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Hematology 2 > Coagulation System (Part II) > Flashcards

Coagulation System (Part II) Flashcards

1
Q

Must be tested within 24 hours of the time of collection

A

PT

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2
Q

Must be tested within 4 hours of the time of
collection

A

APTT

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3
Q

PT reagents (or thromboplastin, tissue thromboplastin) consists of:

A

tissue factor
phospholipids
calcium chloride.

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4
Q

It is most sensitive to factor VII deficiencies

A

Prothrombin Time (PT)

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5
Q

Is used most often to monitor the e ects of
therapy with Coumadin

A

Prothrombin Time (PT)

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6
Q

Prolonged PT results in:

A

• DIC
• Liver disease
• Vitamin K deficienc

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7
Q

Is employed to monitor the e ects of UFH and to detect LAC and specific coagulation factor antibodies (anti-factor VIII antibody)

A

Partial Thromboplastin Time (APTT)

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8
Q

Is prolonged in all congenital and acquired procoagulant deficiencies (except VII and XIII)

A

Partial Thromboplastin Time (APTT)

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9
Q

PTT Negatively charged particulate activator

A

kaolin, ellagic acid, silica, or celite

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10
Q

PTT Is prolonged when there is a deficiency of one or more of the following coagulation factors:

A

• II, V, VIII, IX, X, XI, XII
• I (if <100 mg/dL)

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11
Q

Most common deficiencies of PTT

A

• Factor VIII (Hemophilia A)
• Factor IX (Hemophilia B)
• Factor XI (Rosenthal syndrome)

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12
Q

Distinguish LACs from specific inhibitors and factor deficiencies

A

PTT Mixing Studies

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13
Q

In PTT Mixing Studies UFH may be neutralized with

A

polybrene or heparinase

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14
Q

Commercially prepared bovine thrombin reagent cleaves fibrinopeptides A and B from plasma fibrinogen to form a detectable fibrin polymer

A

Thrombin Clotting Time

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15
Q

Is used to determine whether UFH is present
whenever the PTT is prolonged

A

Thrombin Clotting Time

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16
Q

May also assess the presence of the oral direct
thrombin inhibitor dabigatran.

+ drug = markedly prolonged

A

Thrombin Clotting Time

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17
Q

provides quantitative measure of dabigatran

A

Plasma-diluted TCT

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18
Q

Reptilase is a thrombin-like enzyme isolated from the venom of

A

Bothrops atrox (lancehead viper)

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19
Q

Venom Activated Assays:

Cleaves fibrinopeptide A only

A

Reptilase Time

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20
Q

Venom Activated Assays:

Useful for detecting hypofibrinogenemia or
dysfibrinogenemia

A

Reptilase Time

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21
Q

Russell Viper Venom (RVV) from the

A

Daboia russelii viper

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22
Q

Venom Activated Assays:

triggers coagulation at the level of factor X

A

Russell Viper Venom Test

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23
Q

List the Coagulation Factor Assays

A
  1. Fibrinogen Assay
  2. Single-Factor Assays using the PTT
  3. Nijmegen-Bethesda Assay
  4. Single-Factor Assays using the PT
  5. Factor XIII Assay
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24
Q

Clot-based method of Clauss

A

Fibrinogen Assay

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25
Q

• A modification of TCT
•Is the recommended procedure for estimating fibrinogen function

A

Fibrinogen Assay

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26
Q

Reagents of Fibrinogen Assay

A

• Owren bu er
• Bovine thrombin

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27
Q

Explain what happened in Single-Factor Assay using the PTT

A

● Factor VIII-depleted PPP (alone): ➡️ prolonged PTT
● Factor VIII-depleted PPP + Normal patient plasma: ➡️ PTT reverts to normal
● Factor VIII-depleted PPP + Factor VIII-deficient patient plasma: ➡️prolonged

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28
Q

Confirms and quantifies anti-factor VIII inhibitor (typically IgG4-class immunoglobulin)

A

Nijmegen-Bethesda Assay

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29
Q

The principles and procedures described in the section on single-factor assay using the PTT system may be applied except that PT reagent replaces the PTT reagent in the test system, and the PT protocol is followed

A

Single Factor Assays using the PT

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30
Q

is defined as any single or multiple coagulation factor or platelet deficiency

A

Coagulopathy

31
Q

Accounts for most instances of fatal hemorrhage

A

Trauma-Induced Coagulopathy

32
Q

Resembles the pathophysiology of TTP

A

Trauma-Induced Coagulopathy

33
Q

TIC Management

A

✅ Plasma
✅ FP-24
✅ VWF and Factors V and VIII activities decline to approximately 60% after 5 days of refrigerator storage

34
Q

the key TIC management component

A

Plasma

35
Q

alters the production of the Vitamin K-dependent factors

A

Liver Disease Coagulopathy: Procoagulant deficiency

36
Q

In Liver Disease Coagulopathy: Procoagulant deficiency this serves as the sensitive early marker

