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Heme / Onc > SM_257b: Thrombophilia > Flashcards

SM_257b: Thrombophilia Flashcards

1
Q

____ is the way blood vessels, blood components, and procoagulants stop bleeding

A

Hemostasis is the way blood vessels, blood components, and procoagulants stop bleeding

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2
Q

____ is physiologic control of bleeding by clot formation

A

Coagulation is physiologic control of bleeding by clot formation

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3
Q

___ is pathological occlusion of blood vessels

A

Thrombosis is pathological occlusion of blood vessels

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4
Q

___ is increased tendency to form thrombi

A

Thrombophilia is increased tendency to form thrombi

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5
Q

____ is bleeding tendency

A

Hemophilia is bleeding tendency

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6
Q

Describe hemostatic balance

A

Hemostatic balance

  • Maintaining blood flow while preserving ability to respond to vessel injury
  • Designed to prevent clots within vessels
  • When vessel injury occurs, coagulation system is activated to prevent or lessen hemorrhage
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7
Q

Procoagulant factors include ____ and ____

A

Procoagulant factors include primary hemostasis and secondary hemostasis

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8
Q

Describe anticoagulant factors

A

Anticoagulant factors

  • Rapid pulsatile blood flow
  • Endothelial surface: non-wettable, NO, prostacyclin, ecto-ADPase, TFPI, thrombomodulin, proteoglycans
  • Natural anticoagulants
  • Fibrinolytic system
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9
Q

Coagulation is ___, ___, and ___

A

Coagulation is rapid, self-limited, and reversible

  • Cells and plasma proteins form a clot in response to vessel injury
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10
Q

Describe phases of clot formation

A

Clot formation

  1. Primary hemostasis: formation of platelet plug at site of endothelial injury, involves endothelium (collagen) / platelets / vWF
  2. Secondary hemostasis: strengthening of clot by coagulation cascade, interaction of platelets / proteins / fibrin
  3. Termination: natural anticoagulants
  4. Breakdown of clot: fibrinolysis
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11
Q

Thrombosis occurs when ___

A

Thrombosis occurs when hemostatic balance is shifted in favor of procoagulants

  • Artery: MI, stroke
  • Vein: PE, DVT
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12
Q

Virchow’s triad consists of ____, ____, and ____

A

Virchow’s triad consists of endothelial injury, alterations in normal blood flow, and hypercoagulability of blood

  • Endothelial injury: physical distribution of endothelium, disruption of balance of pro- and anti-thrombotic effects of endothelium
  • Alterations in normal blood flow: stasis, turbulence
  • Hypercoagulability of blood
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13
Q

Describe arterial thrombosis

A

Arterial thrombosis

  • High flow state
  • Typically more dependent on vascular abnormalities and more rarely a result of coagulation abnormality
  • Platelet rich thrombus (white)
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14
Q

Describe mechanisms of arterial thrombosis

A

Arterial thrombosis mechanisms

  • Injury to vessel wall (most common)
  • Embolism from other source (less common): majority from arteries, rarely “paradoxical” embolism from venous circulation
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15
Q

Describe arterial thrombus on disrupted plaque

A

Arterial thrombus on disrupted plaque

  • Many arterial thrombi form on top of disrupted atherosclerotic plaques
  • Thin fibrous cap and lipid-ruch core prone to disruption
  • Plaque rupture exposes thrombogenic material in lipid core to blood
  • Triggers platelet activation and thrombin generation
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16
Q

Describe examples of arterial thrombi

A

Arterial thrombi

  • Coronary artery: MI, unstable angina (temporary occlusion)
  • Cerebral artery: stroke, TIA (temporary occlusion)
  • Peripheral / lower extremity artery: limb ischemia / gangrene
  • Small vessel peripheral arteries: digital ischemia
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17
Q

Describe venous thrombosis

A

Venous thrombosis

  • Low flow state
  • Occurs with venous stasis: valve cusps, muscular sinuses
  • Red thrombi: contain more RBCs that accumulate on fibrin strands
  • More dependent on coagulation factors than platelets
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18
Q

Describe examples of venous thrombosis

A

Venous thrombosis

  • DVT of legs and arms
  • Pulmonary embolus
  • Portal vein thrombosis
  • Cerebral sinus thrombosis
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19
Q

Compare arterial and venous thrombsis

A

Comparison

  • Arterial thrombosis: rich in platelets (white clot), high shear, antiplatelet drugs are first-line
  • Venous: mostly fibrin and trapped RBCs with fewer platelets (red clot), low shear, anticoagulants are first-line
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20
Q

Describe loss of function inherited thrombophilias

A

Loss of function inherited thrombophilias: loss of anticoagulant activity

  • Protein C deficiency
  • Protein S deficiency
  • Antithrombin deficiency
21
Q

Describe gain of function inherited thrombophilias

A

Gain of function inherited thrombophilias: procoagulant activity

  • Factor V Leiden
  • Prothrombin gene mutation 20210
  • Increased clotting factor VIII
22
Q

Factor V Leiden results from ____

A

Factor V Leiden results from a substitution in base 1691 position 506 resulting in glutamic acid instead of the normal arginine

23
Q

Factor V Leiden mutation renders ___

A

Factor V Leiden mutation renders FVa relatively resistant to cleavage by APC

  • Factor V Leiden does not function as a cofactor for the cleavage of FVIIIa by APC
  • Persistence of activated factors V and VIII increases risk of thrombosis
24
Q

Prevalence of heterozygous Factor V Leiden is ___ than that of homozygous Factor V Leiden

