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Hematology 2 > FINALS - LABORATORY > Flashcards

FINALS - LABORATORY Flashcards

1
Q
  • serve the important function of regulating the coagulation process to avoid unnecessary blood clotting
A

Control Proteins

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2
Q

the substrate for the enzymatic action of thrombin, the primary enzyme of the coagulation system.

A
  • fibrinogen
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3
Q

Consumed during the process of coagulation

  • Calcium dependent
  • Vitamin K independent
A

Fibrinogen Group - I, V, VIII, XIII

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4
Q

Adsorbable and affected by coumadin (PIVKAS)

  • Calcium and vitamin K dependent
  • Inhibited by warfarin
A

Prothrombin Group - II, VII, IX, X

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5
Q

Not consumed during the process of coagulation
- Calcium and vitamin k independent
Involved in intrinsic coagulation pathway

A

Contact Group - XI, XII, PK, HMWK

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6
Q

Intrinsic pathway

- Reaction system that begins with

A

FXII

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7
Q

makes up TF

A

Fibroblast and EDc

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8
Q

activates plasminogen to plasmin

A

TPA and UPA

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9
Q

fibrin polymer when fibrinolysed will produce

A

FDP

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10
Q

cross linked fibrin when fibrinolysed will produce

A

fragment D-dimer

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11
Q

soluble fibrin

A

fibrin polymer

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12
Q

Insoluble fibrin

A
  • cross linked fibrin
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13
Q

Intrinsic pathway tests

A

APTT and PT (intrinsic)

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14
Q

refers to extrinsic tenase complex formation and generation of small amounts of FXa, FIXa, and thrombin

A

Initiation Phase

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15
Q

1-2% normally present in blood in activated form

A

FVIIa

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16
Q

Reactions occur on the surface of the activated platelet, which now has all the components needed for coagulation

A

Propagation Phase

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17
Q

Activated by thrombin in the initiation phase bind to platelet membranes and become receptors for FXa and FIXa

A

Cofactors FVa and FVIIIa

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18
Q

Generated in the initiation phase binds to FVIIIa on the platelet membrane to form the intrinsic tenase complex IXa:VIIIa

A

FIXa

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19
Q

Coagulation Assay (Micro method)

A

Drop or Slide

Capillary Tube/Dale & Laidlaws Method

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20
Q

Coagulation Assay (Macro method)

A

Lee-White Method/Whole Blood Clotting
Single-tube method
Three-tube method (modified LWCT)

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21
Q

Is a coagulation test used to monitor low-dose heparin therapy and to screen for function of the intrinsic and common pathways of hemostasis

A

Activated Partial Thromboplastin Time (APTT)

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22
Q

the reagent used in performing the APTT

A

PARTIAL THROMBOPLASTIN: liquid portion of tissue thromboplastin

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23
Q
  • Manufactured from rabbit or bovine brain tissues as well as from vegetable sources such as soybeans (bovine-cow, porcine-pig)
  • Performs the function of platelet factor 3 (PF3) in the APTT test
  • Contains activators such as: kaolin or silica to activate the contact factors in the intrinsic pathway
A

Partial Thromboplastin Reagent

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24
Q

2nd reagent used in the test and is added to supply the ionized calcium required to activate prothrombin in the common pathway

A

Calcium Chloride (CaCl2)

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25
Q
  • Early coagulation test developed by Dr. A.J. Quick
  • Evaluates the function of Extrinsic and common pathway
  • Major use: monitor warfarin (coumadin) anticoagulant therapy
A

Prothrombin Time (PT) Test

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26
Q

Pre-surgery coagulation screening test

A

Prothrombin Time (PT) Test

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27
Q

vitamin K antagonist, which means it blocks the action of vitamin K, prolongs prothrombin time

A

Warfarin

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28
Q

APTT Reference value

A

20-35 seconds

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29
Q

PT Reference value

A

10-13 seconds

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30
Q
  • assigned by the manufacturer to each reagent lot is used with the prothrombin time to calculate the INR
A

