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🩸Hema🎀 > 7.1: Disorders of the Coagulation System > Flashcards

7.1: Disorders of the Coagulation System Flashcards

1
Q

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

A

Coagulopathy

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2
Q

Accounts for most instances of fatal hemorrhage

A

Trauma-Induced Coagulopathy

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3
Q

Is triggered by the combination of injury-related acute inflammation, hypothermia, acidosis, and hypoperfusion (elements of systemic shock)

A

Trauma-Induced Coagulopathy

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4
Q

Resembles the pathophysiology of TTP

A

Trauma-Induced Coagulopathy

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5
Q

Is defined as:
- Blood loss exceeding total blood volume within 24 hours
- Loss of 50% blood volume within a 3 hour period
- Blood loss exceeding 150 mL/min
- Blood loss that necessitates plasma and platelet transfusions

A

Massive Hemorrhage

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6
Q

is the key TIC management component

A

Plasma

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7
Q

Liver Disease Coagulopathy:

are a complication of chronic alcohol cirrhosis

A

Esophageal varices

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8
Q

Liver Disease Coagulopathy:

occurs in liver disease associated thrombocytopenia

A

Mucocutaneous bleeding

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9
Q

Liver Disease Coagulopathy:

is the consequence of procoagulant dysfunction and deficiency

A

Anatomic bleeding

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10
Q

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

A

Factor VII

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11
Q

is a more specific marker of liver disease than deficient factors II, VII, IX, and X (used in conjunction with the factor VII assay

A

Factor V

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12
Q

fibrinogen is coated with excessive sialic acid (in moderately to severely diseased liver)

A

Dysfibrinogenemia

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13
Q

fibrinogen may fall to this level in end-stage liver disease

A

<100 mg/dL

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14
Q

Treatment to Resolve Liver Disease-Related Hemorrhage

A
  1. Oral or intravenous vitamin K therapy
  2. Plasma transfusion
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15
Q

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

A

Chronic Renal Failure and Hemorrhage

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16
Q

Fibrin deposits in renal microvasculature reduce glomerular function

A

Chronic Renal Failure and Hemorrhage

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17
Q

Guanidinosuccinic acid or phenolic compounds coat the platelets

A

Chronic Renal Failure and Hemorrhage

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18
Q

What have been detected in urine in Nephrotic Syndrome and Hemorrhage

A

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

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19
Q

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

A

Warfarin (Coumadin)

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20
Q

the most common acquired autoantibodies

A

Autoanti-factor VIII

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21
Q

Factor Inhibitors other than Autoanti-factor VIII:

develop aslupus anticoagulant

A

Antiprothrombin antibodies

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22
Q

Factor Inhibitors other than Autoanti-factor VIII:

documented in patients receiving isoniazid treatment for tuberculosis

A

Autoanti-factor XIII

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23
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

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24
Q

Factor Inhibitors other than Autoanti-factor VIII:

in amyloidosis

A

Autoanti-factor X

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25
Leads to decreased platelet adhesion to injure vessel walls
von Willebrand Disease
26
vWF gene: supports the receptor site for collagen and GP Ib/IX/V
Domain A
27
vWF gene: provides a site that binds GP IIb/IIIA
Domain C
28
vWF gene: provides the carrier site for factor VIII
Domain D
29
Quantitative vWF deficiency
Type 1 von Willebrand Disease
30
Qualitative vWF deficiency
Type 2 von Willebrand Disease
31
Type 2 von Willebrand Disease Arises from an autosomal dominant point mutations in A2 and D1 structural domains of the vWF molecule
Subtype 2A
32
Type 2 von Willebrand Disease vWF is susceptible to ADAMTS-13
Subtype 2A
33
Type 2 von Willebrand Disease Mutations within the A1 domain
Subtype 2B
34
Type 2 von Willebrand Disease Raised affinity to GP Ib/IX/IV
Subtype 2B
35
Type 2 von Willebrand Disease “Gain-of-function” mutation
Subtype 2B
36
Type 2 von Willebrand Disease HMW-VWF multimers spontaneously bind to resting platelet
Subtype 2B
37
Type 2 von Willebrand Disease a platelet mutation that raises GP Ib affinity for normal HMW-VWF multimers
Subtype 2B, Platelet-type vWD (PT-VWD) or pseudo-vWD
38
Type 2 von Willebrand Disease Possess poor platelet receptor binding despite generating a normal multimeric distribution pattern in electrophoresis
Subtype 2M
39
Type 2 von Willebrand Disease Missence mutation in the D9 domain impairs the protein’s factor VIII binding site
Subtype 2N
40
Type 2 von Willebrand Disease Factor VIII deficiency despite a normal vWF antigen concentration assay result, normal vWF activity, and a normal multimeric pattern
Subtype 2N
41
Type 2 von Willebrand Disease Also known as Autosomal Hemophilia
Subtype 2N
42
Subtype 2N is also known as
Normandy Variant
43
“Null allele” vWF gene translation or deletion mutations
Type 3 von Willebrand Disease
44
Is the most rare form of vWD
Type 3 von Willebrand Disease
45
Partial quantitative deficiency of vWF
1
46
Qualitative deficiency of vWF
2
47
Decreased platelet-dependent vWF function and selective deficiency of high molecular weight multimers
2A
48
Increased affinity to platelet glycoprotein1B
2B
49
Decreased platelet dependent vWF function with high molecular weight multimers present
2M
50
Markedly decreased binding of factor VIII to vWF
2N
51
Complete deficiency of vWF
3
52
Standard VWD test panel
A. VWF:Ag (quantitative) B. VWF:RCo assay C. Factor VIII assay
53
Standard VWD test panel: Most prominent member of the primary VWD laboratory profile
VWF:Ag (quantitative)
54
Standard VWD test panel: Uses Ristocetin and it unfolds the VWF molecule and reduces repelling negative charges, enabling HMW-VWF multimers to bind reagent platelet membrane GP Ib/IX/V receptors
VWF:RCo assay
55
Standard VWD test panel: May parallel VWF:Ag in subtypes 2A, 2B, and 2M, but are markedly reduced in subtype 2N.
Factor VIII assay
56
Von Willebrand Disease Treatment:
- PRICE (protection, rest, ice, compression, elevation)
57
are congenital single-factor deficiencies marked by anatomic soft tissue bleeding
Hemophilias
58
used to detect female carriers of hemophilia A
Ratio of FVIII activity to VWF:Ag concentration
59
Also called Christmas disease
Hemophilia B
60
Also called Rosenthal syndrome, Factor XI deficiency
Hemophilia C
61
More than half of the cases have been described in Ashkenazi Jews
Hemophilia C
62
patients form weak (non-crosslinked) clots that dissolve within 2 hours when suspended in 5M Urea solution (traditional factor XIII assay)
Factor XIII Deficiency
63
Give the INHERITED COAGULOPATHIES and ACQUIRED COAGULOPATHIES of this clotting factor: Factor I
INHERITED COAGULOPATHIES: - Afibrinogenemia - Dysfibrinogenemia ACQUIRED COAGULOPATHIES: - Severe liver disease - DIC - Fibrinolysis
64
Give the INHERITED COAGULOPATHIES and ACQUIRED COAGULOPATHIES of this clotting factor: Factor II
INHERITED COAGULOPATHIES: - Prothrombin deficiency ACQUIRED COAGULOPATHIES: - Liver disease - Vitamin K deficiency - Anticoagulant therapy
65
Give the INHERITED COAGULOPATHIES and ACQUIRED COAGULOPATHIES of this clotting factor: Factor V
INHERITED COAGULOPATHIES: - Factor V deficiency (Owren’s disease/Parahemophilia) ACQUIRED COAGULOPATHIES: - Severe liver disease - DIC - Fibrinolysis
66
Give the INHERITED COAGULOPATHIES and ACQUIRED COAGULOPATHIES of this clotting factor: Factor VII
INHERITED COAGULOPATHIES: - Factor VII deficiency ACQUIRED COAGULOPATHIES: - Liver disease - Vitamin K deficiency - Anticoagulant therapy
67
Give the INHERITED COAGULOPATHIES and ACQUIRED COAGULOPATHIES of this clotting factor: Factor VIII
INHERITED COAGULOPATHIES: - Hemophilia A - vWD ACQUIRED COAGULOPATHIES: - DIC - Fibrinolysis
68

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