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Hematology II > THROMBOTIC DISORDERS > Flashcards

THROMBOTIC DISORDERS Flashcards

1
Q

Is the inappropriate formation of a platelet or fibrin clot that obstructs a blood vessel

A

Thrombosis

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2
Q

Is a multifaceted disorder resulting from circulatory stasis and abnormalities in the coagulation system, coagulation control mechanisms, platelet function, the blood vessel wall, or leukocyte activation molecules

A

Thrombosis

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3
Q

Causes ischemia and necrosis

A

Thrombosis

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4
Q

Also known as hypercoagulability

A

Thrombophilia

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5
Q

Is the predisposition to thrombosis secondary
to a congenital or acquired condition

A

Thrombophilia

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6
Q

Known causes of Thrombophilia

A

• Physical, chemical, or biological events.
• Uncontrolled platelet activation and blood coagulation system activation.
• Blood coagulation control protein deficiencies. • Uncontrolled suppression of fibrinolysis

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7
Q

Confer a risk of venous/arterial thrombosis (a condition called

A

antiphospholipid syndrome or APS

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8
Q

A cardinal sign of APML is DIC secondary to the release of procoagulant granule contents from malignant promyelocytes

A

Myeloproliferative neoplasms

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9
Q

Caused by stem cell mutation that modifies membrane-anchored platelet activation suppressors

A

PNH

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10
Q

most common inherited thrombosis risk factor

A

FVL gene mutation

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11
Q

second most common inherited thrombophilia in patients with a personal and family history of deep vein thrombosis

A

Prothrombin G20210A gene mutation

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12
Q

Thrombosis is often associated with a combination of genetic defect, disease, and lifestyle influences

A

Thrombosis Double Hit

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13
Q

Laboratory Evaluation of Thrombophilia

A

1.
Antiphospholipid antibodies (LAC, ACL, and Anti-B2-GPI)
Activated protein C resistance and Factor V 2.
Leiden mutation Prothrombin G20210A 3.
4. Antithrombin
5. Protein C control pathway

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14
Q

Comprise a family of immunoglobulins that bind protein-phospholipid complexes

A

Antiphospholipid Antibodies

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15
Q

APLAs arise as what immunoglobulin

A

IgG or IgG

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16
Q

Antiphospholipid Antibodies are sometimes called

A

Nonspecific inhibitors

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17
Q

the plasma protein most often bound
to APLAs

A

B2-GPI

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18
Q

Most APLAs arise in response to a bacterial, viral, fungal, or parasitic infection or to treatment with one of a variety of drugs

A

Transient alloimmune APLAs

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19
Q

autoantibodies that arise in collagen vascular diseases, SLE, RA, scleroderma, and Sjogren’s syndrome

A

Aitoimmune APLA

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20
Q

sign of occult adenocarcinoma such as cancer of the pancreas or colon.

A

Migratory thrombophlebitis, or Trousseau syndrome

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21
Q

creates protein imbalances that lead to thrombosis through loss of plasma proteins such as antithrom- bin.

A

Nephrotic Syndrome

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22
Q

throm- botic event occurs in young adults; occurs in unusual sites such as the mesenteric, renal, or axillary veins; is recurrent; or occurs in a patient with a family history of thrombosis (Table 39.3). Because thrombosis is multifactorial, however, even patients with congenital thrombophilia are most likely to experience thrombotic events because of a combination of constitutional and acquired conditions.

A

Congenital Thrombosis Risk Factors

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23
Q

inadequate dietary folate, vitamin B6, or vitamin B12 levels and with polymorphisms affected the function of methylene tetrahydrofolate reductase (MTHFR) in the methionine metabolic pathway.

A

antithrombin

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24
Q

may exist in the absence of the FVL mutation and is occasionally acquired in pregnancy or in association with oral contraceptive therapy

A

APC Resistance

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25
Q

most common inherited thrombosis risk factor,

A

FVL gene mutation

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26
Q

mutation is the second most common inherited thrombophilia in patients with a personal and family history of deep vein thrombosis.

A

prothrombin G20210A

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27
Q

associated with a combination of genetic defect, disease, and lifestyle influences.

A

Thrombosis Double Hit

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28
Q

Antiphospholipid antibodies

A

comprise a family of immuno- globulins that bind protein-phospholipid complexes.

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29
Q

detected by clot-based profiles;

A

APLAs include LACs

30
Q

detected by immunoassay

A

ACL and anti-!2-GPI antibodies,

31
Q

nonspecific inhibitors

A

Because they may bind a variety of protein-phospholipid complexes, they are sometimes

32
Q

Clot-based screen employs PTT with factor V-depleted plasma.

