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Bailey and Love + Sabiston 20e > Shock and Transfusion > Flashcards

Shock and Transfusion Flashcards

1
Q

Most common cause of death in surgical patients?

A. Sepsis
B. Shock
C. Post-operative complications
D. Technical complications

A

Ans B - Shock -

B&L page 12

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2
Q

which of the following is the most common form of shock?

A. Septicemic
B. Hypovolemic
C. Endocrine
D. Cardiogenic

A

Ans B -
hypovolemic shock is probably the most common form of shock, and to some degree it is the component of all other forms of shock.

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3
Q

obstructive shock is characterized by -

A. Increased preload
B. Decreased Preload
C. increased afterload
D. Decreased afterload

A

Ans B -
Obstructive shock there is reduced preload due to mechanical obstruction of cardiac filling. Common causes are cardiac tamponade, tension pneumothorax, massive pulmonary embolus or air embolus. There is reduced filling of the left and/or right heart leading to reduced preload and fall in cardiac output.

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4
Q

All of the following are the features of distributive shock except

A. Low systemic vascular resistance
B. high afterload
C. Vascular dilation
D. High cardiac output

A

Ans B -

Distributive shock is seen in septicemic shock, anaphylaxis, spinal cord injury.

characterised by

  • inadequate organ perfusion with vascular dilation
  • hypotention and low systemic vascular resistance
  • inadequate afterload
  • abnormally high cardiac output.
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5
Q

high cardiac output and low systemic vascular resistance is a feature of ?

A. Hypovolemic shock
B. Cardiogenic shock
C. Obstructive shock
D. Distributive shock

A

Ans D -

Cardiac output is low, and systemic vascular resistance is high in hypovolemic, cardiogenic and obstructive shock.

Whereas cardiac output is high, and systemic vascular resistance is low in distributive shock.

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6
Q

Low venous pressure is a feature of which of the following?

A. Hypovolemic shock
B. Distributive shock
C. cardiogenic shock
D. both A and B

A

Ans D -
both hypovolemic shock and distributive shock have low venous pressure, whereas obstructive and cardiogenic shock have raised venous pressure.

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7
Q

high mixed venous saturation is a feature of which of the following?

A. hypovolemic shock
B. Distributive shock
C. Obstructive shock
D. Cardiogenic shock

A

ans B -
Mixed venous saturation is low in hypovolemic, obstructive and cardiogenic shock where the low perfusion of the tissues means that the oxygen extraction by the tissues is high.

In distributive shock, specificially septicemic shock, the mixed venous saturation is high because there is failure of cellular utilisation of oxygen.

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8
Q 
hypothyroidism produces a shock state similar to ? 
A. Hypovolemic shock
B. Obstructive shock
C. Distributive shock
D. Cardiogenic shock
A

Ans C -
Hypothyroidism causes a shock state similar to that of neurogenic shock - due to disordered vascular and cardiac responsiveness to circulating catecholamines.
There may also be an associated cardiomyopathy.

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9
Q

in compensated shock blood to all of the following organs is preserved except -

A. Kidney
B. Brain
C. Lungs
D. Small bowel

A

Ans D -

In compensated shock there is adequate compensation to maintain central blood volume and preserve flow to the kidneys, lungs and brain.
This cardiovascular state is maintained by reducing perfusion to the skin, muscle and gastrointestinal tract.

Apart from tachycardia and cool peripheries there may be no other signs of hypovolemia.

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10
Q

decreased urine output is suggestive of which grade of shock

A. Compensated
B. Mild
C. Moderate
D. both B and C

A

ans - C

Urine output is maintained in mild shock.

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11
Q

what percentage of loss of volume is within the normal compensatory mechanisms -

A. 5%
B. 15%
C. 30%
D. 50%

A

Ans B - 15%

In general around 15% of the circulating blood volume is within normal compensatory mechanism.

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12
Q 
Fall in blood pressure is seen at loss of circulatory volume of - 
A. 5 - 15%
B.  15-25%
C. 30-40%
D. 40-50%
A

Ans C-

Blood pressure is usually well maintained and only falls after 30-40% of circulating volume has been lost.

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13
Q

All of the following are seen in mild shock except

A. High pulse rate
B. Normal urine output
C. low respiratory rate
D. Lactic acidosis

A

Ans C -

mild shock is characterised by

  • tachycardia
  • tachypnea
  • mild reduction urine output
  • mild anxiety
  • blood pressure maintained
  • decreased pulse pressure
  • peripheries are cool and sweaty with prolonged capillary refill times.
  • lactic acidosis is present.
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14
Q

low respiratpry rate is a feature of -

A. Mild shock
B. moderate shock
C. Severe shock
D. none of the above

A

Ans C -

laboured breathing or low respiratory rate is a feature of severe shock.

Severe shock -

  • lactic acidosis . +++
  • anuria
  • comatose patient
  • laboured breathing
  • severe tachycardia
  • severe hypotension
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15
Q

low respiratpry rate is a feature of -

A. Mild shock
B. moderate shock
C. Severe shock
D. none of the above

A

Ans C -

laboured breathing or low respiratory rate is a feature of severe shock.

Severe shock -

  • lactic acidosis . +++
  • anuria
  • comatose patient
  • laboured breathing
  • severe tachycardia
  • severe hypotension
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16
Q

unresuscitable shock is characterised by -

A. myocardial depression
B. unresponsiveness to fluids and inotropes.
C. loss of systemic vascular resistance
D. All of the above

A

Ans D -

There is myocardial depression, and loss of responsiveness to fluid or inotropic therapy.

Peripherally there is loss of the ability to maintain systemic vascular resistance and further hypotension ensues.

Peripheries no longer respond to vasopressor agents.

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17
Q

unresuscitable shock is characterised by -

A. myocardial depression
B. unresponsiveness to fluids and inotropes.
C. loss of systemic vascular resistance
D. All of the above

A

Ans D -

There is myocardial depression, and loss of responsiveness to fluid or inotropic therapy.

Peripherally there is loss of the ability to maintain systemic vascular resistance and further hypotension ensues.

Peripheries no longer respond to vasopressor agents.

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18
Q

moratlity of multiple organ failure in shock is

A. 10%
B. 20%
C. 40%
D. 60%

A

Ans D -

Multiple organ failure currently carries a mortality of 60%.

Effects of organ failure -

A. Lung : ARDS
B. Kidney : AKI
C. Clotting : Coagulopathy
D. Cardiac : Cardiovascular failure.

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19
Q

Ideal replacement fluid in case of hemorrhagic shock -

A. Ringer’s lactate
B. Hartmann’s solution
C. Fresh whole blood
D. Hexastarch

A

Ans C -

Oxygen carrying capacity of colloid and crystalloids is zero.
If blood is being lost, the ideal replacement fluid is blood. Although crystalloid therapy may be required while awaiting blood products.

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20
Q

Ideal replacement fluid in case of hemorrhagic shock -

A. Ringer’s lactate
B. Hartmann’s solution
C. Fresh whole blood
D. Hexastarch

A

Ans C -

Oxygen carrying capacity of colloid and crystalloids is zero.
If blood is being lost, the ideal replacement fluid is blood. Although crystalloid therapy may be required while awaiting blood products.

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21
Q

Hypotonic solutions such as dextrose may be considered for resucitation in which of the following cases -

A. Hypernatremia
B. Cirrhosis
C. Diabetes insipidus
D. all of the above

A

Ans D -

Hypotonic solutions are poor volume expanders and they should not be used in the treatment of shock unless the deficit is free water such as Diabetes insipidus, or patients are sodium overloaded such as cirrhosis.

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22
Q

Hypotonic solutions such as dextrose may be considered for resucitation in which of the following cases -

A. Hypernatremia
B. Cirrhosis
C. Diabetes insipidus
D. all of the above

A

Ans D -

Hypotonic solutions are poor volume expanders and they should not be used in the treatment of shock unless the deficit is free water such as Diabetes insipidus, or patients are sodium overloaded such as cirrhosis.

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23
Q

all of the following are true regarding dynamic fluid response except -

A. 250-500 mL bolus of fluid over 5-10 minutes
B. responders require no further treatment
C. Blood pressure, heart rate and CVP are used to measure the response.
D. transient responders usually revert in 10-20 minutes.

A

ans B -

Shock status can be determined dynamically by cardiovascular response to the rapid administration of a fluid bolus.

In total 250-500 mL of fluid is rapidly given over 5-10 minutes, and the cardiovascular response in terms of HR, BP and CVP is observed.

Responders -
improvement in cardiovascular status is sustained. These patients are not actively losing fluid but require a filling to a normal volume status.

Transient responders -
have an improvement but revert to previous state over 10-20 minutes. They have moderate ongoing fluid loss.

Non-responder - severely volume depleted and are likely to have major ongoing loss of intravascular volume.

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24
Q

all of the following are true regarding dynamic fluid response except -

A. 250-500 mL bolus of fluid over 5-10 minutes
B. responders require no further treatment
C. Blood pressure, heart rate and CVP are used to measure the response.
D. transient responders usually revert in 10-20 minutes.

A

ans B -

Shock status can be determined dynamically by cardiovascular response to the rapid administration of a fluid bolus.

In total 250-500 mL of fluid is rapidly given over 5-10 minutes, and the cardiovascular response in terms of HR, BP and CVP is observed.

Responders -
improvement in cardiovascular status is sustained. These patients are not actively losing fluid but require a filling to a normal volume status.

Transient responders -
have an improvement but revert to previous state over 10-20 minutes. They have moderate ongoing fluid loss.

Non-responder - severely volume depleted and are likely to have major ongoing loss of intravascular volume.

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25
Q

which of the following statements is false

A. Crystalloids should be administered to patients in hypovolemic shock while waiting for blood products
B. Inotropic agents are the first line therapy in hypovolemia
C. vasopressin is effective inotrope in relative steroid deficiency
D. dobutamine is agent of choice in cargiogenic shock

A

Ans B -

In a patient with ongoing hemorrhage, blood is the ideal resuscitation fluid, however crystalloids can be given while waiting for blood products.

Inotropic agents are not indicated as first line therapy in hypovolemia. Administration of these agents in the absence of adequate preload rapidly leads to decreased coronary perfusion and depletion of myocardial oxygen reserves.

Vasopressin may be used as alternative vasopressor in absolute or relative steroid deficiency where vasodilation is resistant to catecholamines.

Inodilator dobutamine is agent of choice in cardiogenic shock.

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26
Q

Minimum standard for monitoring of patient in shock includes all of the following except -

A. Continuous heart rate monitoring

B. Continuous Oxygen saturation monitoring

C. Invasive blood pressure monitoring

D. Hourly urine output measurements

A

ans C -

minimum standard for monitoring of patient in shock is -

continuous heart rate monitoring (ECG)
continuous oxygen saturation monitoring
frequent non-invasive blood pressure monitoring
Hourly urine output monitoring

Additional modalities -

  • CVP
  • Invasive blood pressure
  • Cardiac output
  • Base deficit and serum lactate.

Cardiovascular monitoring at minimum should include -

  • continuous heart rate via ECG
  • oxygen saturation
  • pulse waveform
  • non-invasive BP

Patients whose state of shock is not rapidly corrected with small amount of fluid should have central venous pressure monitoring and continuous blood pressure monitoring via arterial line.

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27
Q

Normal CVP response to a fluid bolus of 250-500 mL over 5-10 minutes is -

a. rise of 2-5cm water
b. rise of 5-10cm water
c. rise of 10-15cm water
d. rise of 15-20cm water

A

Ans A -

The normal CVP response is a rise of 2-5cm of water which gradually drifts back to original level within 10-20minutes.

No change in CVP - empty and require further fluid resuscitation

Large change in CVP - high preload and an element of cardiac insufficiency or volume overload.

