrate is commonly used to prevent clotting and can potentiate hypocalcemia
18
Q

what are some acute (within 24hrs) S/S of transfusion reactions?

A
  • respiratory: tachypnea, dyspnea, wheezing, rales, stridor, hypoxia
  • CV: tachy/bradycardia, hyper/hypoTN, JVD, arrhythmia
  • immune: fever (>1C), chills, rigors
  • cutaneous: pruritus, uticaria, erythema, flushing, petechiae, cyanosis
  • GI: n/v
  • pain: HA, chest, ab, back/flank, infusion site
  • renal: red urine (hemolytic, non-antibody mediated)
19
Q

how would you manage acute hemolytic reactions (antibody mediated)?

A
  • anticipate hypotension, renal failure, and DIC
  • prophylactic measures to reduce risk of renal failure may include vigorous hydration with crystalloid solutions, and osmotic diuresis with 20% mannitol
  • if DIC is documented and bleeding requires treatment, transfusions of frozen plasma, pooled cryo, and/or platelet concentrates may be indicated
20
Q

how would you manage acute hemolytic reactions (non-antibody mediated)?

A
  • transfusion of serologically compatible, although damaged, RBCs usually does not require rigorous management
  • diuresis induced by an infusion of 500ml of NS/hr or as tolerated by pt, until red urine subsides