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HEMA 256 MB > Module 4: Disorders of Hemostasis (from review- Coagulation disorders) > Flashcards

Module 4: Disorders of Hemostasis (from review- Coagulation disorders) Flashcards

1
Q

coagulation disorders are due to (4)

A

Failure of synthesis
Production of abnormal molecules
Excessive destruction or consumption of factors
Inactivation of factor by circulating anticoagulants

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2
Q

Screening tests

A

PT

PTT

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3
Q

PT test is for which factors

A

Extrinsic
Factors II, V, VII, X, I

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4
Q

PTT test is for which factors

A

Intrinsic
All factors except III, VII, XIII

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5
Q

Inherited disorders

A

all factors can be deficient

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6
Q

3 common inherited disorders

A 
Hemophilia A (factor VIIIc)
Hemophilia B (factor IX), christmas disease
Von Willebrands Disease
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7
Q

Severity of bleeds %

A

For factors IX, VIII, X, V, II, I

Severe

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8
Q

What factors cause a marked prolonged PTT but no clinical bleeding (3)

A

XII, HMWK, PK

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9
Q

What factors cause a disproportionate mild bleed (2)

A

XI, VII

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10
Q

What factors cause a disproportionate severe bleed (1)

A

XIII

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11
Q

Normal male and normal female

A

children all normal unless there is a mutation

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12
Q

Normal male and carrier female (undiagnosed)

A

most common combination which perpetuates the disease

produces XhX, XX, XhY, XY

50% normal (male and female)
25% carriers (female)
25% hemophiliacs (male)

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13
Q

What is the most common bleeding disorder

A

von willebrands disease

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14
Q

what is the most common hemophilia

A

Hemophilia A

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15
Q

Hemophilia A

A

Factor deficient: VIIIc
Gene affected: Xq28
Therapy: factor VIII infusion
Complication: development of immune VIII antibodies

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16
Q

Hemophilia B

A

Factor deficient: IX
Gene affected:Xq27
Therapy: Prothrombin group concentrate or IX concentrate

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17
Q

Which hemophilia therapy lasts longer and why

A

IX because of its longer half-life

Therapy is given less often which reduced the chance of developing antibodies against the therapy

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18
Q

What type of disorder is Von Willebrands disease

A

platelet adhesion

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19
Q

von Willebrands Disease

A

What chromosome is affected: 12
Treatment: VIII concentrate
Tests for workup: Plt agglutination with ristocetin, plt aggregation with ristocetin (reduced)

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20
Q

3 types of von Willebrands Disease

A

Type 1 (most common)
Type 2
Type 3

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21
Q

Lab findings for Hemophilia A

A

Plt count: normal
Bleeding time: normal
PT: normal
PTT: prolonged

22
Q

Lab findings for Hemophilia B

A

Plt count: normal
Bleeding time: normal
PT: normal
PTT: prolonged

23
Q

Lab findings for von Willebrands Disease, Type 1

A

Plt count: normal
Bleeding time: usually prolonged
PT: normal
PTT: usually normal but may be prolonged

24
Q

Acquired coagulation deficiencies (5 types)

A 
Much more common than inherited
Circulating abnormal anticoagulants and antifactors
Vitamin K deficiency
Liver Disease
DIC
Disorders of Fibrinolysis
25
Q

Circulating abnormal anticoagulants and antifactors

A

A) specific factor antibodies
B) non-specific inhibitors “antiphospholipid antibody”
-Lupus anticoagulant
-Anticardiolipin antibody

Test used to differentiate deficiency from circulating anticoagulants or antifactors: mixing study

26
Q

Vitamin K deficiency

A

factors are not caboxylated and cannot bind calcium
Factors involved: Prothrombin group (II, VII, IX, X) and Protein C and S

PIVKA stands for: Proteins induced by vitamin K absence = non carboxylated, inactive abnormal prothrombin factor molecules