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28
Q

subslingual capnometry is a monitor for perfusion of -

A. Muscle
B. Gut
C. Kidney
D. Brain

A

Ans B -

Gut perfusion can be monitored with

  • sublingual capnometry
  • Gut mucosal pH
  • Laser Doppler Flowmetry

Muscle and brain perfusion can be monitored with

  • IR spectroscopy
  • tissue oxygen electrode
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29
Q

Clinical indicators of perfusion of muscle and GIT

A. Infra-red spectroscopy
B. Blood pressure and HR
C. Base Deficit
D. Mucosal pH

A

ans C -

currently the only clinical indicators of perfusion of the GIT and muscle are the global measures of lactic acidosis and the mixed venous oxygen saturation.

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30
Q

Base deficit levels associated with higher morbidity and mortality -

A. >2 mmol/L
B. >4 mmol/L
C. >6 mmol/L
D. >8 mmol/L

A

Ans C -

Patients with a base deficit more than 6 mmol/L have a much higher morbidity and mortality than those with no metabolic acidosis.

length of time in shock with an increased base deficit is important even if all other vital signs have returned to normal.

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31
Q

All of the following are true regarding mixed venous oxygen saturation -

A. Most accurate via a sample drawn from Right atrium

B. Estimates from SVC tend to have a higher value than those from right atrium

C. Normal levels are 50-70%

D. levels below 50% are suggestive of distributive shock.

A

Ans D -

Accurate measurement is via analysis of blood drawn from a long central line placed in the right atrium.

Estimations from a sample drawn from SVC are slightly higher since the lower half of the body has more oxygen extraction

Normal values are 50-70%.

Values below 50% are s/o hypovolemic or cardiogenic shock - with tissues extracting more oxygen.

Values above 70% are s/o septicemic shock or distributive shock with tissues unable to adequately utilise oxygen.

If patient is septic with a mixed venous oxygen saturation of less than 70% then there is also a component of hypovolemia.

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32
Q

signs suggestive of occult hypoperfusion -

A. Lactic acidosis
B. Low mixed venous oxygen saturation
C. Decreased Urine output
D. Both A and B

A

Ans D -

Occult hypoperfusion is a state of normal vital signs and continued hypoperfusion of GIT, muscle and skin.

This is marked by Lactic acidosis and base deficit and low mixed venous oxygen saturation.

Decreased urine output is a sign of overt hypoperfusion.

Patients with occult hypoperfusion for more than 12 hours have 2-3 times the mortality of patients with a limited duration of shock.

Resuscitation algorithms directed at correction of base deficit, lactic acidosis and Mixed Venous oxygen saturation have shown improved mortality and morbidity in high risk surgical patients.

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33
Q

All of the following are true except -

A. Acute traumatic coagulopathy is endogenous coagulopathy as a result of tissue trauma and hypovolemic shock

B. ATC is associated with 4 fold increase in mortality

C. Development of ATC can be completely avoided by rapid control of hemorrhage and adequate resuscitation.

D. ATC is an important component of Trauma induced coagulopathy

A

Ans C -

Hemorrhage leads to hypovolemic shock.

Combination of tissue trauma and shock lead to the development of Acute-Traumatic coagulopathy.
Upto 25% of trauma patients will develop this within minutes of injury.
ATC exists whenever there is combination of shock and tissue trauma.

Hypoperfusion causes activation of Thrombomodulin on the surface of endothelial cells and this combines with thrombin to induce a anti-coagulant state in Acute traumatic coagulopathy.

ATC is associated with 4 fold increase in mortality.

components of Trauma induced coagulopathy

  1. Hypovolemic shock - leading to acidemia and hypothermia due to hypoperfusion.
  2. Tissue trauma leading to fibrinolysis and inflammation
  3. Genetic factors
  4. ATC as a result of combination of tissue trauma and shock.
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34
Q

concealed hemorrhage can occur in all except -

A. chest cavity
B. Pelvis
C. Limbs
D. Cranial cavity

A

ans D -

Hemorrhage may be concealed within chest, abdomen, pelvis or in the limbs.

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35
Q

Reactionary hemorrhage usually occurs at

  1. <24 hours of surgery
  2. <48 hours of surgery
  3. <72 hours of surgery
  4. <1 week of surgery
A

ans 1.

Reactionary hemorrhage is delayed haemorrhage within 24 hours - usually due to dislodgement of a clot by resuscitation, normalisation of blood pressure and vasodilation or technical failure d/t slippage of ligature.

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36
Q

average amount of blood in a neonate is -

A. 60 mL/kg
B. 70 mL/kg
C. 80 mL/kg
D. 90 mL/kg

A

Ans C -

child and adults have 70 ml/kg
neonates have 80 ml/kg.

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37
Q

Components of damage control surgery are all except

A. Arrest hemorrhage
B. Control sepsis
C. Protect from further injury
D. Correct coagulopathy

A

Ans D -

Damage control surgery is defined by - 
arrest hemorrhage
control sepsis
protect from further injury
nothing else

Correction of coagulopathy is part of damage control resuscitation.

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38
Q

Components of damage control surgery are all except

A. Arrest hemorrhage
B. Control sepsis
C. Protect from further injury
D. Correct coagulopathy

A

Ans D -

Damage control surgery is defined by - 
arrest hemorrhage
control sepsis
protect from further injury
nothing else

Correction of coagulopathy is part of damage control resuscitation.

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39
Q

Strategies central to damage control resuscitation include all of the following except -

A. Anticipate and treat ATC
B. Permissive hypotension until hemorrhage control
C. Limit crystalloid and colloid infusion to avoid detrimental coagulopathy
D. Steroids to aid catecholamine responsiveness
E. Damage control surgery

A

Ans D -

Four central strategies of DCR are -

  • anticipate and treat ATC (Immediate release and administration of pre-defined blood products - RBCs, Plasma, platelets in ratios similar to whole blood)
  • Permissive hypotension until hemorrhage is controlled
  • Limit crystalloid and colloid infusion to avoid dilutional coagulopathy
  • Damage control surgery to control Haemorrhage and preserve physiology
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40
Q

Blood drawn from a donors is usually

A. upto 200mL
B. upto 450mL
C. upto 300mL
D. upto 500 mL

A

Ans C -

In the uk upto 450 mL of blood is drawn.

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41
Q

maximum number of blood donations allowed in a year

A. one
B. two
C. Three
D. Four

A

Ans C -

Maximum number of donations are three in a year.

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42
Q

maximum number of blood donations allowed in a year

A. one
B. two
C. Three
D. Four

A

Ans C -

Maximum number of donations are three in a year.

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43
Q 
Donated blood is mandatorily tested for A/E - 
A. HIV-1
B. HIV-2
C. HCV
D. Malaria
A

Ans D -

HIV-1, HIV-2, HCV, HBV and Syphilis.

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44
Q

leukodepletion of donated blood protects against -

A. HIV
B. HBV
C. Creutzfeldt-Jakob disease
D. Kaposi Sarcoma

A

Ans C -

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45
Q

which of the following is false ?

A. each unit of packed RBCs has a hematocrit of 50-70%.

B. Packed cells are stored in SAG-M at 2-6C

C. Shelf life of PRBC - 5 weeks

D. PRBC are more metabolically active than whole blood

A

Ans D -

Whole blood transfusion has significant advantages over packed cells -

  • it is rich in coagulation factors.
  • if fresh, it is more metabolically active than stored blood.

Packed RBC are stored in Saline-adenine-Glucose-Mannitol or SAG-M solution which provides a shelf life of 5 weeks at 2-6 C.
Usually 330 mL of PRBC with hematocrit 50-70% constitutes one unit.

Previously Citrate-phosphate-dextrose solution was used which provided a shelf life of 2-3 weeks.

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46
Q

FFP is stored at

A. - 40 C
B. - 20 C
C. - 4 C
D. 0 C

A

ans A -

FFP is rich in coagulation factors and is removed from fresh blood and stored at - 40C to - 50C with a 2 year shelf life.

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47
Q

Which of the following is false ?

A. Rhesus antigen positive FFP can be transfused to Rhesus negative individuals

B. There is no risk seroconversion with transfusion of Rh+ FFP to RH- individual

C. FFP has a shelf life of 2 years.

D. Rhesus D antigen is not present on platelets.

A

Ans B -

Rhesus D + FFP may be given to a Rhesus D - woman although it is possible for seroconversion to occur with large volumes due to the presence of red cell fragments.

FFP can be stored for upto 2 years at -40 to -50C

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48
Q

Which of the following is false

A. Cryoprecipitate is a supernatant precipitate of FFP

B. Cryoppt is rich in factor VIII

C. Cryoppt is rich in fibrinogen

D. it has a shelf life of 2 years when stored at 30C

E. Both A and B

A

Ans E -

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49
Q

Which of the following is true

A. Cryoprecipitate is a supernatant precipitate of FFP

B. Cryoppt is rich in factor VIII

C. Cryoppt is rich in fibrinogen

D. it has a shelf life of 2 years when stored at 30C

E. all of the above

A

Ans E -

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50
Q

Which of the following statements is true?

A. Platelet concentrate contain 250 x 10^9/L platelets.

B. Platelet concentrates are stored at 20-24 C on a special agitator

C. Shelf life of platelets is 5 days

D. All of the above

A

ans D -

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51
Q

Not true about Prothrombin concetrates -

A. Derived from pooled plasma

B. Contain factor II, IX, X and XIII

C. Factor VII can be included

D. indicated for emergency reversal of warfarin

A

Ans B -

Contain factor II, IX and X. Factor VII may be included or produced separately.

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52
Q

Autologous transfusion are done upto -

A. 3 weeks before the surgery
B. 2 weeks before the surgery
C. 4 weeks before the surgery
D. 1 weeks before the surgery

A

A -

Autologous transfusions can be done for upto 3 weeks before the surgery.

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53
Q

Autologous transfusion are done upto -

A. 3 weeks before the surgery
B. 2 weeks before the surgery
C. 4 weeks before the surgery
D. 1 weeks before the surgery

A

A -

Autologous transfusions can be done for upto 3 weeks before the surgery.

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54
Q

All patients below ____ level of Hb should recieve transfusion preoperatively

A. 5 mg/dL
B. 6 mg/dL
C. 7 mg/dL
D. 8 mg/dL

A

ans D -

<6 - probably will benefit from transfusion.

6-8 mg/dL - transfusion unlikely to be of benefit in the absence of bleeding or impending surgery

> 8 - no indication for transfusion in the absence of other risk factors.

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55
Q

no circulating antibodies are found in which blood group

A. AB+
B. AB-
C. O+
D. O-

A

Ans A -

AB+ is the universal recipient since it has no circulating antibodies.

O- is the universal donor since it has no antigens.

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56
Q

no circulating antibodies are found in which blood group

A. AB+
B. AB-
C. O+
D. O-

A

Ans A -

AB+ is the universal recipient since it has no circulating antibodies.

O- is the universal donor since it has no antigens.

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57
Q

what percentage of the normal circulating platelets can be sequestered in the spleen -

A. 10%
B. 20%
C. 30%
D. 40%

A

Ans C.

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58
Q

average life span of platelets -

A. 5-7 days
B. 7-10 days
C. 10-14 days
D. 15-20 days

A

Ans B.

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59
Q

Which of the following is true -
A. vWF is present in the sub-endothelial layers and exposed during injury

B. vWF binds to gp I/IX/V on the platelet.

C. binding of vWF to platelets initiates the release reaction which recruits other platelets into primary hemostasis

D. heparin does not interfere with this reaction.

E. All of the above

A

Ans E

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60
Q

Principal mediator of platelet aggregation -

A. Adenosine diphosphate
B. Serotonin
C. PGI2
D. Both a and b

A

Ans D -

Principal mediator of platelet aggregation is ADP and Serotonin.
TxA2 is also increases platelet aggregation.

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61
Q

which of the following statements is false -

A. Platelets aggregation is a reversible process.

B. Platelet aggregation is not associated with secretion

C. Platelets are irreversibly inhibited by NSAID

D. COX2 inhibitors do not affect platelet

A

Ans C -

Platelet aggregation is a reversible process and not associated with secretion.

