Hematology Flashcards
One unit PRBCs increases Hb by
human blood volume
universal donor and recipient
1.5 g/dL
70ml/kg = about 5 liters in 70kg adult
Type O and AB
Benefits of PRBCS over a whole blood (5)
–Less volume / less fluid overload
–More RBCs per volume transfused
–Decreased citrate infusion = better coagulation
–Decreased infusion of protein antigens
(less autoimmunization)
–Decreased infusion of potassium
(from lysed RBCs)
Massive blood transfusion constituents
relationship to ARDS
packed cells, FFP and platelets
Microaggregates from RBC, WBC, platelet debris showered into pulmonary capillary bed causing ARDS – use 40 micron filter to decrease this risk
Etiology of acute hemolytic transfusion reaction
consequences of RBC destruction (2)
ABO incompatible
immunologic reaction (fever, chills, hypotension) and the consequences of free hemoglobin and RBC stroma in the blood stream (ATN, breathlessness, respiratory failure, hemoglobinuria [pink urine])
Acute hemolytic transfusion reaction
treatment
labs (3)
- Free hemoglobinemia and hemoglobinuria
- Haptoglobin (binds to free hemoglobin) is decreased
- Coombs testing of pre- and post-transfusion blood (a test for globulin antibodies on the surface of RBCs)
etiology of acute febrile non-hemolytic transfusion reaction and tx
etiology of acute allergic reaction and tx
Febrile:
–Due to interaction between recipient and donor non-RBC components
–Must stop transfusion and exclude hemolysis
Allergic:
–Due to plasma protein incompatibilities
–Reaction severity not dose-related
–Discontinuation of transfusion not always required
Other transfusion reactions
delayed hemolytic etiology electrolyte imbalance (3) and etiologies
Delayed: –Antigen-antibody reaction after 7-10 days
electrolytes:
–Hyperkalemia from lysed RBCs
–Low calcium from excess citrate causing chelation (causes prolonged QT)
–Hypokalemia from citrate being metabolized to bicarbonate and resultant plasma alkalosis (causes shift of K into cells and increased K excretion)
Transfusion infection related risks
hepatitis B
Titus C
HIV
other (3)
1: 500k
1: 2 million
1: 2 million
bacterial infections, chlamydia, rare viral like West Nile
Platelets
one units raises count by
type specific?
10,000
yes due to contamination of a small amount of RBCs in the platelet pack
note: our institution does not do this
Thrombocytopenia thresholds
30,000 to 50,000
10,000 to 30,000
less than 10,000
–50,000-30,000 = excess bruising with minor trauma
–30,000-10,000 = spontaneous petechiae and bruising
–< 10,000 = spontaneous visceral hemorrhage
Significance of palpable versus non-palpable purpura
causes of dysfunctional platelets (increased bleeding time) - (4)
- Nonpalpable purpura – think low or dysfunctional platelets
- Palpable purpura – think angiopathy / vasculitis
Causes of dysfunctional platelets (increases the bleeding time / platelet function test):
–Aspirin (for the life of the platelet)
–NSAIDS (only as long as in the blood stream)
–Ticlopidine (Ticlid) / clopidogrel (Plavix)
Other meds
Thrombocytopenia primary mechanisms (4)
–Decreased platelet production: Aplastic anemia, viral infections, drugs (ethanol, thiazides, estrogens, chemotherapy drugs, heparin)
–Increased platelet destruction: •ITP / TTP / HUS / DIC / viruses / drugs (heparin)
–Splenic sequestration: Hypersplenism - malaria, rheumatoid arthritis, TB
- Platelet loss from bleeding
ITP cause/features
versions (2)
Autoimmune destruction of platelets, isolated platelets
pediatric version acute, usually after an illness and usually self-limited
adult version insidious and chronic
ITP treatment thresholds
treatment (2) (1) OR (1)
Tx Thresholds: A platelet count of 20-30,000 or Active bleeding with a 30-50,000 count
All patients: prednisone and replace platelets at 2 to 3 times the rate calculated to get to 50,000
