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Circulation > Thrombotic disorders > Flashcards

Thrombotic disorders Flashcards

1
Q

_ are clots that form within blood vessels, usually within the venous system

A

Thrombi are clots that form within blood vessels, usually within the venous system

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2
Q

_ are pieces of clot that travel through the bloodstream to other places in the body where they become lodged in vessels

A

Emboli are pieces of clot that travel through the bloodstream to other places in the body where they become lodged in vessels

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3
Q

A _ is a clot that forms in one of the deep veins of an extremity, such as the femoral or brachial vein

A

A deep vein thrombosis (DVT) is a clot that forms in one of the deep veins of an extremity, such as the femoral or brachial vein

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4
Q

_ is most commonly caused by a piece of clot that breaks off from a DVT and lodges in the pulmonary arterial system

A

Pulmonary embolism (PE) is most commonly caused by a piece of clot that breaks off from a DVT and lodges in the pulmonary arterial system

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5
Q

DVT patients usually present with _

A

DVT patients usually present with unilateral swelling of the leg often with pain and redness
* A palpable cord may be present

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6
Q

What is a positive Homan sign

A

Positive homan sign: increased pain with passive dorsiflexion of the ankle with a DVT

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7
Q

Three components of Virchow Triad

A
  1. Endothelial damage
  2. Hypercoagulable state
  3. Abnormal blood flow/venous stasis
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8
Q

Name some common causes of endothelial damage

A
  • Smoking
  • Hypertension
  • Surgery
  • Trauma
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9
Q

Name some common causes of abnormal blood flow

A

Abnormal blood flow means blood either moves in a disorganized manner (turbulence) or slows down (stasis); this allows platelets and clotting factors to mingle
* Immobility
* Central venous catheters
* Varicose veins
* Atrial fibrillation

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10
Q

Name some common causes of hypercoagulability

A
  • Cancer
  • Estrogen-containing contraceptives
  • Pregnancy
  • Obesity
  • Hereditary disorders
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11
Q

Postthrombotic syndrome is _ that occurs in up to 50% of patients after a DVT

A

Postthrombotic syndrome is chronic venous insufficiency that occurs in up to 50% of patients after a DVT
* Causes leg pain, edema, skin ulcers, discoloration

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12
Q

_ is a massive iliofemoral DVT that completely occludes the venous drainage of the extremity –> edema, cyanosis, gangrene

A

Phlegmasia cerulea dolens is a massive iliofemoral DVT that completely occludes the venous drainage of the extremity –> edema, cyanosis, gangrene

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13
Q

Patients with a low to moderate Wells score will first get _ testing for DVT; Patients with high Wells score will first get _ test

A

Patients with a low to moderate Wells score will first get D-dimer test for DVT; Patients with high Wells score will first get D-dimer and ultrasonography

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14
Q

An elevated D-dimer test indicates _

A

An elevated D-dimer test indicates thrombus formation and breakdown

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15
Q

D-dimer test has high (specificity/sensitivity) but low (specificity/sensitivity)

A

D-dimer test has high sensitivity but low specificity
* Smoking, infection, surgery, pregnancy can cause D-dimer to be positive

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16
Q

_ is the best radiographic modality to diagnose DVT

A

Compression ultrasonography is the best radiographic modality to diagnose DVT
* If there is a clot present in the vein, the ultrasound transducer will fail to collapse the vein like a normal vein

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17
Q

Patients at risk of DVT in the hospital normally get _ and _ as prophylaxis

A

Patients at risk of DVT in the hospital normally get low-molecular-weight heparin and leg-compression devices

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18
Q

The prefered DVT treatment is _

A

The prefered DVT treatment is direct oral anticoagulants
* Ex: Rivaroxaban (Xarelto)
* Ex: Apixaban (Eliquis)

19
Q

_ is the most common hereditary thrombotic disease

A

Factor V Leiden is the most common hereditary thrombotic disease

20
Q

Factor V Leiden involves a _ mutation in the _ gene

A

Factor V Leiden involves a single-point mutation in the factor V gene
* Makes it invinsible to protein C cleavage and inactivation
* Causes fibrin to continuously be made –> clots

21
Q

Factor V Leiden is a _ to _ substitution; specifically at the location where _

A

Factor V Leiden is a arginine to glutamine substitution; specifically at the location where protein C cleaves factor V to inactivate it

22
Q

When should we be concerned about herditary thrombosis disorders?

A
  • Young age (< 45)
  • Family history
  • Lack of risk factors
23
Q

How do we test for Factor V Leiden?