Arachidonic acid released from platelets is converted by COX-1 to PGG2 which in turn is converted to PGH2 and finally TxA2. AA may also shuttled to adjacent endothelial cells and converted to prostacyclin (PGI2) which is a vasodilator and acts to inhibit platelet aggregation.

Platelet COX-1 is irreversibly inhibited by Aspirin, and reversibly inhibited by NSAID but it is not affected by COX-2 inhibitors.

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62
Q

which of the following statements is false -

A. Platelets aggregation is a reversible process.

B. Platelet aggregation is not associated with secretion

C. Platelets are irreversibly inhibited by NSAID

D. COX2 inhibitors do not affect platelet

A

Ans C -

Platelet aggregation is a reversible process and not associated with secretion.

Arachidonic acid released from platelets is converted by COX-1 to PGG2 which in turn is converted to PGH2 and finally TxA2. AA may also shuttled to adjacent endothelial cells and converted to prostacyclin (PGI2) which is a vasodilator and acts to inhibit platelet aggregation.

Platelet COX-1 is irreversibly inhibited by Aspirin, and reversibly inhibited by NSAID but it is not affected by COX-2 inhibitors.

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63
Q

Platelet release reaction - all are true except

A. Fibrinogen is required cofactor

B. Fibrinogen acts as a bridge to connect Gp IIb/IIIa receptors of two activated platelets.

C. ADP, Calcium, TxA2, Serotonin and alpha-granule proteins are released.

D. formation of the platelet plug as a result of the platelet release reaction is a reversible process

A

Ans D -

platelet plug formation as a result of compaction of platelets following the release reaction is an irreversible process.

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64
Q

All of the following are present in the alpha granules of platelets except -

A. Thrombospondin
B. Platelet Factor 4
C. Alpha thromboglobulin
D. TxA2

A

Ans D -

Thrombospondin - stabilises fibrinogen binding to activated platelets surface and strengthens the platelet-platelet interaction.

Platelet Factor 4 - potent heparin antagonist.

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65
Q

Which of the following are inhibitors of second wave of platelet aggregation except -

A. Nitric oxide
B. cAMP
C. Aspirin
D. Heparin
E. NSAIDS
A

Ans D -

The second wave of platelet aggregation is inhibited by

  • aspirin
  • NSAID
  • cAMP
  • NO
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66
Q

Intrinsic Pathway begins with the activation of -

A. Factor XI
B. Factor XII
C. Factor VIII
D. Factor IX

A

Ans B -

intrinsic pathway begins with the activation of factor XII which activates Factor XI, IX and VIII in that order.

In this pathway each of the primary factors are intrinsic to the plasma and therefore no surface is required.

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67
Q

Extrinsic pathway begins with

A. Release of Tissue factor
B. Activation of factor VII
C. Activation of factor X
D. None of the above

A

Ans A - extrinsic pathway begins with the release of tissue factor by vascular injury. Tissue factor is also present on the exposed surface of the endothelium.

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68
Q

Extrinsic pathway begins with

A. Release of Tissue factor
B. Activation of factor VII
C. Activation of factor X
D. None of the above

A

Ans A - extrinsic pathway begins with the release of tissue factor by vascular injury. Tissue factor is also present on the exposed surface of the endothelium.

TF binds to VIIa and forms a complex. This complex activates Factor X to Xa.
This complex is 4x more potent at converting factor X to Xa than Factor VIIa alone.

TF-VIIa also activates factor IX to IXa.

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69
Q

which of the following factors in involved in cross-linking of fibrin monomers into polymers -

A. Factor IX
B. Factor XIII
C. Factor XII
D. Calcium

A

Ans B - factor XIII or Hagemann factor is involved in the cross-linking of fibrin monomers into the polymers.

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70
Q

which of the following factors in involved in cross-linking of fibrin monomers into polymers -

A. Factor IX
B. Factor XIII
C. Factor XII
D. Calcium

A

Ans B - factor XIII or Hagemann factor is involved in the cross-linking of fibrin monomers into the polymers.

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71
Q

abnormal elevation of aPTT is linked with dysfunction of all of the following except -

A. Factor IX
B. Factor XI
C. Factor X
D. Factor VII

A

Ans D

aPTT is associated with abnormal function of the intrinsic arm of the cascade i.e. factor II, IX, X, XI, XII

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72
Q

abnormal elevation of the Prothrombin Time is associated with dysfunction of all of the following except -

A. Factor X
B. Factor VIII
C. Factor II
D. Factor VII

A

Ans B

PT is associated with the extrinsic arm of the cascade - i.e. factor II, X and VII.

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73
Q

Vitamin K deficiency or warfarin use is associated with the depletion of all of the following except -

A. Factor II
B. Factor VII
C. Factor IX
D. Facrtor VIII

A

ans D -

Vitamin K deficiency or warfarin use affects factor 2, 7, 9 and 10.

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74
Q

Prothrombinase complex is formed by all of the following except -

A. Factor Xa
B. Factor Va
C. Calcium
D. Factor VIIIa

A

Ans D -

Factor Xa + Va + calcium + phospholipid form the prothrombinase complex - converts Factor II to IIa.

This prothrombinase complex is significantly more active at converting prothrombin to thrombin than factor Xa alone.

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75
Q

Thrombin activates all of the following except -

A. Factor V
B. Factor VII
C. Factor VIII
D. Factor IX
E. Factor XIII
F. Factor X
A

ans F -

thrombin is involved in conversion of fibrinogen to fibrin and the activation of

  • factor 5
  • factor 7
  • factor 8
  • factor 9
  • factor 13
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76
Q

Intrinsic factor complex is formed by -

A. Factor IXa
B. Factor VIIIa
C. Factor VIIa
D. Both A and B

A

ans D -

Intrinsic factor complex is formed by Factor IXa-VIIIa.

Factor IXa - responsible for the bulk of conversion of Factor X to Xa.

Whereas the intrinsic factor complex is upto 50x more effective than the extrinsic complex (TF-VIIa) at converting Factor X to Xa.

Intrinsic factor complex is 5x-6x more effective at converting Factor X to Xa than Factor IXa alone.

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77
Q 
Bulk of the conversion of Factor X to Xa is done by - 
A. Factor IXa
B. Extrinsic complex
C. Intrinsic factor complex
D. VIIa
A

Ans A -

Factor IXa is responsible for the bulk of conversion of Factor X to Xa.

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78
Q

Most potent activator of factor X to Factor Xa -

A. Factor IXa
B. Extrinsic complex
C. Intrinsic factor complex
D. VIIa

A

Ans C -

Intrinsic factor complex (IXa-VIIIa) is the 50x times more potent than extrinsic complex (TF-VIIa) at converting factor X to Xa.

Intrinsic factor complex IXa-VIIIa - is 5-6x times more effective than factor IXa alone.

Extrinsic factor complex (TF-VIIa) is 4x times more effective at converting Factor X to Factor Xa than VIIa alone.

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79
Q

Thrombin cleaves fibrinogen into all of the following except

A. Fibrinopeptide A
B. Fibrinopeptide B
C. Fibrinopeptide C
D. Fibrin

A

Ans C -

Thrombin breaks fibrinogen into

  • Fibrin
  • Fibrinopeptide A
  • Fibrinopeptide B

Removal of Fibrinopeptide A - allows end-to-end polymerisation of fibrin.

Removal of Fibrinopeptide B - allows side to side polymerisation of fibrin.

The removal of these fibrinopeptides is done by Thrombin Activable Fibrinolysis Inhibitor (TAFI)

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80
Q

Which of the following is referred to as the Thrombin sink ?

A. Protein C
B. Protein S
C. Thrombomodulin
D. Tissue plasminogen Activator

A

Ans C -

Thrombomodulin presented by endothelium serves as a “thrombin sink” by forming complex with thrombin rendering it no longer available to cleave fibrinogen.

This complex of thrombomodulin and thrombin, also activates protein C.

Notably, thrombin-thrombomodulin complex also activates TAFI - which increases the polymerisation of fibrin and therefore Thrombin-TM complex has a mixed effect on clot stability.

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81
Q

Activated protein C acts by inhibition of

A. Factor V
B. Factor IX
C. Factor VIII
D. Plasminogen activator inhibitor-1
E. A, C and D
A

Ans E -

Activated protein C reduces further thrombin generation by inhibiting factor V and VIII.

Activated protein C also consumes the Plasminogen activator inhibitor-1 (PAI-1) which leads to increased activity of tissue plasminogen activator (tPA)

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82
Q

Tissue plasminogen activator - all are true except -

A. Released from the endothelium following injury
B. Cleaves plasminogen to initiate fibrinolysis
C. tPA is a non-selective plasminogen activator
D. Plasmin is a serine protease

A

Ans C -

tPA is released from endothelium and other cells of the vascular wall and it is the main circulating form of this family of enzymes.

It cleaves plasminogen into plasmin and initiates fibrinolysis.

Plasmin is a serine protease derived from plasminogen.

tPA is selective for fibrin-bound plasminogen, so that endogenous fibrinolytic activity occurs predominately at the site of clot formation.

tPA and plasminogen bind to fibrin as it forms and this trimolecular complex cleaves fibrin very efficiently.

Urokinase plasminogen activator - produced by the urothelium - not selective for fibrin bound plasminogen.

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83
Q

TAFI -
Thrombin Activable Fibrinolysis inhibitor -

  • activated by thrombin-thrombomodulin complex
  • inhibits fibrinolysis directly
  • removes the fibrinopeptide A and B from the fibrin and therefore allows end-to-end and side-to-side polymerisation of fibrin.
  • the removal of lysine on the fibrin molecule by TAFI renders the clot more susceptible to lysis by plasmin.
  • the removal of the lysine residues however also renders binding of plasminogen less likely.
A

nothing.

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84
Q

the most potent mechanism for thrombin inhibition -

A. Thrombomodulin
B. Activated Protein C
C. tPA
D. PAI-1

A

ans B -

the most potent mechanism for thrombin inhibition involves the activated protein C system.

APC forms a complex with its co-factor Protein S on a phospholipid surface.

This complex of APC-Protein S then cleaves the factor Va and Factor VIIIa so that they are no longer able to form extrinsic complex and the prothrombinase complex.

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85
Q

Factor V leiden mutation lead to -

A. deficiency of Factor Va
B. resistance of factor Va to cleavage by APC.
C. Inability of Factor Va to form prothrombinase complex with factor Xa.
D. Increased ability of factor Va to bind Factor Xa leading.

A

ans B -

Factor V leiden mutation renders factor V resistant to cleavage by APC, thereby remaining active as a pro-coagulant.
Patients are predisposed to venous thromboembolism.

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86
Q

Which of the following is false

A. Plasmin degrades the fibrin mesh at various places leading to production of FDPs.

B. FDPs are cleared by kidneys and liver.

C. kallikrien is cleaved into bradykinin by kininogen

D. bradykinin enhances the release of tPA

A

Ans C -

Bradykinin - potent endothelial dependent vasodilator.

Bradykinin cleaved from the high-molecular weight kininogen.

Cleavage of kininogen done by Kallikrien.

Bradykinin enhances the release of tPA.

87
Q

Plasmin is inhibited by -

A. alpha-2 antiplasmin
B. circulating tPA
C. Circulating urokinase
D. all of the above

A

Ans D -

Fibrinolysis is kept in check by several mechanisms -

  1. tPA activates plasminogen more efficiently when it is bound to fibrin, so that plasmin is formed selectively on the clot.
  2. Plasmin is inhibited by alpha-2 aniplasmin which is a protein cross linked to fibrin by factor XIII - this ensures that clot lysis does not occur too quickly
  3. circulating plasmin is also inhibited by alpha-2 antiplasmin and circulating tPA and Urokinase.
88
Q

true regarding FDP are all except =

A. FDP include E-nodules and D dimers.

B. smaller fragments interfere with normal platelet aggregation

C. larger fragments are incorporated into the clot in lieu of normal fibrin monomers.

D. None of the above

A

D =

Clot lysis by plasmin yields FDPs including E nodules and D dimers.