International Sensitivity Index (ISI)-

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31
Q

Reference Value: INR

A

1.0-1.4

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32
Q

Used to measure the availability of functional fibrinogen

A

Thrombin Time (TT) Test

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33
Q

Thrombin Time (TT) Test prolonged in cases of:

A
  1. Low levels of fibrinogen
  2. Non-functional fibrinogen
  3. Presence of heparin | fibrin/fibrinogen products | thrombolytic agents
    (streptokinase)
34
Q

determines the rate of thrombin-induced cleavage of fibrinogen to fibrin monomers and the subsequent polymerization of hydrogen-bonded fibrin polymers

A

Thrombin Time (TT) Test

35
Q

Mixing Studies also known as

A

Circulating Anticoagulant Screen

screening for circulating inhibitor

36
Q

indicated when the APTT is prolonged in the absence of heparin therapy

A

APTT mixing study

37
Q

can be used to identify specific coagulation factor deficiencies

A

Substitution studies

38
Q

Substitution studies may be performed using

A

adsorbed plasma and

aged serum with the APTT

39
Q

APTT (ABNORMAL)

Associated with bleeding

A

VIII, IX and XI defects

40
Q

APTT (ABNORMAL)

Not associated with bleeding

A

XII, prekallikrein (PK), HMWK, lupus anticoagulants

41
Q

PT (ABNORMAL)

A

Factor VII defects

42
Q

APTT & PT (ABNORMAL)

A

Medical conditions: Anticoagulants, DIC, liver disease, vitamin K deficiency, massive transfusion
Rarely dysfibrinogenemia: factor X, V and II defects

43
Q

What deficiency
Hemophilia A
Most common severe congenital bleeding disorder in patients with VWD

A

Factor VIII deficiency

44
Q

What disease
Unique VWF abnormality: missense mutation in VWF that impairs its capacity to bind to and promote FVIII secretion into plasma

A

Von Willebrand Disease “Normandy” | Type 2n

45
Q

Hemophilia B/Christmas disease: causes a severe congenital bleeding disorder
Hemophilia B Leyden: rare form of FIX deficiency
FVIII & FIX genes- located on the X chromosome, x-linked recessive disorders primarily affecting males, females carrying a hemophilia mutation on one of their 2 x chromosomes (carriers)
- Laboratory evaluation: APTT and PT
- Diagnosis is confirmed by: FVIII | FIX assay
- Treatment: recombinant factor products
A. Factor VIII deficiency
B. Factor IX Deficiency
C. FXII, Prekallikrein and HMWK
D. Factor XI Deficiency

A

B

46
Q 
Common in Ashkenazi Jews
- Rarely have spontaneous hemorrhage
- Bleeding typically occurs following injury or surgery
- Replacement therapy: FFP (prepared within 8 hours), PF24 (prepared within 24 hours)
A. Factor VIII deficiency
B. Factor IX Deficiency
C. FXII, Prekallikrein and HMWK
D. Factor XI Deficiency
A

D

47
Q

Associated with prolonged APTT but are not associated with any bleeding risk
- Most common, occurring in all racial and ethnic backgrounds
A. Factor VIII deficiency
B. Factor IX Deficiency
C. FXII, Prekallikrein and HMWK
D. Factor XI Deficiency

A

C

48
Q
  • Commonly acquired in association with liver disease
  • Prolonged APTT & PT: plasma concentration of protein (<100 mg/dL)
  • Replacement: cryoprecipitate
    A. Factor VIII deficiency
    B. Disorders of fibrinogen
    C. FXII, Prekallikrein and HMWK
    D. Factor II deficiency
A

B

49
Q
  • Rarest inherited coagulation factor deficiency (1:2,000,000)
  • True prothrombin deficiency (mouse) - incompatible with life after birth
    A. Factor VIII deficiency
    B. Disorders of fibrinogen
    C. FXII, Prekallikrein and HMWK
    D. Factor II deficiency
A

