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Unit 2 SPATH UFCOM > H. Testing of Primary Hemostasis (L6, L7, L9 & Lab 3) > Flashcards

H. Testing of Primary Hemostasis (L6, L7, L9 & Lab 3) Flashcards

1
Q

Broadly speaking what are the 2 main aspects of primary hemostasis that are assessed?

A

Platelet number

Platelet & VWF function

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2
Q

What is the quantitative assessment of platelets and when is it performed?

A
  • Platelet count

* Routinely performed as part of a CBC

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3
Q

How commonly are platelet function tests ordered?

A
  • Relatively infrequently due to high cost and the cumbersome nature of the tests
  • Generally only do functional analysis if quantitative tests don’t explain symptoms
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4
Q

Platelet functional analysis can be performed on what 2 types of samples? Which is easier to use?

A
  • Platelet rich plasma
  • Whole blood
  • Whole blood is easier to use because it does not have to be prepared
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5
Q

How is platelet aggregation tested on platelet rich blood?

A
  • Optical density for the sample is measured –> relatively little light passes through as most is scattered by the platelets that are even dispersed through the sample –> high adsorption –> high OD
  • Add platelet agonist –> continuing measuring OD –> platelets aggregate leaving more “open spaces” in the sample –> more light passes through –> plot OD on graph as it lowers overtime
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6
Q

What is the shape of the OD vs. time graph for the platelet aggregation test? How does it look for somebody deficient in agonist response?

A
  • OD decreases over time after agonist is added
  • The decrease is in 2 distinct phases. The first phase is due to the agonist which is added and the second phase is due to the agonist being released by platelets themselves
  • If there is a deficient response to the agonist the curve begins to decrease and then “flat lines”
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7
Q

There are 2 groups of agonist used in platelet aggregation studies. Name the agonists in both groups and the mechanism they are testing:

A
  • ADP, Epinepherine, Thrombin, Collagen and TxA2 –> test GPIIb/GPIIIa & fibrinogen
  • Ristocetin –> GpIb & VWF
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8
Q

How is a whole blood aggregometer different than aggregation studies performed on platelet rich plasma?

A

• Instead of using spectrophotometry, it measures electrical impedance

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9
Q

What agonists are used in whole blood aggregometry?

A
  • ADP, Collagen, Arachidonic acid and Ristocetin

* Epinepherine is not used

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10
Q

What disorders cause impaired clotting in response to ristocetin?

A
  • Von Willebrand Deficiency

* Bernard Soulier Disease (GPIb deficiency)

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11
Q

What is Benard Soulier Disease?

A

• Impaired clotting due to a deficiency of GPIb (receptor for VWF) –> impaired coagulation

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12
Q

How is it determined whether impaired clotting to Ristocetin is the result of VWF deficiency or a deficiency of the platelet receptor for WVF (GPIb)?

A

• Ristocetin cofactor test

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13
Q

What is the Ristocetin Cofactor Test?

A

• Repeat Ristocentin test but use platelets from another healthy individual –> only the patients WVF is being used

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14
Q

What is suspected with an abnormal Ristocetin Induced Platelet Aggregation (RIPA) and normal Ristocetin Cofactor test?

A
  • Bernard Soulier syndrome

* Normal cofactor test –> VWF from patient is fine –> must be problem with platelet –> def of GPIb

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15
Q

What is suspected with an abnormal Ristocetin Induced Platelet Aggregation (RIPA) and abnormal Ristocetin Cofactor test?

A
  • VWF deficiency

* Abnormal cofactor test –> VWF from patient is not functioning

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16
Q

What 3 supplemental laboratory procedures can test VWF?

A
  • Elisa tests the amount of VWF in the plasma
  • Western Blot –> probe with anti-VWF –> VWF size distribution (Larger multimers are more active)
  • Can test VWF ability to adhere to collagen to tests its ability to initiation adhesion
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17
Q

What is type 1 Von Willebrand Disease? What is it’s pattern of inheritance? Is it heterozygous or homozygous?

A
  • Normal ratios of different sized VWF but absolute deficiency of all sizes
  • Autosomal dominant
  • Heterozygous
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18
Q

What is type 2 Von Willebrand Disease?