Smaller fragments interfere with platelet aggregation.

Larger fragments are incorporated into the clot instead of fibrin monomers and result in unstable clot - this is seen in severe coagulopathy such as hyperfibrinolysis seen with Trauma induced coagulopathy and DIC.

the presence of D dimers in circulation is a marker of thrombosis or significant activation of fibrinolytic system.

89
Q

Three most common coagulation factor deficiencies include all except -

A. Factor VIII
B. Factor IX
C. Factor X
D. Factor XI

A

Ans C -

the three most frequent coagulation factor deficiencies are

  1. Factor VIII (Hemophilia A and vW disease)
  2. Factor IX (Hemophilia B or Christmas disease)
  3. Factor XI deficiency.
90
Q

All of the following are true regarding Hemophilia A and B

A. Sex linked recessive disease
B. Almost exclusive in males.
C. Severe disease is levels <5% in plasma
D. severe disease have spontaneous bleeds into joints

A

Ans C -

Hemophilia A (Factor VIII) and Hemopilia B (Factor IX) are sex linked recessive disorders - almost exclusively seen in males.

Clinical severity depends on measurable levels of factor VIII and Factor IX respectively.

Severe disease <1%
Moderate disease 1-5%
Mild disease 1-30%.

Patients with severe hemophilia have spontaneous bleeds into the joints - crippling arthropathies, intracranial bleeds, intramuscular hematomas, retroperitoneal hematomas, GI/GU/Retropharyngeal bleeds.

Patients with moderate disease - less spontaneous bleed but likely to bleed severely after trauma and surgery.

Mild disease - no spontaneous bleed, minor bleeding after trauma or surgery.

these patients have a normal platelet response with platelet activation and formation of the platelet plug.

91
Q

Treatment of choice for Hemophilia A in a newly diagnosed patient -

A. Factor VIII concentrate
B. Recombinant factor VIII
C. Cryoppt
D. FFP

A

Ans B -

Patients with Hemophilia A and B are treated with factor VIII or IX concentrates.

Recominant Factor VIII is strongly recommended for patients who are both HIV and HCV seronegative.

Similarly for Hemophilia B the recommended products are recombinant factor IX or high purity factor IX.

92
Q

Recommended levels of activity of factor VIII in hemophilia A patients with severe bleeding.

A. 10-20%
B. 30-40%
C. 50%
D. 80-100%

A

Ans C -

Activity levels should be restored to

  • 30-40% - for mild hemorrhage
  • 50% for severe hemorrhage
  • 80-100% for life threatening hemorrhage.
93
Q

Alternative treatment options for hemophilia A patients with high titres of inhibitors of FVIII
are all except

A. High dose of recombinant Factor VIII
B. Recombinant Factor VIIa
C. Porcine Factor VIII
D. prothrombin-complex concentrates. 
E. activated prothrombin complex concentrates.
A

Ans A -

upto 20% of hemophiliacs with factor VIII deficiency develop inhibitors that can neutralize factor VIII.

Low titres - higher doses of Factor VIII

High titres - Porcine Factor VIII, Prothrombin complex concentrates, activated prothrombin complex concentrates, recombinant factor VIIa.

94
Q

which of the following is the most common congenital bleeding disorder -

A. Hemophilia A
B. Von-Wildebrand disease
C. Hemophilia B
D. Factor XI deficiency

A

ans B -

Von Willebrand’s disease or vWD is the most common congenital bleeding disorder.

95
Q

vWF all are true except -

A. large glycoprotein
B. carries factor VIII
C. responsible for platelet adhesion
D. only quantitative defects lead to vWD

A

ans D -

vWF is a large glycoprotein responsible for carrying factor VIII and platelet adhesion.

Platelet adhesion is important for normal platelet adhesion to exposed sub-endothelium and for aggregation under high shear stress conditions.

96
Q

All of the following are true regarding vWD except -

A. Sponatneous bleeds into the joint, retroperitoneum etc.

B. type I is a partial quantitative defect.

C. Type II is a qualitative defect

D. Type III requires vWD concentrates.

E. Type I responds well to desmopressin

A

Ans A -

Bleeding in vWD is similar to platelet disorders - i.e. easy bruising and mucosal bleeding. Mennorrhagia is common.

Type I - partial qualitative defect - usually responds to DDAVP or desmopression

Type II - qualitative defect - depending on the particular defect it may respond to DDAVP.

Type III - total deficiency - do not respond to DDAVP and therefore require vWF concentrates.

97
Q

Hemophilia C is deficiency of

A. Factor VII
B. Factor V
C. Factor XIII
D. Factor XI

A

ans D -

Factor XI deficiency is sometimes called Hemophilia C.

98
Q

All of the following are sex linked recessive disorders except -

A. Hemophilia A
B. Hemophilia B
C. Hemophilia C
D. Duchene muscular dystrophy
E. Red Green color blindness
A

Ans C - hemophilia C - factor XI deficiency is a autosomal recessive inherited disorder.

99
Q

All of the following are false regarding Factor XI deficiency except -

A. Autosomal dominant
B. Spontaneous bleeding is common
C. FFP is treatment of choice.
D. 1mL of plasma usually contains 10U of Factor XI

A

ans C -

Factor XI deficiency is a autosomal recessive inherited condition.

Spontaneus bleeding is rare.

Bleeding may occur after surgery, trauma or invasive procedures.

Treatment of patients with Factor XI deficiency who present with bleeding is FFP.

Patients who present with mennorrhagia can be given anti-fibrinolytics (Tranexamic acid)

Each mL of plasma contains 1U of Factor XI.

Factor VIIa is recommended for treatment for patients with anti-factor XI antibodies.

There is interest in factor XI inhibitors are anti-thrombotic agents - since patients with factor XI deficiency usually have only mild bleeding risk and at the same time they are protected from thrombosis.

100
Q

All of the following are autosomal recessive inheritance except -

A. Factor II deficiency
B. Factor X deficiency
C. Factor V deficiency
D. Factor XI deficiency
E. Factor VIII deficiency
A

Ans E -

Factor II, V and X are rare coagulation defects with autosomal recessive inheritance.

Factor XI also has a autosomal recessive inheritance.

Factor VIII or hemophilia A has a sex linked recessive inheritance.

101
Q

All of the following are true except -

A. Factor II has a half life of 72 hours.

B. only 25% of normal plasma activity of factor II is needed for hemostasis.

C. one mL of FFP contains one unit each of factor II, V and X.

D. Weekly infusion of FFP are used for treatment of bleeding in Factor V deficiency

A

Ans D -

Significant bleeding occurs in factor II, V and X deficiencies with levels less than 1% of normal activity.

Bleeding with any of these deficiencies is treated by FFP

one mL of FFP contains one unit of activity of factor II, V, X and XI

Half life of prothrombin (Factor II) is long approximately 72 hours.
About 25% of a normal level is needed for hemostasis.

Factor V is inherently unstable and daily infusion of FFP is needed to treat bleeding in factor V deficiency with a goal of 20-25% activity.

Prothrombin complex concentrates can be used to treat deficiencies of prothrombin or factor X.

102
Q

Factor V deficiency is often co-inherited with deficiency of factor -

A. VIII
B. X
C. II
D. VII

A

Ans A -

Factor V deficiency may be coinherited with factor VIII deficiency.

Treatment of such individuals - Factor VIII + FFP

Some patients with factor V deficiency also lack the factor V normally present in platelets and may need platelet transfusion as well as FFP.

103
Q

Bleeding in factor VII deficiency usually occurs at -

A. <1%
B. <3%
C. <5%
D. <10%

A

ans B

Bleeding is uncommon unless the levels is less than 3%.

104
Q

All of the following are true regarding factor VII deficiency except -

A. Autosomal recessive disorder

B. Bleeding correlates with levels of Factor VII in plasma

C. Half life of rFVIIa is 2 hours

D. Half life of Factor VIIa in FFP is 4 hours.

E. most common bleeding is easy bruising and mucosal bleeding especially epistaxis

A

Ans B -

Autosomal recessive disorder.

Clinical bleeding can vary widely and does not always correlate with level of Factor VII coagulant activity in plasma.

Bleeding is uncommon unless levels is less than 3%.

Most common manifestation is easy bruising, mucosal bleeding especially epistaxis

Post operative bleeding is also common - 30% of procedures.

105
Q

Factor XIII deficiency all are true except -

A. Autosomal recessive condition

B. Acquired in case of IBD, myeloid leukemia and liver failure.

C. Atleast 20-25% of the normal activity level must be attained for homeostasis

D. Clots form normally

A

Ans C -

Congenital factor XIII deficiency is autosomal recessive condition.

Acquire condition occurs in -

  • liver failure
  • IBD
  • Myeloid Leukemia

Bleeding is typically delayed since the clot forms normally but it is susceptible to fibrinolysis.

Spontaneous abortions are common in women with factor XIII deficiency unless they recieve replacement therapy.

Umbilical stump bleeding is also a characteristic feature.

Replacement can be done using -

  • FFP
  • Cryppt
  • Factor XIII concentrate.

Level 1-2% of the normal are adequate for homeostasis.

106
Q

Glanzmann thrombasthenia is a defect in function of . -

A. Gp I/IX/V
B. Gp IIa/IIIb
C. Gp IIb/IIIa
D. Gp Ia/IIb

A

Ans C -

Glanzmann thrombasthenia is a autosomal recessive disease in which platelet glycoprotein IIb/IIIa complex is either lacking or present but dysfunctional.

Treatment is with platelet transfusion.

while gp I/IX/V is involved in adhesion of platelets via the vWF to the exposed sub-endothelium.

gp IIb/IIIa is involved in adhesion of the platelets to other platelets via a fibrinogen bridge.

107
Q

Bernard soulier syndrome is caused by a defect in the -

A. Gp Ia/IX/V
B. Gp Ib/IX/V
C. Gp IIb/IIIa
D. Gp IIa/IIIb

A

ans B -

Bernard Soulier syndrome is caused by a defect in the gp Ib/IX/V receptor for vWF which is necessary for the platelet adhesion to the sub-endothelium.

Rx - platelet transfusion.

108
Q

Dense granule deficiency is associated with -

A. Bernard Soulier syndrome
B. Glanzmann thrombasthenia
C. Hermansky Pudlak syndrome
D. Hemophilia B

A

Ans C -

Dense granules deficiency is the most prevalent intrinsic platelet defect or storage pool disease. Dense granules contain - ADP, ATP, Calcium and Inorganic phosphate.

It is associated with partial albinism in Hermansky-Pudlak syndrome.

Bleeding is variable depending on the severity of granule defect due to the decrease in release of ADP.

Mild cases - DDAVP : DDAVP increases the levels of vWF in the plasma and this may somewhat compensate for the lack of dense granules.

109
Q

All of the following represent a failure of production of platelets except -

A. Leukemia
B. Vitamin B12 deficiency
C. Acute Alcohol intoxication
D. Secondary thrombocytopenia

A

Ans D -

Failure of production of platelets are seen due to impairment of the bone marrow function.

  • leukemia
  • Myeloproliferative disorder
  • B12 or folate deficiency
  • Chemotherapy or radiation therapy
  • Acute alcohol intoxication
  • Viral infections.
110
Q

All of the following are related to immune mediated destruction of platelets except -

A. ITP
B. Heparin Induced Thrombocytopenia
C. B-cell malignancies
D. Hemolytic Uremic syndrome

A

Ans D -

Immune mediated destruction of platelets is seen in -

  • Idiopathic thrombocytopenia
  • Heparin induced thrombocytopenia
  • Autoimmune disoders.
  • B cell malignancies
  • Secondary thrombocytopenia

Decreased survival of platelets is also seen in DIC, and thrombi related consumption of platelets is seen in TTP, HUS.