Rhogam if Rh positive otherwise IgG
PT/INR: pathway measured
PTT: pathway measured
PTT: causes of elevation
Extrinsic
intrinsic
Elevated PTT
- Heparin
- Hemophilia
- von Willebrand’s disease
- Lupus anticoagulant
DIC pathway affected leading causes (4)
DIC basic descrption
Extrinsic
- Causes: meningococcemia (most extreme form of DIC), trauma (especially head), sepsis, retained products of conception
- liberation of tissue activating factor ® small fibrin and blood clots deposited in the microcirculation (consume clotting factors; can cause tissue hypoxemia) ® fibrinolysis ® fibrin degradation products and d-dimer
DIC laboratory findings (5)
Elevated INR number thrombocytopenia, elevated fibrin degradation products, low fibrinogen (low sensitivity), fragmented RBCs
DIC treatment (5)
Treat underlying problem, follow INR for response
give PCC
FFP, vitamin K, folate
platelets
consider heparin is thrombosis predominant
TTP pentad
causes (4)
treatment (3)
treatment contraindication
similar to DIC: Thrombocytopenia, MAHA, transient neuro- deficits, ARF, fever
Causes: idiopathic, drug-induced, pregnancy, infection
Tx: steroids, plasmapheresis, FFP
NO platelets (can exacerbate)
Heparin pathway
reversal agent
pregnancy consideration
Intrinsic
protamine
doesn’t cross placenta
Vitamin K dependent clotting factors
leading cause of coagulopathy for warfarin patients
optimal reversal
Two, seven, nine, 10
drugs especially oral antibiotics including effects on gut bacteria which decrease vitamin K synthesis
four factor prothrombin complex concentrate
Xarelto, Eliquis etc mechanism
naming convention
reversal
Factor X a inhibitors
end in “xaban”
reversal: time-normal hemostasis about 12 to 24 hours after the last dose; due to renal metabolism, dialysis may be needed for patients with renal failure, consider TXA, PCC
Sickle cell acute chest criteria (4)
morbidity
treatment (2+)
- New pulmonary infiltrate involving at least one complete lung segment (usually lower lobes)
- Chest pain
- Fever (more than 38.5C)
- Concomitant tachypnea, wheezing or cough
treatment: oxygen, antibiotics, bronchodilator, transfusion, incentive spirometry
Sickle cell anemia
describe CNS crisis
renal crisis
hand-foot syndrome
Priaprism
possible common treatment
possible common treatment: exchange transfusion
•CNS crisis: painless, cerebral infarction in children / hemorrhage in adults
–Other CNS problems: TIAs, strokes, seizures, paresthesias
- Renal crisis: infarction, hematuria, flank pain, papillary necrosis
- Hand-Foot Syndrome: in first two years of age, swelling of hands or feet due to avascular necrosis due to vasoocclusion - may be first sign of sickle cell disease
- Priapism – exchange transfusion / corpus cavernosum (lateral corpora) epi and aspiration
Sickle cell-aplastic crisis
etiology
precipitant
prognosis
–Failure of bone marrow erythropoiesis
–Reticulocyte count low
–Precipitants: infection (parvovirus is the most common precipitant), ¯ folate
–Usually self-limited
Sickle cell-infection risks (3+)
Bacterial and viral
Encapsulated organisms: pneumococcus, salmonella, Haemophilus influenza, staff, E. coli, Mycoplasma
viral: influenza and parvovirus
Sickle cell crises, general treatment pathway (5)
- Hydration
- Analgesics
- Oxygen
- Transfusions if indicated
- Emergent exchange transfusion for serious sickle crisis (CNS infarction, sequestration)
- Antibiotics if indicated
Hemophilia etiology (A and B)
Test results
treatments
Factor eight and factor IX deficiency respectively
normal PT, increased PTT, decreased factor levels
low threshold for the DDAVP (increases VWB/factor 7), factor replacement
Von Willebrands Disease
Lab
treatment (2)
Lab: normal PT, elevated bleeding time, variable PTT
Treatment
–DDAVP (induces release of VWF from storage sites within the endothelium)
–Factor VIII concentrate has large amounts of VWF