D

50
Q

Manifests as a concomitant reduction in prothrombin activity and antigen levels
A. Factor VIII deficiency
B. Disorders of fibrinogen
C. Hypoprothrombinemia (Type I deficiency)
D. Factor II deficiency

A

C

51
Q

presents with reduced activity and normal antigen levels
A. Dysprothrombinemia (Type II deficiency)
B. Disorders of fibrinogen
C. Hypoprothrombinemia (Type I deficiency)
D. Factor II deficiency

A

A

52
Q

-Heterozygous: asymptomatic
- Homozygous: rare | presenting in children with easy bruising and mucosal bleeding
- Prolong APTT and PT, NORMAL TT
- Confirmed by: PT reagent-based, single stage FV assay
- Replacement product: FFP
A. Dysprothrombinemia (Type II deficiency)
B. Factor V deficiency
C. Hypoprothrombinemia (Type I deficiency)
D. Factor II deficiency

A

B

53
Q

-Heterozygous: asymptomatic
- Homozygous: severe bleeding disorders that present in infancy
- Most common factor deficiency associated with primary amyloidosis
A. Dysprothrombinemia (Type II deficiency)
B. Factor V deficiency
C. Hypoprothrombinemia (Type I deficiency)
D. Factor X deficiency

A

D

54
Q

Rare autosomal recessive disorder that results from a single gene defect
Testing usually demonstrates disproportionate prolongation of the APTT compared with the PT
A. Dysprothrombinemia (Type II deficiency)
B. Factor V deficiency
C. Combined FV and FVIII deficiency
D. Factor X deficiency

A

C

55
Q
  • Affecting multiple vitamin K-dependent coagulation factors (II, VII, IX and X) occurs with vitamin K deficiency and hepatic dysfunction
  • Also results from: heritable dysfunction of hepatic enzyme y-glutamyl carboxylase (Type I)
  • Vitamin K epoxide reductase enzyme complex (Type II)
  • Diagnosis: established by prolongation of both the APTT and PT and associated reduction in levels of vitamin K-dependent clotting factors. These patients may respond to vitamin K (oral or parenteral) with normalization of the APTT, PT and factor levels, as well as resolution of bleeding symptoms.
    A. Dysprothrombinemia (Type II deficiency)
    B. Factor V deficiency
    C. Combined deficiency of vitamin-K dependent clotting factors
    D. Factor X deficiency
A

C

56
Q

Common compared with the other rare hereditary coagulation factor deficiencies
A. Dysprothrombinemia (Type II deficiency)
B. Factor V deficiency
C. Combined deficiency of vitamin-K dependent clotting factors
D. Factor VII deficiency

A

D

57
Q
  • autosomal recessive | often presenting shortly after birth, and may have dramatic presentation with intracranial hemorrhage.
    A. Dysprothrombinemia (Type II deficiency)
    B. Severe FVII deficiency
    C. Combined deficiency of vitamin-K dependent clotting factors
    D. Factor VII deficiency
A

B

58
Q

Factor XIII deficiency APTT & PT result

A

both normal

59
Q 
clot dissolves in 5M urea
A. Dysprothrombinemia (Type II deficiency)
B. Severe FVII deficiency
C. FXIII deficiency
D. Factor VII deficiency
A

C

60
Q

Activation of the coagulation and fibrinolysis systems results in the simultaneous formation of thrombin and plasmin with consumption of coagulation factors and inhibitors of the system
A. Liver disease
B. Disseminated Intravascular Coagulation (DIC)
C. Vitamin K deficiency
D. Massive transfusion

A

B

61
Q

Laboratory feature of DIC

A

a. Prolonged APTT & PT

b. Thrombocytopenia

62
Q

It is important to be recognized in patients
A. Liver disease
B. Disseminated Intravascular Coagulation (DIC)
C. Vitamin K deficiency
D. Massive transfusion