111
Q

Secondary immune thrombocytopenia - all are true except -

A. Platelet counts are usually only mildly decreased.

B. Large platelets can be seen on peripheral smear.

C. Initial treatment with steroids and IVIG.

D. common manifestations are petechiae, purpura and epistaxis

A

Ans A -

Secondary immune thrombocytopenia usually associated with other autoimmune disorders or low grade B cell malignancies, or HIV, drug, etc.

Platelet counts are very low.

Petechiae, purpura and epistaxis are common.
CNS bleeding can occur.

Large platelets are seen on peripheral smear.

Initial treatment . -

  • steroids
  • IVIG
  • Anti-D immunoglobulin in patients who are Rh+

IVIG and Anti-D Ig are rapid acting.

Platelet transfusions - in case of CNS bleed or active bleed from other sites.

112
Q

Primary ITP all are true except -

A. In children it is usually chronic and has no identifiable cause.

B. Impaired platelet function is seen

C. T cell mediated destruction of platelets.

D. First line treatment is IVIG, Anti-D immunoglobulin, Corticosteroids

A

Ans A -

Primary ITP
- usually acute in children often following a viral illness.

  • usually chronic in adults with no identifiable cause.
  • Both Impaired platelet function as well as T cell mediated destruction are seen.

Management -
1. First line - Corticosteroids (Majority respond), IVIG and Anti-D (For clinical bleeding.

  1. in case of drug induced - only withdrawal of drug may be needed. But First line measures can quicken the recovery.
  2. Second line - require in most patients -
    - Splenectomy (Severe thrombocytopenia, high risk of bleeding, continued need for steroids)
    - Rituximab (anti-CD20 monoclonal antibody)
    - Thrombopoeitin (TPO) receptor agonists such as Romiplostim, eltrombopag.
  3. Third line - after failure of splenectomy and rituximab
    - Romiplostim
    - immunosupressants.
113
Q

Heparin induced thrombocytopenia -
All are true except -

A. antibodies against Platelet Factor 4.

B. intravascular thrombosis and thrombocytopenia occur

C. Counts fall within 48 hours of first exposure

D. can occur with prophylactic doses.

A

Ans C -

Heparin induced thrombocytopenia - it is a type of drug induced thrombocytopenia.

Antibodies formed against PF4 affect platelet activation and endothelial function with resultant thrombocytopenia and intravascular thrombosis.

Platelet counts fall start after 5-7 days after heparin has been started - but if it is a re-exposure the decrease in count may occur within 1-2 days.

Suspect HIT if - counts < 1lac or drop by more than 50% from baseline.

HIT is more common in full dose UFH (1-3%), it can also occur with prophylactic doses and LMWH.

17% patients receiving UFH and 8% receiving LMWH develop antibodies against PF4, but very few develop clinical HIT.

The characteristic feature is the high incidence of thrombosis.

114
Q

All of the following are false regarding HIT except -

A. A negative serotonin release assay excludes HIT

B. A positive ELISA confirms the diagnosis of HIT

C. Once HIT diagnosed, UFH stopped and LMWH started.

D. All of the above

A

Ans D -

Serotonin release assay - has a very high specificity and very low sensitivity and therefore,

  • Positive SRA confirms HIT
  • Negative SRA does not rule out HIT

ELISA for PF4 Ab - very high sensitivity but not very specific.

  • positive ELISA does not confirm HIT
  • negative ELISA essentially rules out HIT.

Once HIT is suspected, UFH and LMWH stopped.
Patients should be placed on
- adequate renal function - Lepirudin, Danaparoid, Argatroban
- poor renal function - Argatrobran.

And eventually shifted to Warfarin.

115
Q

ADAMtS13 inhibition leads to which of the following -

A. ITP
B. TTP
C. HUS
D. HIT

A

Ans B -

Thrombotic thrombocytopenic purpura - is a condition in which thrombocytopenia results from the activation of platelets and formation of platelet thrombi.

Large vWF molecules which are normally supposed to be cleaved by ADAMtS13 are allowed to interact with platelets and cause their activation.

116
Q

TTP is associated with all of the following except -

A. Micro-angiopathic hemolytic anemia

B. Shcistocytes on peripheral smear

C. Rituximab is drug of choice in acute setting for management of acquired TTP.

D. Neurologic and renal signs and symptoms are common.

A

Ans C -

Thrombotic thrombocytopenic purpura is related to activation and platelets and formation of thrombi - which eventually leads to Microangiopathic Hemolytic Anemia - and this hemolysis also leads to renal failure. Whereas thrombosis leads to neurologic signs and symptoms.

Plasma exchange and FFP is used for treatment of choice in acute setting.

However in case of Acquired TTP of autoimmune origin, immunomodulatory treatment can be given with Rituximab (Anti-CD20).

117
Q

which of the following is related to the development of HUS

A. Salmonella
B. E.Coli O157:H7
C. Pasteurella
D. Klebsiella

A

Ans B -

Hemolytic uremic syndrome often occurs secondary to infection by E. Coli O157:H7 or other Shiga-toxin producing bacteria.
The metalloproteinase is normal in these cases.

118
Q

most common abnormality of hemostasis that causes bleeding in surgical patients

A. Hepatic Failure
B. Hemophilia
C. Thrombocytopenia
D. Uremia

A

Ans C -

Thrombocytopenia is the most common abnormality of hemostasis that results in bleeding in the surgical patient.

119
Q

Which of the following condition is not associated with a reduced number megakaryocytes with thrombocytopenia

A. Cytotoxic therapy
B. Secondary Thrombocytopenia
C. Leukemia
D. Uremia

A

Ans B -

When thrombocytopenia occurs in patients with leukemia/uremia/cytotoxic therapy there are generally reduced number of megakaryocytes in the marrow.

120
Q

Major surgery can be taken up with platelets counts more than -

A. 100,000 /uL
B. 50,000/uL
C. 30,000/uL
D. 20,000/uL

A

Ans B -

When thrombocytopenia is present in a patient for whom an elective operation is being considered, management is contingent upon the extent and cause of platelet reduction - A count of more than 50,000/uL generally requires no specific therapy.

121
Q

One unit of platelet concentrate is expected to increase the platelet counts of a 70 kg man by

A. 5000/uL
B. 10,000/uL
C. 15000/uL
D. 20000/uL

A

Ans B -

One unit of platelet concentrate contains approximately 5.5 x 10^10 platelets and this would be expected to increase the platelet counts of a 70 kg man by 10,000/uL

effectiveness is reduced by -

  • fever
  • Hepatosplenomegaly
  • antiplatelet Ab
  • infection

in patients refractory to standard platelet transfusions - the use of HLA-compatible Platelets couped with special processors has proven effective.

122
Q

All of the following are associated with qualitative defects in platelet function except

A. Sarcoidosis
B. Massive transfusion
C. Uremia
D. Polycythemia Vera

A

Ans A -

Sarcoidosis leads to a quantitative defect in platelet function by causing hypersplenism.

Qualitative defect in platelet function -

  • Massive transfusions leads to impairment of ADP stimulated aggregation.
  • Uremia - impaired aggregation.
  • Polycythemia vera
  • thrombocythemia
  • myelofibrosis

Platelet dysfunction of uremia can be corrected by dialysis and administration of DDAVP.
Platelet transfusion is of no use.

Monoclonal gammopathies - treatment with chemotherapy or plasmapheresis.

123
Q

All of the following are correctly matched except -

A. Aspirin - irreversible acetylation of platelet PG synthase.

B. Clopidogrel irreversible inhibition of ADP induced platelet aggregation.

C. Abciximab - Gp IIb/IIIa inhibitor

D. Prasugrel - Gp IIb/IIIa inhibitor

A

Ans D -

Aspirin - irreversible acetylation of platelet prostaglandin synthase.

Clopidogrel, Prasugrel
irreversible inhibition of ADP induced platelet aggregation.

Abciximab, Tirofiban, Roxifiban, Orbofiban, eptifibatide - gp IIb/IIIa inhibitors.

Tirofiban is derived by alteration of a chemical derived from saw Scaled Viper.

124
Q

Diagnosis of DIC depends on all of the following except -

A. Inciting etiology with thrombocytopenia

B. Low fibrinogen levels

C. Raised D-Dimer and FDPs

D. Prolongation of PT

E. All of the above

A

Ans E -

DIC - can be caused by -

  • Embolisation of brain matter, marrow or amiotic fluid.
  • Severe pancreatitis
  • liver failure
  • malignancy
  • snake bites
  • transfusion reactions
  • sepsis.

Activated protein C is effective in septic patients with DIC.

Diagnosis is based on -

presence of inciting etiology with thrombocytopenia, raised PT, raised D-Dimer and Low fibrinogen.

125
Q

Main stay of treatment of DIC is -

A. Treatment of the primary etiology
B. Heparin
C. FFP
D. Cryoppt with platelets

A

Ans A -

Most important aspect of treatment of DIC - relieving the primary medical or surgical problems.

If there is active bleeding, hemostatic factors should be replaced with FFP.

Heparin therapy has not been found to be useful in treatment of acute forms of DIC, however it may be used in cases where thrombosis predominates and severe purpura fulminans.

126
Q

All of the following are synthesized by liver except -

A. Plasminogen
B. Protein C
C. Protein S
D. vWF

A

Ans D -

Factors synthesized by liver

Vitamin K dependent (2,7,9,10)
Fibrinogen (Factor I)
Factor V
Factor VIII
Factor XI, XII, XIII
Antithrombin III
Plasminogen
Protein C and Protein S.
127
Q

Patients with impaired liver functions are at -

A. Increased risk of thrombosis
B. Increased risk of bleeding
C. Increased risk of platelet dysfunction
D. All of the above

A

Ans D -

Liver produces both non-endothelial cell derived procoagulants and anticoagulants.

Therefore these patients are at an increased risk of both bleeding and thrombosis.

Thrombocytopenia in liver disease is mediated by three mechanisms -

  • Hypersplenism
  • Decreased production of thrombopoeitin
  • immune mediated thrombocytopenia especially in PBC, HCV.
128
Q

What percentage of patients have trauma induced coagulopathy at the time of admission -

A. 15%
B. 25%
C. 30%
D. 40%

A

ans C -

one third of injured patients have evidence of coagulopathy at the time of admission.

These patients are at significantly higher risk of mortality especially in the first 24 hours after the injury.

129
Q

all of the following are true regarding Antiphospholipid Syndrome

A. ALPS includes the lupus anti-coagulant and anti-cardiolipin antibodies.

B. ALPS is associated with increased risk of venous and arterial thrombosis

C. ALPS can be seen in Systemic lupus, RA, Sjogren’s syndrome.

D. aPTT is essentially normal in these patients.

A

Ans D -

ALPS includes the lupus anticoagulant and anti-cardiolipin antibodies.

These antibodies can induce both arterial and venous thrombosis.

ALPS is very common in SLE. 
Can also be seen in - 
 - RA
 - Sjogren's syndrome
 - Transiently after infection or drug induced.

Hallmark of ALPS is prolonged aPTT in vitro and increased risk of thrombosis in vivo.

130
Q

Which of the following drugs is associated with increased effect of warfarin requiring dose reduction -

A. Barbiturates
B. OCPs
C. Anabolic steroids
D. Corticosteroids
E. ACTH
A

Ans C -

Warfarin effect is decreased by the following -

  • Barbiturates
  • OCP
  • Corticosteroids
  • ACTH

Warfarin effect is increased by the following

  • Phenylbutazone
  • Clofibrate
  • Anabolic steroids
  • Quinidine
  • amiodarone
  • Glucagon
  • Cephalosporin
131
Q

An elderly patient who was on warfarin develops intracranial hemorrhage. Best option for rapid reversal is

A. Vitamin K
B. FFP
C. Cryoppt
D. Prothrombin complex concentrate

A

Ans D -

There are several reversal options for Warfarin induced coagulopathy

Vitamin K
Plasma
Cryoppt
rFVIIa
Prothrombin complex concentrate

Urgent reversal for life threatening bleeding should include Vitamin K and rapid reversal agent such as plasma or prothrombin complex concentrate

In the elderly or those with intra-cranial hemorrhage concentrates are preferred.

