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HEMATOLOGY > VENOUS THROMBOSIS > Flashcards

VENOUS THROMBOSIS Flashcards

1
Q

Where may arterial thrombitic events occur?

A
  • coronary
  • cerebral
  • peripheral
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2
Q

Cause of blood clots in arterial system?

A
  • chronic high pressure damages the vascular endothelium leading to eventual atherosclerosis> presents as angina if in heart/ claudication in legs
  • rupture results in PLATELET rich thrombus !
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3
Q

How to treat arterial thrombosis?

A
  • ASPIRIN and ANTI-PLATELET drugs

- modify risk factors (high BP/ smoking)

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4
Q

How does venous thrombosis occur?

A
  • its a low pressure system
  • —tends to be stasis problem
  • which ACTIVATES the coagulation cascade> fibrin clot formation
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5
Q

What is given to treat venous thrombosis?

A
  • Heparin and Warfarin

- Anti-coagulants

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6
Q

What is involved in Virchow’s triad?

A
  • stasis
  • vessel wall (deterioration of the valves) —occurs with AGE and blood clot formation
  • hypercoagulability (Tissue factor/ vWF)
  • —–ANTI-THROMBIN AND PROTEINS S may drop!
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7
Q

How does DVT present as?

A

Blood fails to return to heart!

  • —limb feels HOT, swollen, tender
  • pitting edema
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8
Q

What is a DDX for dvt?

A
  • -CELLULITIS (also unilateral)
  • lymphedema (cancer blocking the lymphatic flow)
  • -CHF is b.l
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9
Q

How does a P.E come about

A

blood clot from DVT travels through the IVC to the heart, through the pulmonary artery into the LUNGS
—occludes small vessel in lungs> tissue hypoxia

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10
Q

How does P.E present as?

A

-hypoxia
- pleuritic pain (STABBING pain on inhalation!) —S1Q3T (ECG) ????
inflammed lung lining rubs on the pleura?

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11
Q

Why is hypercoagulability seen in pregnancy?

A
  • factor VIII RAISES by 5x in pregnancy
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12
Q

What are some hypercoagulable states ?

A
  1. age
  2. Prgenancy
  3. Puerperium
  4. Estrogen therapy
  5. Trauma/ surgery
  6. Malignancy
  7. Infection
  8. Thrombophilia (heritable/ anti-phosholipid syndrome)
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13
Q

What component of the normal haemostatic system is affected in venous thromboembolism?

A

– anticoagulant defences

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14
Q

What is seen with thrombophilia?

A
  • familial/ acquired d.o of the haemostatsis mechanism

- -predisposing one to thrombosis

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15
Q

What is seen with thrombophilia?

A
  • FACTOR 5 normal fxn
  • –but unable to switch off efficiently
  • –5x incr. risk of getting blood clt.
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16
Q

What IS responsible for switching off Factor 5 and 7?

A

Protein C and Protein S

17
Q

When to consider screening for Hereditary thrombophilia?

A

Venous thrombosis <45 years old
Recurrent/ Unusual VENOUS thrombosis
Family history of venous thrombosis
Family history of thrombophilia

18
Q

How to manage hereditary thrombotic events?

A

avoid OCP (

  • short- term prophylaxis (to prevent thrombotic events)
  • short term anticoagulation (to treat thrombotic event)
  • long-term anti-coagulation (if RECCURENT)
19
Q

Are multiple risk synergistic ?

A

YES

  • —if you have family hx and your on OCP
  • —HUGE risk !
20
Q

What occurs with acquired thrombophilia?

A
  • THROMBOSIS IN BOTH arteries and veins
  • —YOUNG pt with stroke
  • -said to be d.t anti-phospholipid syndrome
21
Q

What are the fts of anti-phospholipid syndrome?

A
  • recurrent FETAL loss
  • mild thrombocytopenia
  • recurrent thromboses (TIAs and venous)
22
Q

Why may APTT be prolonged in Antiphospholipid syndrome?

A
  • –Lupus anticoagulants (Abs) interfere with the test

- –prolongation WITHOUT factor deficiency occurring

23
Q

What is A.W antiphospholipid Abs?

A
  • EBV may trigger the autoimmune d.o
  • lymphoproliferative d.o
  • viral infections
  • drugs
  • primary
24
Q

Rx of Antiphospholipid syndrome?

A
  • Warfarin

prevent both Iary and IIary haemostasis

25
Q

What results in arterial and venous thrombosis respectively?

A

Arterial= atjeroscleorsis; subsequent rupture

Venous= Virchow’s triad

26
Q

Which condition holds a HIGHER risk

for thrombosis than hereditary thrombophilias?

A

Antiphospholipid Ab syndrome

27
Q

What occurs with pulmonary embolism pathologically?

A

pulmonary infarction

  • pleuritic chest pain
  • cardiovascular collapse/ death
  • HYPOXIA
  • right heart strain
28
Q

What are the risk factors for STASIS to occur?

A
  • age
  • pregnancy
  • marked obesity
  • DVT/ PE
  • malignancy
  • paralysis
  • surgery/ trauma
29
Q

What vessel wall risk factors predisposes one to venous thrombosis?

A

Age

Previous DVT/PE

30
Q

What is a specific hypercoagulable state? Why does it occur?

A

thrombophilia

  • decr. anti-coagulant activity / decr. fibrinolytic acivity/ incr, coagulation activity (fibrin clot and platelet plug formation)
31
Q

Name some naturally occurring anti-coagulants.

A
  1. Serine Protease Inhibitor (anti-thrombins)
  2. Protein C and Protein S
  3. Tissue Factor pathway inhibtitor
32
Q

What follows IIary haemostasis?

What carries out fibrinolysis?

A

To prevent Inappropriate, dangerous clotting elsewhere- FIBRINOLYTIC cascade follows
—carried out by PLASMIN (breaks down fibrin)

33
Q

What is hereditary thrombophilias?

A
  • gr. of genetic defects

- individuals have INCR. tendency to develop PREMATURE, unusual and recurrent thromboses

34
Q

What is said to be the pathogenesis of anti-phospholipid abs?

A
  • Abs cause a conformational in Bets1 Glycoprotein 1

> activation of Iary and IIary haemostasis and vessel wall abnormalities

35
Q

Most common genetic defect mounting to DVT?

A

Factor V Leiden

HEMATOLOGY (20 decks)

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