A

Add activated protein C to aPTT assay –> clotting time is prolonged in normal patients but not as prolonged in FVL patients

24
Q

Recurrent thrombosis and history of miscarriages are hallmark signs of _

A

Recurrent thrombosis and history of miscarriages are hallmark signs of antiphospholipid antibody syndrome

25
Q

Antiphospholipid antibodies can be idiopathic in some patients; more commonly they are caused by systemic disease like _

A

Antiphospholipid antibodies can be idiopathic in some patients; more commonly they are caused by systemic disease like lupus (SLE)

26
Q

Explain the two hit hypothesis of antiphospholipid antibody syndrome

A
  1. Presence of antiphospholipid antibodies
  2. Additional risk factor for hypercoagulability
27
Q

What are the common clinical manifestations of antiphospholipid antibody syndrome?

A
  • Venous thrombosis
  • Arterial thrombosis
  • Pulmonary embolism
  • Stroke
  • Livedo reicularis
  • Fetal loss
  • Heart valve disease
  • Neuropathy

APS can affect any organ in the body because phospholipids are everywhere

28
Q

_ is discoloration of skin in a reticular pattern due to obstruction of superficial capillaries

A

Livedo reticularis is discoloration of skin in a reticular pattern due to obstruction of superficial capillaries

29
Q

Patients with APS will have a _ PTT and PT

A

Patients with APS will have a prolonged PTT and PT and thrombocytopenia
* Because antiphospholipid antibodies interfere with the reagents in coagulation studies
* The antibodies inhibit coagulation in vitro but act as procoagulants in vivo
* Ex: “lupus anticoagulant”

30
Q

How do we test for APS in the lab?

A
  1. Mixing study: we expect PTT to remain prolonged
  2. We can then add phospholipids to pick up some of the antibodies –> correction of clotting time confirms ddx
  3. ELISA can identify nature of antibody specifically
31
Q

Name 3 ways of acquiring antithrombin deficiency

A
  1. Liver disease (cirrhosis): decreased production of antithrombin
  2. Acute thrombosis, surgery, trauma: consumption of antithrombin
  3. Nephrotic syndromes: urinary loss of antithrombin
32
Q

Antithrombin deficiency will cause excessive clotting due to the inability for AT to shut off its normal clotting factors _

A

Antithrombin deficiency will cause excessive clotting due to the inability for AT to shut off its normal clotting factors XIa, IXa, Xa, VIIa, IIa

33
Q

Hereditary antithrombin deficiency is [inheritance pattern]

A

Hereditary antithrombin deficiency is autosomal dominant

34
Q

Type I antithrombin deficiency. is a _ that results from a _

A

Type I antithrombin deficiency. is a complete loss of the mutant antithrombin that results from a nonsense mutation at the AT gene

35
Q

Type II antithrombin deficiency is a _ that results from _

A

Type II antithrombin deficiency is a functionally defective antithrombin that results from missense mutation at a reactive site; defective antithrombin is still synthesized in normal levels

36
Q

Two key clinical features of antithrombin deficiency:

A
  1. Increased risk of thrombosis
  2. Heparin resistance
37
Q

Heparin mechanism of action:

A

Heparin works by binding antithrombin and inducing a conformational change that increases the affinity of AT for thrombin and factor X
* Increases the inactivating ability of antithrombin and promotes anticoagulation

38
Q

We an use a _ assay to test for antithrombin deficiency; this is then followed by a _ test to measure the level of antithrombin antigen in the plasma

A

We an use a heparin cofactor assay to test for antithrombin deficiency; this is then followed by an ELISA to measure the level of antithrombin antigen in the plasma (and we can distinguish between type I and type II)
* We do not commonly test for AT deficiency because it is very rare

39
Q

Factor _ is very important because it catalyes the conversion of fibrinogen to fibrin; if we have a mutation in this factor that causes its overproduction we tip the balance towards clotting

A

Factor II (thrombin) is very important because it catalyes the conversion of fibrinogen to fibrin; if we have a mutation in this factor that causes its overproduction we tip the balance towards clotting

40
Q

Most patients with an overproduction of factor II have a point mutation known as _

A

Most patients with an overproduction of factor II have a point mutation known as G20210A (guanine –> adenine)

41
Q

How common is factor II genetic mutation?

A

Factor II mutation (G20210A) is the second most common thrombophilia in white people, behind factor V Leiden

42
Q

To test for factor II genetic mutation we can use _

A

To test for factor II genetic mutation we can use PCR

43
Q

Protein S serves as _ while Protein C is able to _

A

Protein S serves as sidekick (cofactor) while Protein C is able to directly inactivate Va and VIIIa

44
Q

Thrombophilias cause _

A

Thrombophilias cause excessive clotting

Circulation (12 decks)

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