In situations with hypovolemia from hemorrhage plasma should be used.

132
Q

Effect of Dabigatran can be measured using -

A. PT
B. ecarin clotting time
C. activated clotting time 
D. anti-factor Xa assays
E. Both B and C
A

ans B and C -

Activated clotting time (Alone or with rapid Thromboelastography) or ecarin clotting time can be obtained in those on dabigatran.

Anti-Xa assays can be used for patients on rivaroxaban.

133
Q

Method of rapid reversal of Dabigatran

A. FFP
B. Vitamin K with FFP
C. Emergent dialysis
D. Prothrombin complex concentrates

A

Ans C -
The only possible strategy to reverse the effect of dabigatran may be emergent dialysis. But very difficult to achieve this in a unstable bleeding patient.

134
Q

Reversal of rivaroxaban may be possible by the use of

A. FFP
B. prothrombin complex concentrates
C. Cryoppt
D. Platelet

A

Ans B -

Four factor complex concentrates containing Factor II, VII, IX and X can reverse the effect of rivaroxaban.

135
Q

Rivaroxaban and Dabigatran can be stopped how many days before surgery to avoid the risk of bleeding

A. 1 day
B. 2 days
C. 5 days
D. 7 days

A

ans B -

Dabigatran and Rivaroxaban can be stopped for 36-48 hours before surgery without increased risk of bleeding in those with normal renal function.

136
Q

reversal of anti-coagulation may not be necessary in patient on heparin with aPTT below

A. 1.5
B. 1.4
C. 1.3
D. 1.2

A

ans C -

aPTT less than 1.3 times control in a heparinized patient and INR less than 1.5 times in a patient on warfarin - reversal of anti-coagulation may not be necessary.

137
Q

prothrombin level considered safe for surgery -

A. 20%
B. 30%
C. 40%
D. 50%

A

ans D -

in a patient receiving coumarin derivative therapy the drug can be discontinued several days before the operation and the prothrombin concentration checked, a level >50% is considered safe.

138
Q

Patient who are on anti-coagulation can undergo

A. Elective Eye Surgery
B. Elective CNS surgery
C. Emergency neurosurgery
D. Elective spinal surgery

A

Ans C -

Certain procedures should not be performed in concert with anti-coagulation, especially where even minor bleeding can cause great morbidity - elective eye surgery and CNS surgery.

Emergency operations are occasionally necessaary in these patients.

139
Q

Protamine sulfate all are true except -

A. Rapid reversal of heparinized patient

B. Significant adverse reactions in patients with fish allergies.

C. Has pro-coagulant effect by itself.

D. aPTT remains elongated even after heparin reversal

A

Ans C -

Emergency operations are sometimes necessary in patients who have been heparinized. The first step in these patients is to discontinue heparin. For more rapid reversal protamine sulfate is effective.
It causes significant adverse reactions in patients with severe fish allergies.

Prolongation of aPTT after heparin neutralisation with protamine can be result of the anti-coagulant effect of protamine.

140
Q

Which of the following is correct regarding therapeutic heparin infusions

A. Stopped 4-6 hours before surgery
B. restarted within 12-24 hours at the end of the procedure
C. Both A and B
D. Heparin infusion can be continued

A

ans C -

A heparin infusion should be held 4-6 hours before surgery and restarted within 12-24 hours.

The primary indication for these aggressive regimes are -

  • Mechanical heart valves
  • MI within 30 days
  • Stroke within 30 days
  • Pulmonary embolism within 30 days

Not required in -

  • AF
  • Hypercoagulable history
  • thromboembolic events more than 30 days prior.
141
Q

Best method for controlling diffuse bleeding from large areas -

A. Argon plasma coagulation
B. rFVIIa with FFP
C. Packing a wound with gauze
D. Electrocautery

A

Ans C -

Direct pressure applied by “packing” a wound with gauze affords the best method of controlling diffuse bleeding from large areas.

Although direct current in the 20-100 mA range have successfully controlled diffuse bleeding from raw surfaces, as has argon gas.

142
Q

Characteristics of ideal topical hemostatic agent include all except -

A. Minimal tissue reaction 
B. Non-antigenic
C. In-vivo biodegradeability
D. Ease of sterilisation
E. Low cost
A

Ans all of the above.

143
Q

DIC can be an adverse effect of which of the following -

A. Abgel
B. Surgicel
C. Avitene
D. Topical Thrombin

A

ans D -

Gelatin foam (Gelfoam) and oxidized cellulose (Surgicel) provide a physical matrix for clot initiation.

Microfibrillar collagen (Avitene) facilitate platelet adherence and activation.

Human or recombinant thrombin derivatives - they avoid FB reactions but entry into large caliber vessels can lead to DIC and death. They are however very effective in controlling capillary bed bleeding when pressure and ligation are insufficient.

144
Q

Rh grouping was described by

A. Edward Jenner
B. Karl Landsteiner
C. Levine
D. Idaho et al

A

Ans C -

Levine and Stetson in 1939 discovered the Rh blood grouping.

145
Q

Increased risk of hemolysis is associated with transfusion of more than _____ units of O- blood without cross matching.

A. 2
B. 3
C. 4
D. 6

A

ans B -

administration of 4 or more units of O negative blood is associated with significant increase in the risk of hemolysis.

146
Q

Maximum number of units of blood that can be collected preoperative for autologous transfusion -

A. 2
B. 3
C. 4
D. 5

A

ans D -
Upto 5 units of blood can be collected for subsequent use in autologous tranfusion.

Patients can donate and store their own blood if their Hb is more than 11 g/dL or hematocrit is more than 34%.

First procurement - 40 days before the planned operation and last one 3 days before operation.

donations are scheduled at interval of 3-4 days.

Recombinant human EPO allows more frequent harvesting.

147
Q

Shelf life of stored red blood cells is -

A. 30 days
B. 21 days
C. 42 days
D. 35 days

A

ans C.

148
Q

which of the following not true

A. Dextran can interefere with cross matching.

B. age of red cells can significantly affect inflammatory response and incidence of Multiple organ failure

C. during storage there is reduction in levels of ADP and 2,3 DPG in red cells.

D. Stored Red cells have reduced levels of Potassium

A

ans D -

Cross matching should always be done before the administration of dextran since it can interfere with cross matching.

Age of red cells can significantly affect the development of inflammatory response and incidence of multiple organ failure.

Changes in red cells that occur during storage include

  • reduction in ADP
  • reduction in 2,3-DPG
  • decreased oxygen transport.
  • increased lactate
  • increased potassium
  • increased ammonia

Frozen red cells have improved viability, and ATP and 2,3 DPG levels are maintained.

149
Q

which of the following is not a benefit associated with use of leukocyte reduced red cells -

A. Hemolytic transfusion rections avoided
B. Allo-immunization to HLA class I Ag decreased.
C. decreased CMV transmission
D. decreased refractoriness to platelet transfusion

A

ans A -

Leukocyte reduced RBCs - prepared by filtration that removes about 99.9% of white blood cells.

Leukocyte reduced/Washed RBCs are prepared by additional saline washing.

They prevent

  • almost all febrile non-hemolytic transfusion reactions.
  • allimmunisation to HLA class I Ag.
  • Platelet transfusion refractoriness
  • CMV transmission.
150
Q

Shelf life of platelets is -

A. 72 hours from donation
B. 96 hours from donation
C. 120 hours from donation
D. 144 hours from donation

A

ans C -

shelf life of platelets is 5 days or 120 hours from donation.

151
Q

What is the volume of one unit of platelets -

A. 50mL
B. 100mL
C. 150mL
D. 200mL

A

ans A -

152
Q

Factor V can be found in -

A. Cryoppt
B. Prothrombin complex Concentrates
C. FFP
D. none of the above

A

ans C -

Fresh frozen plasma is the usual source of -

  • vitamin K dependent factors (II, VII, IX and X)
  • only source of factor V.
153
Q

True or false -

Infectious risks are lower for FFP compared to RBC

A

ans False -

FFP carries the same infectious risks as other component therapies.

154
Q

thawed FFP can be stored for -

A. 6 hours
B. 2 days
C. 5 days
D. 7 days

A

ans C - thawed FFP can be stored for upto 5 days.

155
Q

Tranexamic acid is used in -

A. CABG
B. OLT
C. Hip arhtroplasty
D. Knee arthroplasty
E. all of the above
A

ans E

156
Q

Maximum benefit from administration of tranexamic acid occur when administered within

A. 3 hours
B. 4 hours
C. 6 hours
D. 10 hours

A

ans A - TXA given between 1 and 3 hours after trauma reduced the risk of death by 21%.

157
Q

All of the following are contraindications for the use of Tranexamic acid except -

A. Acquired defective color vision
B. Active intravascular clotting 
C. Intracranial traumatic bleed
D. Urinary tract bleeding
E. Aneurysmal SAH
A

ans C -

TXA has been associated with blurry vision and changes in color perception especially prolonged use.

Contraindicated for use in -

  • Acquired Color vision defects
  • Active intrvascular clotting
  • Urinary tract bleeding - can lead to ureteral obstruction d/t clotting.
  • aneurysmal SAH

TXA should not be given with Prothrombin complex concentrate or Factor IX complex concentrate - they increase the risk of thrombosis.

No reported complications of TXA associated with intra- or extra-cranial hemorrhage associated with trauma.

158
Q

TXA acts by -

A. inhibition of plasminogen activation
B. Plasmin inhibition
C. increased fibrin polymerisation
D. both A and B

A

ans D -

TXA - antifibrinolytic - inhibits both plasminogen activation and plasmin activity.

occupies the Lysine binding site on plasminogen - prevents its binding to lysine residues on fibrin.

159
Q

Which of the following is a more potent anti-fibrinolytic

A. Tranexamic acid
B. Aminocaproid acid
C. Mefenamic acid
D. Clofibrate

A

ans A -

Tranexamic acid is nearly 10 times more active than aminocaproic acid in vitro.

160
Q

Transfused blood has poor oxygen offloading due to -

A. Decreased 2,3DPG
B. Decreased P50
C. deformation of the red cells
D. All of the above

A

ans D -

161
Q

Transfused blood has poor oxygen offloading due to -

A. Decreased 2,3DPG
B. Decreased P50
C. deformation of the red cells
D. All of the above

A

ans D -

162
Q

Most indication for blood transfusion in surgical patients is -

A. Volume replacement
B. Anemia
C. Oxygen transport
D. Acidosis

A

ans A -

163
Q

In a previously healthy patient, what percentage of blood loss can be replaced with crystalloids

A. None
B. 10%
C. 20%
D. 30%

A

ans C - In patients with normal preoperative values blood loss upto 20% of the total blood volume can be replaced with crystalloid or colloid.

Above this value addition of balanced resuscitation including red blood cells, FFP and platelets is needed.

164
Q

In civilian trauma systems, what perentage of deaths occur before patient reaches hospital -

A. 15%
B. 50%
C. 70%
D. 90%

A

ans B - nearly half of all deaths happen before a patient reaches the hospital.

165
Q

significant transfusion is defined as . -

A. 4 or more units of PRBC
B. 8 or more units of PRBC
C. 10 or more units of PRBC
D. 2 or more units of PRBC

A

ans A -

Significant transfusion is generally defined as 4 or more (Sometimes 6 or more) units of RBCS transfused within 4-6 hours of admission.

