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Pulmonary Vascular Disease (week 5) > Thrombo embolic disease > Flashcards

Thrombo embolic disease Flashcards

1
Q

Normal clot formation - 2 types

A

1) Primary clotting

2) Secondary clotting

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2
Q

Components of primary clot

A

-platelet plug

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3
Q

Components of secondary clot

A
  • coagulation cascade

- negative feedback

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4
Q

The clotting cascade components

A

1) Intrinsic
2) Extrinsic
3) Common
enzymes (proteases) = most of the factors
coenzymes = V & VIII
cofactors = calcium , phopholipids

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5
Q

Coagulation cascade

A

X

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6
Q

Negative feedback mechanisms

A
  1. Anticoagulants
    - antithrombin (inhibits proteases)
    - TFPI (inhibits proteases, mainly VIIa/TF)
  2. Fibrinolysis
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7
Q

why called D-dimers

A

-2 D globulins and one E subunit

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8
Q

Classification of diseases of clotting

A

1) Which vessels they occur in
- venous thromboembolism (VTE)
- arterial thrombosis
- capillary thrombosis

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9
Q

Why venous system is high risk of clotting

A

-Stuff is sitting there for awhile

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10
Q

Common cause arterial thrombosis

A

Atherosclerosis

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11
Q

Cause Capillary thrombosis

A

Mainly due to microangioathic hemolytic anemias

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12
Q

Types of VTE diseases

A
  1. Superficial vein thrombosis (SVT)
  2. Migratory SVT
  3. Deep vein thrombosis (DVT)
  4. DVT complicatins
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13
Q

SVT causes

A

-from IV, catheters etc

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14
Q

Complications from SVT

A

Are rare

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15
Q

What are migratory SVT a sign of

A

Malignancy

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16
Q

DVT common complications

A
  • pulmonary embolism

- postphlebitic syndrome

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17
Q

Etiology /Risk of VTE- acquired VTE

A
  • immobility
  • age
  • pregnancy (to compensate for excess breathing in birth)
  • obesity
  • trauma
  • surgery
  • malignancy
  • meds -birth control pill
  • inflammation (autoimmune disorders)
  • hyperviscosity (blood get thicker occuring in rare disorders -i.e. get lots of RBCs)
  • antiphospholipid antibody syndrome (APLAS)- make autoantibody to phospholipids
18
Q

Etiology/Risk of VTE - hereditary

A
  • factor V leiden
  • prothrombin gene mutation
  • protein C deficiency
  • protein S deficiency
  • antithrombin-3 deficiency
  • increased factor 8
  • increased homocysteine
19
Q

Virchows triad

A

1) Stasis
2) Vascular injury
3) Hypercoag

20
Q

What risks propagate clotting through vascular injury

A

1) Surgery
2) Trauma
3) Malignancy
4) Inflammation
5) Homocysteine

21
Q

What risks propagate clotting through stasis

A
  • immobility
  • age
  • pregnancy
  • obesity
22
Q

What risks propagate clotting through hypercoag

A
  • hereditary thrombophilias
  • pregnancy
  • age
  • malignancy
  • hyperviscosity
  • meds -OCP
23
Q

Risks with multiple mechanisms leading to clotting

A
  • pregnancy
  • age
  • malignancy
24
Q

Unknown mechanisms of clotting

A
  • hyperhomocysteinemia ( does it cause the clot or is it consequence)
  • antiphopholipid antibody syndrome (APALS)
25
Q

Classification of hereditary thrombophilias

A
  1. Loss of anticoagulant function
    - antithrombin 3 deficiency
    - protein C deficiency
    - protein S deficiency
  2. Gain of factor function
    - factor V leiden
    - prothrombin gene
    - elevated Factor VIII
26
Q

Accumulative risk

A

2 or more risk factors - risk of clot goes up exponentially

27
Q

Postphlebitic synrome MOA

A

Chronic venous insufficiency leads to venous hypertension which then causes edema, hypoxia, inflammation

28
Q

Signs of DVT

A
  • swelling, painful

- red, warm (inflmmation signs)

29
Q

Signs of PE

A

typical: SOB, chest pain, hemoptysis
Atypical: abdominal pain, syncope, fever, cough, seizure

30
Q

Postphlebetic syndrome

A
  • swelling
  • pain
  • ulcers
  • rash
31
Q

Radiological testing

A

1) Ultrasound

2) CT

32
Q

Lab testing

A
  1. DDimers
    - high sensitivity
    - low specificity
  2. Etiologic testing
33
Q

DD dimers high sensitiivity

A

If negative, excludes VTE

34
Q

DD dimer low specificity

A

If positive, can be due to thrombosis, infection, trauma, surgery

35
Q

Etiologic testing

A

Figure out what could be the trigger for the clot
What ??(tests for)
a) is it hereditary?
b) is it acquired?

When to do these panel of testing

1) unprovoked +/-recurrent VTE
2) Strong family history
3) Purpura fulminans in neonates and children (requires urgent protein C and S testing)

36
Q

When not to test for hereditary factors

A

1) provoked (obvious trigger)
2) not recurrent
3) Arterial thrombosis

37
Q

General guideline when to test for hereditary disorder

A

1) Change in management
- duration of anticoagulant
- prophylaxis required
- alternative to OCP or HRT required

38
Q

Goal of treatment

A

To prevent further clot formation

dont want to bust clot because huge risk of emboli-travelling to the lungs

39
Q

Treatment

A

-heparin + coumadin (warfarin)
-5 day overlap
because:
heparin acts more rapidly (increases AT-3 activity) but is given IV
-Coumadin is PO but acts slower and has potential transient procoagulant state (inhibts vitamin K dependent factors + protein C&S)

40
Q

How long continue treatment

A 
Typically 6 months on coumadin
3 months (with transient risk factor)
Indefinite (for recurrent DVT)

Pulmonary Vascular Disease (week 5) (3 decks)

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