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
Classification of hereditary thrombophilias
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
Accumulative risk
2 or more risk factors - risk of clot goes up exponentially
27
Postphlebitic synrome MOA
Chronic venous insufficiency leads to venous hypertension which then causes edema, hypoxia, inflammation
28
Signs of DVT
- swelling, painful | - red, warm (inflmmation signs)
29
Signs of PE
typical: SOB, chest pain, hemoptysis Atypical: abdominal pain, syncope, fever, cough, seizure
30
Postphlebetic syndrome
- swelling - pain - ulcers - rash
31
Radiological testing
1) Ultrasound | 2) CT
32
Lab testing
1. DDimers - high sensitivity - low specificity 2. Etiologic testing
33
DD dimers high sensitiivity
If negative, excludes VTE
34
DD dimer low specificity
If positive, can be due to thrombosis, infection, trauma, surgery
35
Etiologic testing
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
When not to test for hereditary factors
1) provoked (obvious trigger) 2) not recurrent 3) Arterial thrombosis
37
General guideline when to test for hereditary disorder
1) Change in management - duration of anticoagulant - prophylaxis required - alternative to OCP or HRT required
38
Goal of treatment
To prevent further clot formation | dont want to bust clot because huge risk of emboli-travelling to the lungs
39
Treatment
-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
How long continue treatment
``` Typically 6 months on coumadin 3 months (with transient risk factor) Indefinite (for recurrent DVT) ```