A

A

63
Q

1st protein to decreased in liver disease

A

PK

64
Q

last protein to decreased in liver disease

A

Fibrinogen

65
Q

absent in hepatic stage of live transplantation

A

FV & FVIII

66
Q

elevated in patients with inflammatory hepatocellular disease

A

FVIII

67
Q

Anti-thrombin and other serpin plasma protein inhibitors

increased or decreased in liver disease

A

decreased

68
Q

Has a critical role in the y-carboxylation reaction of a number of glutamic acid residues within coagulation factors II, VII, IX and X and proteins C, S and Z.

A

Vitamin K

69
Q

result from dilution of clotting factors, DIC, or acquired platelet dysfunction

A

Hemostatic failure

70
Q

replacement of more than 1.5 blood volume in 24 hours

A

Massive transfusion

71
Q

results from replacement with packed red blood cells and normal saline and lack of clotting factors of platelets

A

Dilutional coagulopathy

72
Q

most common severe acquired coagulation protein inhibitor is that against

A

FVIII

73
Q

associated with decreases in plasma factor X or IX as a result of adsorption of the coagulation proteins onto the amyloid protein
A. Lupus Anticoagulant or Antiphospholipid antibody
B. Systemic Amyloidosis
C. Hypergammaglobulinemic States

A

B

74
Q

Seen with multiple myeloma or waldenstrom’s macroglobulinemia (IgM) can be associated with pan-inhibitors to coagulation protein function.
A. Lupus Anticoagulant or Antiphospholipid antibody
B. Systemic Amyloidosis
C. Hypergammaglobulinemic States

A

C

75
Q

Influences coagulation protein reactions, variably interfere with APTT, less common in PT
A. Lupus Anticoagulant or Antiphospholipid antibody
B. Systemic Amyloidosis
C. Hypergammaglobulinemic States

A

A

76
Q 
Whole-blood volume less than 90% of required volume less than manufacturer specified minimum. PT and PTT are falsely prolonged
A. short draw
B. Visible hemolysis
C. Specimen clot 
D. Tourniquet application >1 minute
A

A

77
Q 
Each specimen is inspected visually before centrifugation or during analysis; even a small clot interferes with hemostasis test results
A. short draw
B. Visible hemolysis
C. Specimen clot 
D. Tourniquet application >1 minute
A

C

78
Q 
Pink or red plasma indicates in vitro activation of platelets and coagulation; unpredictable hemostasis test interference. Further, hemolysis interferes with optical endpoint coagulometer results
A. short draw
B. Visible hemolysis
C. Specimen clot 
D. Tourniquet application >1 minute
A

B

79
Q 
Optical instruments may fail to measure clots in cloudy or highly colored specimens. Interferes with chromogenic substrate methods. The practitioner must employ an electro-mechanical detection method instrument
A. short draw
B. Visible hemolysis
C. Lipemia or icterus
D. Tourniquet application >1 minute
A

C

80
Q 
Blood stasis activates endothelial cells and elevates the concentration of Von Willebrand factor and fibrinogen, falsely shortening clot-based test results
A. short draw
B. Visible hemolysis
C. Lipemia or icterus
D. Tourniquet application >1 minute
A

D

81
Q 
Storage at refrigerator temperatures causes precipitation of large Von Willebrand factor multimers, activation of coagulation factor VII, activation of platelets, and destruction of platelet integrity
A. Specimen storage at 1-6 degC
B. Visible hemolysis
C. Lipemia or icterus
D. Tourniquet application >1 minute
A

A

82
Q

Storage at above standard room temperature causes coagulation factors V and VIII to deteriorate

A. Specimen storage at 1-6 degC
B. Visible hemolysis
C. Specimen storage at >25 degC
D. Tourniquet application >1 minute

A

C

Hematology 2 (8 decks)

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