166
Q

Which of the following statements is false -

A. Plasma:PRBC ratios of 1:2 were 4 times more likely to die than ratios of 1:1.

B. Well developed massive transfusion protocol leads to improved outcomes independent of the transfusion protocol.

C. Both

D. None

A

and D -

167
Q

which of the following has the shortest lifespan or half life in-vivo

A. Factor VII
B. Factor V
C. Factor VIII
D. Factor X

A

ans A -

Factor I : 72 hours. 
Factor II : 72 hours
Factor V : 36 hours
Factor VII: 5 hours
Factor VIII : 6-12 hours
Factor IX : 24 hours
Factor X : 40h
Factor XI : 40-80h
Factor XIII : 4-7 days
Platelets : 8-11 days
168
Q

Deficiency of which of the following is not associated with any known bleeding tendency

A. Factor X
B. Factor XI
C. Factor XII
D. Factor XIII

A

ans C -

Factor XII or Hagemann factor deficiency leads to no bleeding tendency.

Therefore Factor XII also does not require any replacement.

169
Q

All of the following are considered labile in stored blood except -

A. Factor II
B. Factor V
C. Factor VIII
D. Platelets

A

ans A -

Bank blood (Acid-citrate-dextrose) 4C

Factor I - very stable
Factor II - stable
Factor V - Labile (40% of normal at 1wk)
Factor VII - stable
Factor VIII - Labile (20-40% of normal level at 1wk)
Factor IX - stable
Factor X - stable
Factor XI - probably stable
Factor XII - stable
Factor XIII - stable
Platelet - very labile (40% of normal level at 20hours and 0 at 48 hours)
170
Q

Normal level of fibrinogen in plasma are . -

A. 60-100 mg/dL
B. 100-150 mg/dL
C. 200-400 mg/dL
D. 400-500 mg/dL

A

ans C -

Normal levels of fibrinogen in blood - 200-400 mg/dL

Minimal levels required for safe hemostasis: 60-100 mg/dL

171
Q

Type specific non-cross matched blood should be available within

A. 2-4 minutes
B. 5-10 minutes
C. 10-15 minutes
D. 30 minutes

A

ans B -

O-negative uncross matched - avaialble immediately

Type Specific uncross matched blood - 5-10 minutes (Bailey: 10-15 minutes)

Complete cross matched - 40 minutes. (Bailey - 45 min)

172
Q

the plasma:platelet:RBC ratio of 1:1:1 should ideally attained with

A. first 2 units of RBC
B. first 4 units of RBC
C. first 6 units of RBC
D. first 8 units of RBC

A

ans A -

First 2 units of RBC.

173
Q

MTG stops at -

A. once 6 units each of plasma, platelet and RBC have been transfused

B. once pt stops actively bleeding

C. Once 10 units of RBC are transfused

D. once cross matched blood available

A

ans B.

174
Q

Tests that should be performed after 6 units of each of RBC, Platelet, FFP are transfused include all except

A. CBC
B. INR
C. pH
D. Factor X assay

A

ans D -

Tests performed are -

CBC
INR or Fibrinogen
pH and/or base deficit
Thromboelastography

175
Q

Transfusion reactions are seen in

A. 5% of all transfusion
B. 10% of all transfusion
C. 15% of all transfusion
D. 20% of all transfusion

A

ans B -

transfusion related events are estimated to occur in 10% of all transfusions, but less than 0.5% are serious in nature.

176
Q

Most common cause of tranfusion related deaths is -

A. TRALI
B. ABO hemolytic Transfusion reactions
C. Bacterial contamination of platelets
D. Non-hemolytic transfusion reactions

A

ans A -

TRALI causes 16-22% of all deaths
ABO hemolytic reactions cause 12-15% of all deaths
Bacterial contamination causes 11-18% of all deaths.

177
Q

Most common cause of bacterial contamination of infused blood -

A. Gram Positive Cocci
B. Gram Positive Bacilli
C. Gram negative organisms
D. Anerobes

A

ans C -

Gram negative organisms that are capable of growing at 4C are the most common cause.

Bacterial contamination can lead to sepsis and death in upto 25%.

If suspected - discontinue transfusion and send Blood culture.

178
Q 
Blood product that is most liable to bacterial contamination is - 
A. PRBC
B. Platelets
C. Cryoppt
D. FFP
A

ans B -

Platelets are the cause for most of the bacterial contaminations since they are stored 20C and more so with apheresis platelets which are stored at room temperature.

179
Q

all of the following are true regarding febrile reactions except

A. They are non-hemolytic reactions

B. due to preformed Cytokines in the recipient

C. Pretreatment with PCM can reduce the severity

D. Leukocyte reduced RBC greatly reduce the incidence

A

ans B -

They are due to performed cytokines within the donated blood.

Febrile reactions are defined as a rise in temperature more than 1C.

Febrile reactions are seen in nearly 1% of all transfusions.

180
Q

one apheresis platelets equals -

A. 6 random donor platelet packs
B. 4 random donor platelet packs
C. 2 random donor platelet packs
D. 1 random donor platelet pack

A

ans A -

6 random donor platelet packs = 1 apheresis platelet unit.

181
Q

Cryoppt is indicated after 6 units of RBCs if fibrinogen levels are -

A, <60 mg/dL
B. <100 mg/dL
C. <200 mg/dL
D. <400 mg/dL

A

ans C -

After first 6 units of RBCs fibrinogen levels should be checked. If they are <200 mg/dL then 20 Units of Cryoppt are given i.e. 2000mg or fibrinogen.

(1 unit of Cryoppt = 100mg of fibrinogen)

182
Q

Allergic reactions are most common after the administration of . -

A. PRBCs
B. Leukocyte reduced PRBC
C. FFP
D. Whole Blood

A

ans C -

Allergic reactions are caused by -
1. transfusion of antibodies from a hypersensitive donor

  1. transfusion of antigens to which the recipient is hypersensitive

Allergic reactions are most commonly associated with FFP and Platelets.

183
Q

All of the following are true regarding TRALI

A. Defined as Non-cardiogenic pulmonary edema related to tranfusion.

B. Bilateral infiltrates on chest x ray.

C. Develops between 6-12 hours after transfusion.

D. ventilatory support varying from oxygen supplementation to mechanical ventilation

A

ans C -

TRALI -

non-cardiogenic pulmonary edema related to transfusion.

Can occur with administration of any plasma containing blood product.

Symptoms are similar to circulatory overload - dyspnea and associated with hypoxemia.
Often accompanied with Fever, rigors and bilateral pulmonary infiltrates on chest x ray

Most commonly occurs within 1-2 hours after the onset of tranfusion but virtually always within 6 hours of tranfusion.

Decrease in incidence has been reported with -

  • reduction transfusion of plasma from female donors - due to
    a. reduced tranfusion of strong cognate HLA class II antibodies
    b. reduced transfusion of HNA Ab in patients with risk factors for acute lung injury.

Treatment

  • discontinuation
  • notify tranfusion service
  • pulmonary support - ranging from supplemental oxygen to mechanical ventilation.
184
Q

Which of the following is least likely to cause TRALI

A. FFP
B. PRBC
C. Cryoppt
D. Whole Blood

A

ans B -

Any plasma containing blood product can cause TRALI.

185
Q

Tranfusion associated cardiac overload all are true except -

A. it is an avoidable complication
B. Central venous pressure monitoring can help
C. Can occur with rapid infusion of blood products, colloids, plasma expanders and colloids.
D. Transfusion has to be discontinued.

A

ans D -

Treatment consists of diuresis, slowing the rate of administration and minimisation of fluids while blood products are being tranfused.

Usually occurs from FFP.

186
Q

which of the following is the most common symptom of acute transfusion reactions -

A. Fever
B. pain at the site of tranfusion
C. Hypotension
D. Respiratory distress

A

ans B -

Most common symptomsof acute tranfusion reactions include -

  • pain at the site of tranfusion
  • facial flushing
  • back and chest pain.

Associated symptoms include - fever

  • respiratory distress
  • hypotension
  • tachycardia.
187
Q

All of the following are true regarding immediate hemolytic reactions

A. Hemoglobinuria and Tubular necrosis
B. Intravascular hemolysis
C. Pain at the site of tranfusion is the most common symptom
D. Anamnestic reaction is the cause

A

Ans D -

Immediate hemolytic reaction
- intravascular destruction of red blood cells leading to hemoglobinemia, hemoglobinuria and tubular necrosis.

  • DIC can also occur due to Ag-Ab complexes activating factor XII and Complement.
  • Tubular necrosis occurs due to ppt of Hb in renal tubules.

Hemolytic reactions are due to incompatible ABO transfusions and fatal in upto 6% cases.

Anamnestic reaction is seen in delayed hemolytic reactions.

Two healthcare personnel should check the patient details against the prescription and the label of the donor blood. Donor blood serial number should be checked against the issue slip of patient.

188
Q

all of the following are true regarding delayed hemolytic reactions except

A. Usually occur more than 24 hours after, but within 3 days of transfusion.

B. characterised by extravascular hemolysis

C. Anamnestic reaction leads to rise in Ab titres.

D. Indirect Bilirubinemia with low grade hemoglobinuria

A

ans A -

Delayed hemolytic tranfusion reactions usually occur after 2-10 days.

  • extravascular hemolysis and indirect bilirubinemia.
  • fever, recurrent anemia, jaundice, decreased haptoglobin, low grade hemoglobinemia and hemoglobinuria may be seen.
  • individual has low Ab titres at the time of transfusion but titer increases after tranfusion as a result of ANAMNESTIC reaction.

Reactions to non-ABO Ag involve IgG mediated clearance by the reticuloendothelial system.

Blood bank must identify the Ag to prevent subsequent reactions.

189
Q

Positive coomb’s test in a tranfusion reaction is predictive of all of the following except

A. Tranfused cells coated with patient Antibodies
B. Patient’s cells coated with recipient antibodies
C. Immediate hemolytic reactions
D. Delayed hemolytic reactions

A

Ans B -

A positive Coomb’s test indicates transfused cells coated with patient Ab and it is considered diagnostic of immediate hemolytic reaction. Coomb’s test is also usually positive in delayed hemolytic reactions.

190
Q

Diagnosis of Immediate hemolytic reaction is based on -

A. presence of hemoglobinuria
B. Serologic criteria of incompatibility of donor and recipient blood
C. Positive Coomb’s test
D. All of the above

A

Ans D.

191
Q

Which of the following is correctly matched

A. Immediate hemolytic reaction - preformed IgG antibodies to ABO Ag

B. Delayed Hemolytic reactions - decreased haptoglobin levels

C. Febrile non-hemolytic transfusion reactions - Donor Ab to host Lymphocytes

D. TRALI - limit female donors for prevention

A

ans D -

  1. Febrile non-hemolytic reactions - 0.5-1.5% tranfusions -
    - occurs d/t Host Ab to donor lymphocytes and preformed Cytokines.
    - prevention : use of leukocyte reduced blood, and store platelets for less than 5 days.
  2. Bacterial contamination occurs in less than 0.05% of blood tranfusion, but >0.05% of platelet tranfusions.
  3. Allergic reactions are due to soluble tranfusion constituents. Marked by rash, hives and itching.
  4. Transfusion asso. cardiac overload - marked by pulmonary edema. Occurs in once in 200-10,000 tranfusions. Large volume transfused in older patient with CHF. Rx - diuretics and reduce rate.
  5. TRALI - acute hypoxemia within 6 hours with bilateral lung infiltrates. Caused by Anti-HLA or Anti-HNA Ab in the transfused blood which attacks the circulatory and pulmonary leukocytes. Prevented by limiting female donors.
  6. Immediate hemolytic reactions - once in 33,000 to 1.5 million units - due to preformed IgM Ab against ABO Ag on donor blood.
  7. Delayed hemolytic reactions - occur after 2-10 days. associated with indirect bilirubinemia, decreased haptoglobin and positive Direct Coomb’s test. IgG mediated.
192
Q

Malaria can be transmitted by -

A. Platelets
B. PRBC
C. Cryoppt
D. FFP
E. All of the above
A

ans E -

Malaria can be transmitted by all blood components.
Incubation period 8-100 days.
First manifestation is shaking chills and spiking fever.