A

• Improper ratio of different sized VWF –> deficiency of larger more active VWF

19
Q

What is type 3 Von Willebrand Disease? Is it heterozygous or homozygous?

A
  • Production of VWF is virtually absent

* Homozygous for the mutation that causes type 1

20
Q

What is the most common type of Von Willebrand Disease?

A

Type 1

21
Q

What is necessary for a normal PFA-100 reading?

A
  • Adhesion due to VWF

* Aggregation due to response to agonist

22
Q

How is the PFA-100 (Platelet Function analyzer) performed?

A
  • Have a membrane with a 150 micrometer whole –> suck blood through it and measure how long it takes to clot = closure time
  • Collagen is present on the membrane (adhesion) and either epinephrine or ADP is given as an agonist (aggregation
23
Q

What type of blood sample is the PFA-100 test performed on?

A

Whole blood

24
Q

Platelet aggregation tests are not performed on patients with what bleeding disorder?

A

• Thrombocytopenia, already know that coagulation will be delayed by CBC & the aggregation tests are more expensive

25
Q

Approximate size of a platelet?

A

2 micrometers

26
Q

How is the PFA-100 closure time affected for patients taking aspirin?

A
  • Delayed if epinephrine is used as the agonist

* Normal if ADP is used as the agonist

27
Q

Why is PFA-100 the preferred test for platelet function?

A

• It is cheaper and easier to perform (can use whole blood)

28
Q

If there is impaired platelet adhension there will be a deficient response to what agonist(s) during coagulation testing?

A

Ristocetin

29
Q

If there is impaired platelet aggregation there will be a deficient to what agonist(s) during coagulation testing?

A

• ADP, epinephrine, thrombin, collagen and TxA2

30
Q

What impairs platelet aggregation?

A
  • Acquired = NSAIDs, Plavix, dialysis and cardiopulmonary bypass
  • Inherited = afibrinogenemia, Glanzman thrombasthenia, gray platelet syndrome
31
Q

In patients taking NSAIDs like aspirin, how is aggregation impaired?

A

• NSAIDs –> COX inhibitor –> prevent creation of TxA2 which is a platelet activator

32
Q

In patients taking Plavix/Clopidrogel, how is aggregation impaired?

A

Plavix blocks ADP receptor

33
Q

What is Glanzman Thrombasthenia?

A

Deficiency in GBIIb/IIIa

34
Q

What is gray platelet syndrome?

A

• Storage disorder of granules in platelet  prevents platelets own release of agonist

35
Q

What substance is added to almost all blood samples to reversibly inhibit coagulation?

A
  • Sodium citrate

* Removes Ca ions

36
Q

What must be added to a blood sample before you can begin testing on it (after it has been stored in a refrigerator)?

A
  • Calcium Chloride (to reverse effect of Sodium citrate)
  • Phopholipid (to give factors a surface to work on. Can’t work in suspension)
  • Warm the sample to 37 degrees so the enzymes can function
37
Q

Factor VII circulates bound to what? Why?

A
  • VWF

* Prolongs VII half life

38
Q

What is an alternative to the OD vs. Time graph for platelet function testing?

A
  • Aggregation vs time

* Graph is basically inverted

39
Q

How soon after injury do symptoms present if there is a primary hemostasis disorder? How about for secondary?

A

Immediately

Delayed

40
Q

Can injury to patients with primary hemostasis disorder be controlled with pressure? What about for patients with disorders of secondary hemostasis?

A

Yes

No

41
Q

What are the general set of labs done when trying to diagnose a bleeding disorder?

A 
Platelet count (primary)
PFA (primary)
PT (secondary)
PTT (secondary)
Thrombin Time (secondary)
42
Q

What is the inherited disorder with platelet adhesion? What about aggregation?

A

Bernard Soulier

Glanzman Thrombastenia

43
Q

If all aggregations studies are normal except when ristocetin is used, what is the likely diagnosis?

A

Bernard Soulier

44
Q

If platelet aggregation studies are always abnormal except to ristocetin, what is the likely diagnosis?

A

Glanzman Thrombastenia

Unit 2 SPATH UFCOM (17 decks)

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