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Unit 2 SPATH UFCOM > I. Coagulation Testing of Secondary Hemostasis (L6, L7 & L9 & Lab 3) > Flashcards

I. Coagulation Testing of Secondary Hemostasis (L6, L7 & L9 & Lab 3) Flashcards

1
Q

What are the 4 main tests of secondary hemostasis/coagulation cascade?

A

• PT, PTT, TT and Fibrinogen concentration

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2
Q

What prolongs secondary hemostasis?

A
  • Coagulation factor dysfunction
  • Coagulation deficiency (rare)
  • Drugs like heparin leading to inhibition
  • Antibody inhibition
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3
Q

Why is citrate added to blood samples? What is the downside to this?

A
  • Citrate removes the Ca from the sample –> prevents clotting before the tests can be performed
  • Ca must be added back before coagulation tests are performed
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4
Q

The PTT measures which portions of the coagulation cascade?

A
  • Intrinsic and common

* Think more letters in PTT than PT, PTT measures side with more numbers (more coag factors)

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5
Q

The PT measures which portions of the coagulation cascade?

A
  • Extrinsic and common

* Think more letters in PTT than PT, PTT measures side with more numbers (more coag factors)

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6
Q

What does aPTT stand for?

A

• Activated partial thromboplastic time

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7
Q

What does TT stand for?

A

Thrombin time

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8
Q

What is added to a sample for PTT?

A
  • Ca
  • Negatively charged silica
  • Partial Thromboplastin which is really just phospholipid
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9
Q

What is added to a sample for PT?

A
  • Ca

* Thromboplastin (Phospholipid and Tissue activator)

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10
Q

How does Warfarin/Coumadin act as an anticoagulant?

A

• Prevents Vit K recycling –> Vit K deficiency –> inhibits Vit K dependent coagulation factors –> inhibit 7, 10 & 2

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11
Q

Which coagulation factors are vitamin k deficient?

A

2, 7,9 & 10

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12
Q

A prolonged PT means what? (asking about relationship to cascade, not clinical presentation)

A

• Deficiency, dysfunction or inhibition of VII, X, 5, 2 and/or 1

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13
Q

What clinical presentations cause prolonged PT?

A
  • Liver disease
  • Vit K antagonist (Warfarin or Coumadin)
  • Fibrin/fibrinogen fragments
  • DIC –> factor consumption and fibrin/fibrinogen fragments created which inhibit normal organized interactions
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14
Q

Why does liver disease potentially prolong PT and PTT?

A
  • Vit K is a fat soluble vitamin, therefore liver disease –> decreased bile –> decreased fat absorption –> vit k deficiency
  • Liver if site of production for coagulation factors –> liver disease can cause factor deficiency
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15
Q

Where in the body are coagulation factors created?

A

Liver

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16
Q

A prolonged PT means what? (asking about relationship to cascade, not clinical presentation)

A

• Deficiency, dysfunction or inhibition of 12, 11, 9, 10, 5, 2 and/or 1

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17
Q

What clinical presentations cause prolonged PTT?

A
  • Heparin (inhibits 10 and 2)
  • DIC –> factor consumption and fibrin/fibrinogen fragments created which inhibit normal organized interactions
  • Lupus anticoagulant
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18
Q

How does Heparin work?

A

• Inhibits 10 and 2 –> anticoagulant

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19
Q

What clinical disorder results in a deficiency of factor XI? How is it inherited?

A
  • Hemophilia C

* Autosomal dominant

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20
Q

What clinical disorder results in a deficiency of factor IX? How is it inherited?

A
  • Hemophilia B

* X linked recessive

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21
Q

What clinical disorder results in a deficiency of factor VIII? How is it inherited?

A
  • Hemophilia A

* X linked recessive

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22
Q

Which test (PT and/or PTT) is affected by heparin? Which one is more sensitive?

A
  • Both are prolonged

* PTT is affected more

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23
Q

Which test (PT and/or PTT) is affected by lupus anticoagulant? Which one is more sensitive?

A
  • Both are prolonged

* PTT is affected more

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24
Q

Which test (PT and/or PTT) is affected by Warfarin/Coumidin? Which one is more sensitive?

A
  • Both are prolonged

* PT is affected more

25
Q

Which (PTT or PT) is better for measuring effectiveness of heparin and cumodin?

A
  • Hep = 3 letters, PTT = 3 letters

* Cumodin = PT

26
Q

What is a Thrombin Time (TT)? What does it measure?

A
  • Add exogenous thrombin and Ca –> measure fibrin formation
  • Ability to convert fibrinogen to fibrin
27
Q

What are the 2 types to measure the Thrombin Time and what are the testing for?

A
  • Functional assay = concentration and function

* Mass assay/immune assay = concentration only

28
Q

How is the Functional Assay for TT different than the mass assay?

