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EM Board exam > Hematology > Flashcards

Hematology Flashcards

1
Q

One unit PRBCs increases Hb by

human blood volume

universal donor and recipient

A

1.5 g/dL

70ml/kg = about 5 liters in 70kg adult

Type O and AB

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2
Q

Benefits of PRBCS over a whole blood (5)

A

–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)

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3
Q

Massive blood transfusion constituents
relationship to ARDS

A

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

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4
Q

Etiology of acute hemolytic transfusion reaction

consequences of RBC destruction (2)

A

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])

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5
Q

Acute hemolytic transfusion reaction
treatment
labs (3)

A
  • 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)
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6
Q

etiology of acute febrile non-hemolytic transfusion reaction and tx

etiology of acute allergic reaction and tx

A

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

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7
Q

Other transfusion reactions

delayed hemolytic etiology
electrolyte imbalance (3) and etiologies
A

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)

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8
Q

Transfusion infection related risks
hepatitis B
Titus C
HIV
other (3)

A

1: 500k
1: 2 million
1: 2 million

bacterial infections, chlamydia, rare viral like West Nile

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9
Q

Platelets
one units raises count by
type specific?

A

10,000
yes due to contamination of a small amount of RBCs in the platelet pack
note: our institution does not do this

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10
Q

Thrombocytopenia thresholds
30,000 to 50,000
10,000 to 30,000
less than 10,000

A

–50,000-30,000 = excess bruising with minor trauma

–30,000-10,000 = spontaneous petechiae and bruising

–< 10,000 = spontaneous visceral hemorrhage

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11
Q

Significance of palpable versus non-palpable purpura
causes of dysfunctional platelets (increased bleeding time) - (4)

A
  • 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

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12
Q

Thrombocytopenia primary mechanisms (4)

A

–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

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13
Q

ITP cause/features

versions (2)

A

Autoimmune destruction of platelets, isolated platelets
pediatric version acute, usually after an illness and usually self-limited
adult version insidious and chronic

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14
Q

ITP treatment thresholds
treatment (2) (1) OR (1)

A

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

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15
Q

PT/INR: pathway measured
PTT: pathway measured

PTT: causes of elevation

A

Extrinsic
intrinsic

Elevated PTT

  • Heparin
  • Hemophilia
  • von Willebrand’s disease
  • Lupus anticoagulant
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16
Q 
DIC pathway affected
leading causes (4)

DIC basic descrption

A

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
17
Q

DIC laboratory findings (5)

A

Elevated INR number thrombocytopenia, elevated fibrin degradation products, low fibrinogen (low sensitivity), fragmented RBCs

18
Q

DIC treatment (5)

A

Treat underlying problem, follow INR for response
give PCC
FFP, vitamin K, folate

platelets
consider heparin is thrombosis predominant

19
Q

TTP pentad

causes (4)
treatment (3)

treatment contraindication

A

similar to DIC: Thrombocytopenia, MAHA, transient neuro- deficits, ARF, fever

Causes: idiopathic, drug-induced, pregnancy, infection

Tx: steroids, plasmapheresis, FFP

NO platelets (can exacerbate)

20
Q

Heparin pathway

reversal agent

pregnancy consideration

A

Intrinsic
protamine
doesn’t cross placenta

21
Q

Vitamin K dependent clotting factors

leading cause of coagulopathy for warfarin patients

optimal reversal

A

Two, seven, nine, 10

drugs especially oral antibiotics including effects on gut bacteria which decrease vitamin K synthesis

four factor prothrombin complex concentrate

22
Q

Xarelto, Eliquis etc mechanism

naming convention

reversal

A

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

23
Q

Sickle cell acute chest criteria (4)
morbidity

treatment (2+)

A
  • 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

24
Q

Sickle cell anemia
describe CNS crisis
renal crisis
hand-foot syndrome
Priaprism

possible common treatment

A

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
25
Q

Sickle cell-aplastic crisis

etiology
precipitant
prognosis

A

–Failure of bone marrow erythropoiesis

–Reticulocyte count low

–Precipitants: infection (parvovirus is the most common precipitant), ¯ folate

–Usually self-limited

26
Q

Sickle cell-infection risks (3+)

Bacterial and viral

A

Encapsulated organisms: pneumococcus, salmonella, Haemophilus influenza, staff, E. coli, Mycoplasma
viral: influenza and parvovirus

27
Q

Sickle cell crises, general treatment pathway (5)

A
  • Hydration
  • Analgesics
  • Oxygen
  • Transfusions if indicated
  • Emergent exchange transfusion for serious sickle crisis (CNS infarction, sequestration)
  • Antibiotics if indicated
28
Q

Hemophilia etiology (A and B)

Test results

treatments

A

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

29
Q

Von Willebrands Disease

Lab

treatment (2)

A

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

EM Board exam (18 decks)

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