Oral anticoagulant: Warfarin (Coumadin)

27
Q

Liver Disease

A

reduced production in diseased hepatic cells

Factors involved: II, VII, IX, X, V, I

28
Q

2 liver disorders that affect coagulation

A

Obstructive jaundice :cannot absorb Vitamin K

Severe hepatitis: Damaged cells produce less factor

29
Q

3 things destruction of liver cells may result in

A

DIC: coagulation factors are not removed
Released increased amounts of tPA from hepatic cell triggering fibrinolysis
Spenomegaly, increasing splenic sequestering of platelets

30
Q

DIC results in

A

widespread intravascular coagulation and secondary fibrinolysis

Results in: consumption and destruction of coag factors until they are deficient; thrombocytopenia; abnormal bleeding

31
Q

causes of DIC

A

any situation which causes exposure of a lot of foreign surfaces to the blood, or the widespread release of coagulation activators (FIII) or activators of fibrinolysis

32
Q

DIC laboratory findings should confirm (4)

A

activation of coagulation
activation of fibrinolysis
inhibitor consumption
end organ damage or failure

33
Q

Main lab results for DIC

A 
Factor deficiencies (cause prolonged PT/PTT)
Thrombocytopenia
Increased fdp, FDP
Increased D-dimer
Schistocytes (broken up RBC)
34
Q

Disorders of fibrinolysis

A

Primary: activation of fibrinolysis in the absence of coagulation

Secondary: whenever fibrin is deposited as normal (but if abnormal DIC)

Therapeutic: injection of direct plasminogen activators

Impaired Fibrinolysis: due to decreased production, increased destruction or increased inhibition of plasminogen, plasminogen activators or plasmin

35
Q

Differentiate primary from secondary fibrinolysis

A

Fibrinogen degradation product test:
Primary = pos
Secondary = pos

D dimer test: Fibrin degradation products:
Primary = NEG
secondary = pos

36
Q

Thrombosis is

A

abnormal formation in circulation of solid, localized masses of fibrin and/or platelets that cause partial or complete blockage of vessels

37
Q

Thromboembolism

A

thrombi break away and block smaller vessels

38
Q

pulmonary embolism is

A

obstruction of pulmonary artery or branch of

Usually from DVT (deep vein thrombosis)

39
Q

3 factors involved in forming a thrombus are

A

slowed blood flow
hypercoagulability
vessel wall damage

40
Q

thrombi

A

multiple blood clots

41
Q

thrombus

A

single blood clot

42
Q

Inherited disorders

A 
Factor V leiden gene mutation (protein C resistance)
Antithrombin III
Protein C or S deficiency
Homocysteinuria
Dysfibrinogenemia
Abnormal plasminogen
Prothrombin G20210A Variant
43
Q

What immune condition is an acquired coagulation deficiency and also an acquired disorder that promotes thrombosis

A

lupus anticoagulant

44
Q

Factor V Leiden gene mutation (protein C resistance)

A

most common cause of increased risk of venous thrombosis
Produce an abnormal factor V molecule that resists the action of activated protein C, thus the factor is inappropriately maintained in an active form and therefore continues to promote coagulation

45
Q

Antithrombin III

A

normally works with heparin to inhibit factors

Inadequate inhibition of thrombin, Xa and IXa

46
Q

Protein C or S deficiency

A

inadequate inhibition of V and VIII

impaired activation of fibrinolysis because activated protein C inhibits antiplasmin

47
Q

Homocysteinuria

A

damaged endothelium by deposits of amino acid causes activation of coagulation and atherosclerosis

48
Q

Dysfibrinogenemia

A

abnormal fibrinogen makes abnormal fibrin that will not neutralize thrombin

49
Q

Abnormal plasminogen

A

impaired formation of plasmin

50
Q

Prothrombin G20210A variant

A

abnormal allele of II = increased II levels = increased thrombosis

HEMA 256 MB (9 decks)

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