A
  • You add excess thrombin in the functional

* So if there is just a deficiency of fibrinogen this will be overcome by the excess thrombin

29
Q

What causes a prolonged TT?

A
  • Fibrinogen deficiency, dysfunction or inhibition
  • Thrombin inhibition (heparin or thrombin Ab)
  • Increased fibrin polymerization/fibrin split products
30
Q

When clotting time is prolonged, how can it be determined if there is a deficiency/dysfuntion or inhibition?

A

Mixed Study

31
Q

What is a mixed study? What do the results tell you?

A
  • Mix patients plasma with plasma from a healthy individual
  • If clotting time corrects –> deficiency or dysfunction
  • If clotting time doesn’t correct –> inhibition (whatever is inhibiting the patients’ blood effects the healthy blood)
32
Q

What conditions can increase fibrinogen concentration?

A
  • Estrogen
  • Pregnancy
  • Acute phase response
33
Q

How are blood samples stored in a way to protect damage of coagulation factors?

A

• Stored in refrigerator because coagulation factors are heat sensitive

34
Q

The last step in the common pathway of the coagulation cascade is tested with what?

A

TT

35
Q

What is the purpose of an INR?

A
  • Way to standardize TT across labs (which can report different numbers)
  • Used to test patients response to warfarin/Coumadin
36
Q

What does INR stand for?

A

• International Normalized Ration

37
Q

How is INR calculated?

A
  • = (Patients PT/MNPT)^ISI
  • MNPT (Mean Normal Prothrombin Time) = mean PT for population measured at that lab
  • ISI (International Sensitivity Index) = characteristic of agent used to cause clotting (provided by manufacturer)
38
Q

INR should only be used to test for what? Why should it not be utilized for other therapies/conditions?

A
  • Coumidin/warfarin response
  • The ISI which is used to calculate INR is determined by testing healthy patients and patients on Coumadin (not patients with other conditions)
39
Q

What are the results of a mixing study on patients taking Warfarin/Coumidin and Heparin?

A
  • Haprin does not correct (acts as inhibitor)

* Warfarin does correct (causes factor deficiency)

40
Q

Does Warfarin/Coumidin cause inhibition, deficiency or dysfunction of clotting factors?

A

• Deficiency by removing K which is needed for synthesis

41
Q

Does Heparin cause inhibition, deficiency or dysfunction of clotting factors?

A

Inhibition

42
Q

If want to test for a potential deficiency in a single coagulation factor you can perform what test?

A

Biological assay

43
Q

What is most likely if PT is normal, PTT is prolonged, PTT is corrected with mixing study and Thrombin times are normal?

A

Hemophilia A or B

44
Q

What is suspected if there is a factor VIII deficiency, normal PT and normall PTT (occasionally this disorder presents with prolonged PTT that is corrected with mixing study)?

A

VWF disease

45
Q

What causes bleeding in Von Willebrand Disease?

A
  • Decreased platelet adhesion causes bleeding

* Decrease in VIII half like usually does not cause enough of a deficiency to cause bleeding

46
Q

If the PT is prolonged and the PTT is normal, which pathway(s) are affected?

A

• Extrinsic (if PTT is normal than common is fine)

47
Q

If the PT is prolonged but you do not know the status of the PTT, which pathway(s) could be affected?

A

• Extrinsic or common

48
Q

If the PTT is prolonged but you do not know the status of the PT, which pathway(s) could be affected?

A

• Intrinsic or common

49
Q

If the PTT is prolonged and the PT is normal, which pathway(s) are affected?

A

• Intrinsic (if PT is normal than common is fine)

50
Q

If the PT and the PTT is prolonged, which pathway is affected?

A
  • Common only

* Very unlikely to have 2 unrelated problems in the extrinsic and intrinsic present at the same time

51
Q

Should coagulation tests be performed on somebody without bleeding history?

A

• No, abnormal labs on their own are not sufficient for a disorder unless there are symptoms

52
Q

If a patient with abnormal bleeding history has normal labs, what should be done?

A

• Avoid unnecessary surgeries, but a full work up is not needed

53
Q

What ethnic group gets Hemophilia more often?

A

Hemophilia has the same risk across all ethnic groups

54
Q

Does hemophilia have to be inherited?

A

No spontaneous cases are present about 30% of the time

55
Q

Which is the most common hemophilia?

A

A

56
Q

How do levels of VIII correlate with severity of the disease in Hemophilia A?

A

5-25% = Mild

1-5% = Moderate

<1% = Severe

57
Q

What causes acquired FVIII Inhibitor?

A

Ab against VIII

Present in elderly, pregnant, people with autoimmune disorders

58
Q

When narrow down disorder to common pathway, what is the next test?

A

TT

Unit 2 SPATH UFCOM (17 decks)

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