A

APC RESISTANCE

33
Q

Measured by molecular assay

A

Factor V Leiden mutation* Prothrombin G20210A*

34
Q

Two clot based assays for LAC profile

A

DRVVT
PTT

35
Q

Immunoassay for immunoglobulins of APL family. ACL depends on B2-GPI in reaction mix.

A

ACL antibody

36
Q

Immunoassay for an immunoglobulin of APL family. B2-GPI is key phospholipid-binding protein in family.

A

Anti-B2-GPI antibody*

37
Q

Digests VIIIa and Va. When consistently below reference limit, follow up with PC antigen assay.

A

PC ACTIVITY

38
Q

Serine protease inhibitor suppresses IIa (thrombin), IXa, Xa, XIa. When consistently below reference limit, follow up with AT antigen assay.

A

AT activity

39
Q

Digests VIIIa and Va. When consistently below reference limit, follow up with PC antigen assay.

A

PC activity

40
Q

PC cofactor. When consistently below reference limit, follow up with total and free PS antigen assay, C4b-binding protein assay.

A

PS activity

41
Q

includes a means for detecting unfraction- ated heparin (UFH),

A

MIXING STUDY

42
Q

heparinase

A

Neutralize heparin, although this may be unnecessary because many LAC detection reagents provide heparin-neutralizing poly- brene.

43
Q

In performing mixing studies, the laboratory professional employs only

A

PPP

44
Q

considered the more specific of the LAC assays

A

DRVVT

45
Q

Confirms LAC by mixing an aliquot of the patient specimen with the

A

RVVT high-phospholipid confirmatory reagent,

46
Q
A

If the primary reagent result is prolonged over the DRVVT confirm reagent result by a prede- termined ratio or more, typically 1.2, LAC is confirmed.

47
Q

immunoassay that is not affected by anticoagulant therapy, current thrombosis, or factor deficiencies.

A

ACL TEST (anti)

48
Q

in performing mixing studies, the laboratory professional employ

A

PPP

49
Q

to detect APL antibodies specific for phosphatidylserine or prothrombin.

A

antiphosphatidylserine and anti- prothrombin immunoassays

50
Q

mutation in the factor V

A

substitutes glutamine for arginine at position 506 of the factor V molecule (FV R506Q)

51
Q

factor V R506Q mutation is named for the city

A

The Netherlands in which Bertina first described it, Leiden

52
Q

factor V Leiden [FVL] mutation,

A

APC RESISTANCE

53
Q

chromogenic substrate test

A

detects quantitative and qualitative AT deficiencies and detects mutations affecting the proteolytic site but not the heparin binding site.

54
Q

turbidometric micropar- ticle immunoassay

A

turbidometric micropar- ticle immunoassay

55
Q

uses a suspension of latex microbeads coated with antibody to antithrombin

A

Turbidometric micropar- ticle immunoassay

56
Q

AT concentration is directly proportional to the rate of light absorption change. I LOVE JHOPE

A
57
Q

detect both quantitative and qualitative PC deficiencies.

A

Clot-based or chromogenic functional assays

58
Q

protein c assay venom

A

Agkistrodon contortrix

59
Q

The interval to clot formation is proportional to PS activity ( i love jhope

A
60
Q

APC resistance, LAC, and the presence of the therapeutic direct thrombin in- hibitors

A

argatroban or dabigatran

61
Q

lipoprotein can be measured by

A

EIA

62
Q

Naturally occurring sulfur-containing amino acid intermediate in the metabolism of dietary methionine.

A

HOMOCYSTEINE

63
Q

Which comprises DVT and PE, is the third most common thrombotic disease,

A

Venous Thromboembolic Disease

64
Q

Often the sufferer first misidentifies DVT as

A

muscle strain or charles horse

65
Q

reference method for Pulmonary Embolism

A

multislice” or spiral chest computed tomography (CT) angiography

66
Q

generalized and uncontrolled hemostasis activation secondary to a systemic disorder.

A

DIC

67
Q

BLACK DEATH

A

DIC

68
Q

is the consequence of an immune response to UFH (standard intravenous heparin) and LMWH that is reflected in a reduced platelet count

A

heparin-induced thrombocytopenia

69
Q

heparin induced thrombocytopenia antibodies are specific for

A

platelet factor 4 complexed woth heparin

70
Q

hapten that triggers immune production of IgG isotype anti-H:PF4 anti- bodies that now bind the H:PF4, targeting a neoepitope on PF4 that is expressed with heparin binding.

A

H:PF4

71
Q

pF4 is a positively charged tetrameric protein stored in

A

alpha granules

72
Q
A

Hematology II (17 decks)

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