A

Factor VII

37
Q

In Liver Disease Coagulopathy: Procoagulant deficiency this is a more specific marker of liver
disease

A

Factor V

38
Q

During Dysfibrinogenemia, the fibrin is coated with excessive

A

sialic acid

39
Q

Treatment to Resolve Liver Disease-Related Hemorrhage

A
  1. Oral or intravenous vitamin K therapy
  2. Plasma transfusion
40
Q

Is often associated with platelet dysfunction and mild to moderate mucocutaneous bleeding (anemia and thrombocytopenia)

A

Chronic Renal Failure and Hemorrhage

41
Q

In Chronic Renal Failure and Hemorrhage this coat the platelets

A

Guanidinosuccinic acid or phenolic compounds

42
Q

is a state of increased glomerular permeability associated with a variety of conditions

A

Nephrotic syndrome

43
Q

In Nephrotic syndrome, what are detected in the urine

A

factors II, VII, IX, X, XII,
antithrombin,
protein C

44
Q

Vitamin K Antagonists

A

Warfarin (Coumadin)
Coumadin overdose:
PIVKA factors

45
Q

disrupts the vitamin K epoxide reductase and vitamin K quinone reductase reactions

A

Warfarin (Coumadin)

46
Q

the single most common reason for hemorrhage-associated emergency department visits

A

Coumadin overdose

47
Q

the most common acquired autoantibodies

A

Autoanti-factor VIII

48
Q

Factor Inhibitors other than Autoanti-factor VIII

A
  1. Antiprothrombin antibodies
  2. Autoanti-factor XIII
  3. Autoantibodies to factor V
  4. Autoanti-factor X
49
Q

Factor Inhibitors other than Autoanti-factor VIII

Develop as lupus anticoagulant

A

Antiprothrombin antibodies

50
Q

Factor Inhibitors other than Autoanti-factor VIII

Documented in patients receiving isoniazid
treatment for tuberculosis

A

Autoanti-factor XIII

51
Q

Factor Inhibitors other than Autoanti-factor VIII

May arise spontaneously in autoimmune disorders and after exposure to bovine thrombin in fibrin glue

A

Autoantibodies to factor V

52
Q

Factor Inhibitors other than Autoanti-factor VIII

In amyloidosis

A

Autoanti-factor X

53
Q

The most prevalent inherited mucocutaneous bleeding disorder

A

von Willebrand Disease

54
Q

Leads to decreased platelet adhesion to injure vessel walls

A

von Willebrand Disease

55
Q

Describe the 3 domains in vWF

A

Domain A: supports the receptor site for collagen and GP Ib/IX/V
Domain C: provides a site that binds GP IIb/IIIA Domain D: provides the carrier site for factor VIII

56
Q

● Caused by autosomal dominant frameshifts, nonsense mutations, or deletions
● Comprises 40-70% of vWD cases

A

Type 1 von Willebrand Disease

57
Q

Arises from an autosomal dominant point mutations in A2 and D1 structural domains of the vWF molecule

A

Subtype 2A

58
Q

VWF is susceptible to ADAMTS-13

A

Subtype 2A

59
Q

Mutations within the A1 domain

A

Subtype 2B

60
Q

Raised a nity to GP Ib/IX/V

A

Subtype 2B

61
Q

“gain-of-function” mutation

A

Subtype 2B

62
Q

A platelet mutation that raises GP Ib a nity for normal HMW-VWF multimers

A

Platelet-type vWD (PT-VWD) or pseudo-VWD under Subtype 2B

63
Q

Possesses poor platelet receptor binding despite generating a normal multimeric distribution pattern in electrophoresis

A

Subtype 2M

64
Q

Missense mutation in the D9 domain impairs the protein’s factor VIII binding site

A

Subtype 2N

65
Q

Factor VIII deficiency despite a normal VWF antigen concentration assay result, normal VWF activity, and a normal multimeric pattern

A

Subtype 2N

66
Q

Subtype 2N is also known as

A

Autosomal Hemophilia

67
Q

“Null allele” VWF gene translation or deletion mutations

A

Type 3 von Willebrand Disease

68
Q

Is the most rare form of VWD

A

Type 3 von Willebrand Disease

69
Q

Von Willebrand Disease Treatment

A

PRICE
(protection, rest, ice, compression, elevation)

70
Q

Also called Christmas disease

A

Hemophilia B

71
Q

Also called Rosenthal syndrome, Factor XI deficiency

A

Hemophilia C

72
Q

More than half of the cases have been described in Ashkenazi Jews

A

Hemophilia C

73
Q

an e ective form of therapy of Factor V Deficiency

A

Platelet concentrate

Hematology 2 (18 decks)

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