A

Prevalence of heterozygous Factor V Leiden is greater than that of homozygous Factor V Leiden

(overall most commonly found in Caucasians)

25
\_\_\_\_ is the most common inherited thrombophilic mutation
Factor V Leiden is the most common inherited thrombophilic mutation * Risk for venous thrombosis, arterial thrombosis, pregnancy complications
26
Prothrombin G20210A gene mutation results in \_\_\_
Prothrombin G20210A gene mutation results in gain of function inherited thrombophilia * Heterozygous is more common than homozygous * Most common in Caucasian population
27
Prothrombin G20210A gene mutation is \_\_\_
Prothrombin G20210A gene mutation is mutation in the promoter region of gene leading to an increase in prothrombin synthesis
28
Prothrombin G20210A gene mutation leads to \_\_\_
Prothrombin G20210A gene mutation leads to increased circulating levels of prothrombin (Factor II) * Precursor to thrombin * Protects factor Xa from antithrombin * Higher levels of prothrombin result in greater inhibition of fibrinolysis by activating TAF
29
Elevated factor VII is a ___ inherited thrombophilia
Elevated factor VII is a gain of function inherited thrombophilia * Found in top decile of population * Baseline levels affected by role of FVIII as acute phase reactant
30
Describe quantitative vs qualitative loss of function thrombophilia
Quantitative vs qualitative loss of function thrombophilia * Quantitative: reduced amounts of protein * Qualitative: reduced functional activity, can have normal protein levels but abnormal function * Both can cause reduced activity levels
31
Activated protein C \_\_\_
Activated protein C inactivates factors Va and VIIIa
32
Protein S is a \_\_\_
Protein S is a co-factor of APC * Exists as a free form (1/3) and bound to C4b-binding protein (2/3): free is active form
33
Deficiencies of Protein C and Protein S shift balance toward \_\_\_
Deficiencies of Protein C and Protein S shift balance toward thrombosis * Protein C and Protein S are natural anticoagulants * Congenital: quantitative deficiency or qualitative loss * Acquired: decreased synthesis, increased consumption, increase in C4BP and resultant decrease in free Protein S
34
Homozygous Protein C or S deficiency leads to \_\_\_
Homozygous Protein C or S deficiency leads to purpura fulminans * Rare, life-threatening * Characterized by extensive tissue thrombosis and hemorrhagic skin necrosis
35
Heterozygous Protein C or S deficiency leads to \_\_\_
Heterozygous Protein C or S deficiency leads to increased risk of first thrombosis
36
Protein C or Protein S deficiency confers risk for ____ upon initiation of warfarin
Protein C or Protein S deficiency confers risk for warfarin-induced skin necrosis upon initiation of warfarin * Levels of protein C drop faster than other clotting factors inducing a transient hypercoagulable state
37
Homozygous antithrombin deficiency is \_\_\_
Homozygous antithrombin deficiency is fatal in utero
38
Antithrombin \_\_\_\_
Antithrombin binds to pentasaccharide sequence on heparin and proteoglycans, forming trimolecular complex that inactivates thrombin
39
Congenital mutations leading to antithrombin deficiency can be in \_\_\_
Congenital mutations leading to antithrombin deficiency can be in regions that inactivate thrombin or cause defects in heparin binding to decrease antithrombin deficiency * Lose natural anticoagulant activity
40
Describe when acquired antithrombin deficiency occurs
Acquired antithrombin deficiency * Prematurity * Liver disease * Nephrosis * Malnutrition * IBD * L-asparaginase * Estrogen therapy
41
Antithrombin deficiency leads to \_\_\_
Antithrombin deficiency leads to relative heparin resistance
42
Antiphospholipid antibody syndrome is \_\_\_
Antiphospholipid antibody syndrome is acquired * can be primary or secondary * Associated with arterial and venous thrombosis and pregnancy complications
43
Antiphospholipid antibody syndrome involves autoantibodies directed against ___ and \_\_\_
Antiphospholipid antibody syndrome involves autoantibodies directed against phospholipids and phospholipid binding proteins * Lupus anticoagulant, anti-beta-2 glycoprotein antibody, and anti-cardiolipin antibody * Precise pathogenesis resulting in clinical complications is unknown
44
Diagnosis of antiphospholipid antibody syndrome requires ____ and \_\_\_\_
Diagnosis of antiphospholipid antibody syndrome requires lab and clinical criteria * Positive on 2 occasions separated by at least 12 weeks
45
Describe lupus anticoagulant testing process
Lupus anticoagulant testing 1. Prolongation of clot based assay 2. Does not correct with mixing study 3. Phospholipid dependence 4. Lupus anticoagulant positive
46
Lupus anticoagulant testing can be falsely positive in setting of \_\_\_\_
Lupus anticoagulant testing can be falsely positive in setting of anticoagulation (UFH, warfarin, DOAC)
47
Polymorphisms in MTHFR gene may but do not necessarily ____ so ____ screen
Polymorphisms in MTHFR gene may but do not necessarily increase levels of homocysteine so do NOT screen * Thermolabile variant present in 37% of Caucasians does not increase risk of venous thrombosis or pregnancy complications
48
Describe when to test for inherited thrombophilias
When to test for inherited thrombophilias * Only if information obtained will influence management and outweigh potential risks of testing * Timing of testing: proteins consumed during acute event, take weeks to return to baseline * Testing can also be affected by anticoagulants
49
\_\_\_\_ test for inherited thrombophilia if thrombosis occurs in the setting of a major transient risk factor
Do NOT test for inherited thrombophilia if thrombosis occurs in the setting of a major transient risk factor

Heme / Onc (41 decks)

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