193
Q

All of the following can be transmitted by blood tranfusions except -

A. Brucellosis
B. Chagas’s disease
C. Tuberculosis
D. Syphilis

A

ans C -

Malaria, Chagas’s disease, Brucellosis, CMV and Syphillis can all be transmitted.

194
Q

Which of the following has the highest residual risk of transmission during blood transfusion -

A. HIV-1
B. HIV-2
C. HCV
D. HBV

A

ans D -

the residual risk of HIV and HCV transmission is 1 in 1 million donations.

Whereas the residual risk of HBV transmission is 1 in 300,000 donations.

195
Q

Which of the following cannot be trasmitted by blood transfusion

A. Hepatitis A
B. Creutzfeldt Jakob disease
C. West Nile virus
D. None of the above

A

ans D -

Hepatitis is very rarely transmitted because it has no asymptomatic carriers.

West Nile virus also can be rarely transmitted.

CJ Ds can also be transmitted.

196
Q

Minor sugical procedures can lead to bleeding with platelet counts below

A. 1 lac/uL
B. 50000/uL
C. 30000/uL
D. 20000/uL

A

ans C -

> 10 lac/uL - bleeding or thrombotic complications

<50,000/uL - increased bleeding with major surgical procedures.

<30,000/uL - increased bleeding with minor surgical procedures

<20,000/uL - spontaneous hemorrhage.

197
Q

Platelet transfusions are indicated in opthalamic and neurosurgical procedures at platelet levels of -

A. <1 lac/uL
B. <50,000/uL
C. <30,000/uL
D. <20,000/uL

A

ans A -

198
Q

All of the following is true regarding PT except -

A. Measures the function of Factor I,II,V,VII and X.

B. reagent used contains thromboplastin and calcium.

C. International sensitivity index for thromboplastin should ideally be 1

D. INR is measured as (Test PT/Control PT)^ISI

A

ans C -

PT reagent contains thromboplastin and calcium, that when added to the plasma cause formation of fibrin clot.

PT test measures the function of Factor I, II, V, VII and X.

Factor VII has the shortest half life of all the coagulation factors, and its synthesis is Vitamin K dependent and therefore,
PT is best suited to detect Vitamin K deficiencies and Warfarin therapy.

Due to the variations in thromboplastin there is no normal PT, rather INR is used to report.

International sensitivity index is unique to each batch of thromboplastin.

Human Brain thromboplastin has a value of 1.
Ideally ISI should be between 1.3-1.5

INR = (Measured PT/ Normal PT)^ISI.

199
Q

which of the following vitamin K dependent factors is not measured by PT/INR

A. Factor II
B. Factor VII
C. Factor IX
D. Factor X

A

ans C -

Factor IX is not measured by PT, its activity is measured by aPTT.

200
Q

Therapeutic levels for aPTT in heparin therapy are -

A. less than 1.5
B. 1.5 to 2.5
C. 50-80s
D. Both B and C

A

ans D.

Note -

Low molecular weight heparins are selective for Xa. They mildly elevated aPTT, but therapeutic monitoring is not routinely recommended.

201
Q

All of the following are present in aPTT reagent except -

A. Phopsholipid subsitute
B. Activator
C. Thromboplastin
D. Calcium

A

ans C -

aPTT reagent contains phospholipid subsitute, activator and calcium.

aPTT measures the function of factor I, II and V from the common pathway, and factors VIII, IX, X and XII of the intrinsic pathway.

202
Q

All of the following are true regarding bleeding time -

A. evaluates platelet, vascular and coagulative dysfunction

B. Ivy Bleeding test is the most commonly used.

C. Upper normal limit is 7 minutes.

D. bleeding time is raised in vWD

A

ans A

Bleeding time evaluates platelet and vascular dysfunction.

Ivy Bleeding time is the most commonly used method -

  • syphgmomanometer on the arm and inflate to 40 mmHg.
  • 5mm stab incision on flexor surface of forearm
  • upper limit of normal BT 7 minutes.

An abnormal BT - platelet dysfunction, vWD and certain vascular defects.

In Vitro tests in which blood is sucked through a capillary and platelets adhere to the walls of the capillary and aggregate is being used in some laboratories.
Closure time closely correlates with bleeding in vWD, primary platelet function disorders and patients taking aspirin.

203
Q

Which of the following is true regarding TEG

A. Less expensive than standard coagulation panels.

B. Monitors hemostasis as a dynamic process

C. blood is induced to clot in a high shear environment resembling a artery flow.

D. Whole blood is used.

A

Ans C -

Whole visco-elastic testing are dynamic testing techniques including Thromboelastography and ROTEM (Rotational thromboelastometry)

They are more rapid and less expensive than standard coagulation panels.

TEG monitors hemostasis as a dynamic process.

TEG measures the viscoelastic properties of blood as it is induced to clot in a low shear environment resembling sluggish venous flow.

204
Q

Reagent used in standard TEG is

A. Thromboplastin
B. Calcium
C. Kaolin
D. Tissue Factor

A

ans C

A sample of CELITE activated whole blood is placed into a prewarmed cuvette, and the clotting process is activated with

  • Kaolin in standard TEG
  • Kaolin with Tissue factor in rapid TEG.
205
Q

Which of the following is false regarding TEG

A. Cuvette oscillates in rotation of 4.5 degree arc backwards and forwards.

B. Weak clot does not adequately transmit the movement of the cuvette to the piston.

C. Strong clot transmits the movement of the cuvette to the piston and results in a narrow TEG.

D. Kinetics determine the adequacy of clotting factors

A

ans C -

Celite activated Whole blood is placed in cuvette and clotting is activated using Kaolin in standard TEG and Kaolin with TF is rapid TEG.

Kinetics - determine the adequacy of quantitative factors available for clot formation.

Strength and stability provide information about the ability of clot to perform the work of hemostasis.

Weak clot does not transmit the movement of the cuvette to the piston and therefore leads to a narrow TEG.

Strong clot transmits the movement of the cuvette to the piston simultaneously and proportionally to the cuvette’s movements and thus creates a thick TEG.

206
Q

which of the following is incorrectly matched

A. R-value or reaction time represents the time between initiation of assay and intial clot formation.

B. K-time represents the interaction of clotting factors and platelets.

C. Clot accelaration is reflected by the alpha angle, and reflects interaction of clotting factors and platelets.

D. LY-30 is the percentage of amplitude remaining at 30 minutes after mA is achieved,.

A

Ans D -

Parameters in TEG -
- R-value or reaction time - is the time from the start of assay to the initial clot formation.
Represents Clotting factor activity and initial fibrin formation.

  • K-time - clot kinetics - is the time needed to reach a certain clot strength and represents interaction of clotting factors and platelets.
  • Alpha Angle - is the slope of the tracing and reflects clot accelaration. Reflects the interactions of clotting factors and platelets.
  • maximal Amplitude (mA) is the greatest height of tracing. Represents the clot strength.
  • G value - parametric measure derived from mA value and reflects overall clot strength and firmness.
  • LY-30 - amount of lysis occuring in the clot. Value is the percentage of amplitude reduction at 30 minutes after mA is achieved.
207
Q

Which of the following is matched correctly

A. Raised R value represents hemodilution.

B. Raised K time represents hypofibrinogenemia

C. Slope of alpha angle is reduced in platelet dysfunction.

D. mA is increased in platelet dysfunction

A

ans D-

R value - increased in factor deficiency, hemodilution. Corrected by FFP.

K time increased in hypofibrinogenemia and significant factor deficiency. Corrected with FFP.

Alpha angle decreased with hypofibrinogenemia and platelet dysfunction. Angle can be corrected with Cryoppt, or fibrinogen.

Decreased mA is seen in dysfunction or deficiency of platelets or fibrinogen. Decreased mA is corrected with platelets.
Decreased mA with decreased angle - platelet with cryoppt.

G Value increased in hypercoagulability and decreased in hypocoagulability.

LY-30 when increased represents increased fibrinolysis.

208
Q

Which of the following is true regarding TEG :

A. Can identify patients likely to develop thromboembolic complications after injury or surgery.

B. Useful in predicting need for early transfusion of RBCs, Plasma, platelets and Cryoppt.

C. Can predict the need for life saving interventions shortly after admission.

D. Can predict 24h and 30 day mortality

E. All of the above

A

Ans E

Benefits of using TEG -
– only test measuring all dynamic steps of clot formation until clot lysis or retraction.

– identify on admission those patients likely to develop thromboembolic complications after injury postoperatively.

– Useful in predicting early need for tranfusion of RBCs, plasma, platelets and cryoppt.

– predict need for life saving interventions shortly after arrival

– predict 24 hours and 20 day mortality

– useful to guide administration of TxA to injured patients with hyperfibrinolysis.

209
Q

Excessive bleeding from operative field unassociated with bleeding from other sites suggestive of -

A. Consumptive coagulopathy
B. Undetected hemostatic defect
C. Inadequate mechanical hemostasis
D. Blood transfusion

A

ans C

210
Q

All of the following can be a cause of thrombocytopenia except

A. Massive blood tranfusion
B. Immediate hemolytic transfusion reactions
C. Delayed hemolytic transfusion reaction
D. Tranfusion purpura

A

ans C -

Bleeding following massive blood transfusion can be due to -

  • thrombocytopenia
  • dilutional coagulopathy
  • platelet dysfunction
  • hypothermia
  • thrombocytopenia
  • hypofibrinogenemia

The first sign of a transfusion reaction can be diffuse bleeding. The pathogenesis of this bleeding is release of ADP from the hemolyzed red blood cells resulting in diffuse platelet aggregation, after which platelets are removed out of circulation.

211
Q

All of the following are true regarding transfusion purpura except

A. Occurs with recipient of PlA group of platelets.

B. Thrombocytopenia

C. Considered if bleeding occurs 5-6 days after tranfusion.

D. Self limiting condition

A

ans A -

Transfusion purpura occurs when donor platelets are of uncommon PlA group.

Uncommon cause of thrombocytopenia and subsequent bleeding after transfusion.

Platelets of the donor sensitize the recipient to produce Ab against the foreign platelet Ag.

However the Ag does not disappear with the formation of platelets, rather it attaches to the native platelets, thus causing destruction of these foriegn Ag labelled native platelets to be destroyed by native Ab.

the resultant thrombocytopenia and bleeding may continue for several weeks.

Considered if bleeding occurs 5-6 days after transfusion.

Management -

  • platelet transfusion is of little help
  • corticosteroids - some benefit.
  • self limited condition, inevitably subsides in several weeks.
212
Q

Complications from massive tranfusion include all except -

A. Coagulopathy
B. Hypocalcemia
C. Hypernatremia
D. Hyperkalemia

A

ans C -

Complications associated with massive tranfusion include-

  • Coagulopathy
  • thrombocytopenia
  • Hypocalcemia
  • HypoKalemia
  • Hyperkalemia
  • Hypothermia
213
Q

Each unit of red blood cells contain -

A. 100 mg of elemental iron
B. 250 mg of elemental iron
C. 1g of elemental iron
D. 500 mg of elemental iron

A

ans B.

214
Q

Which of the following statements is false regarding balanced tranfusion

A. Balanced tranfusion is ideal for correction of coagulopathy

B. Balanced tranfusion consists of PRBC:Platelets:FFP in ratios of 1:1:1

C. Balanced tranfusion is central to prevention of dilutional coagulopathy in damage control resuscitation

D. None of the above

A

ans A -

Balanced transfusion approach cannot correct coagulopathy. It can reduce the incidence and severity of dilutional coagulopathy that develops as a result of massive tranfusion protocols.

Underlying coagulopathies should be treated addition to the administration of 1:1:1 balanced tranfusions.

Bailey and Love + Sabiston 20e (4 decks)

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