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PATH 402 > Coagulation disorders: Thrombosis > Flashcards

Coagulation disorders: Thrombosis Flashcards

1
Q

What is thrombosis?

A

Thrombosis is the formation of a platelet or fibrin mass within a vessel

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2
Q

What are the 3 physiologic components responsible for thrombosis?

A
  1. Low velocity in vessel
  2. Activation of coagulation cascade
  3. Vessel damage
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3
Q

What are sources of emboli?

A

From areas of hardening (atherosclerosis causing plaque) in the aorta and other large blood vessels

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4
Q

What is the difference between white (arteries and arterioles) and red thrombus (veins)?
- Mechanism
- Main component

A

WHITE
Main mechanism/risk factors: Atherosclerosis
Main component: Fibrin
Consequence: Stroke

RED
Main mechanisms: Superficial and Deep vein thrombosis
Causes and risk factors:
Superficial
- Blood clot due to IV line or trauma to vein
Deep vein
- Damage to vein from surgery or injury
- Inflammation and damage due to infection/injury
Main component: Erythrocytes

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5
Q

What are the risk factors for arterial thrombosis?

A

Increasing age
Hypercholesterolemia
Hypertension
Smoking
Physical inactivity
Obesity
Diabetes
Chronic diseases and inflammation
- Chronic renal failure
- HIV infection
- Hyperhomocysteinemia

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6
Q

What are the risk factors for venous thrombosis?

A

Stasis
Wall damage
Factor V Leiden and activate protein C resistance (APCR)
Deficiency of protease inhibitor
- PrS, PrC, AntiThrombin, heparin cofactor
Elevated prothrombin level
- Factor II mutation
Antiphospholipid antibody
Decreased fibrinolysis
Hyperhomocysteinemia
Surgery
Malignancy

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7
Q

Hereditary thrombophilia increases the risk of thrombosis because:

A
  1. Increase in procoagulant factors
  2. Decrease in inhibitors of clotting
  3. Combination of inherited and/or environmental factors
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8
Q

*What are the clinical manifestations of herditary thrombophilia?

A
  1. Venous thromboembolism (VTE) < 50
  2. Recurrent VTE
  3. Strong family history
  4. Unusual sites
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9
Q

*What are the hereditary conditions associated with thrombosis? What are the lab investigations for these conditions?

A

Factor V Leiden
- PCR

Prothrombin G20210a
- PCR

PS deficiency
- ELISA for total PS Ag
- Immunoassay for free PS
- Clot based assay showing ability of PS as cofactor for aPC

PC deficiency
- Clot based assay using protein C activators

Antithrombin deficiency
- Chromogenic assay
- Clot based method based on clotting of fibrinogen

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10
Q

What are the secondary (acquired) disorders that can lead to thrombosis?

A
  1. Antiphospholipid syndrom (APLS) - most common of acquired thrombophilia
    - Refers to grp of auto-Ab that includes lupus anticoagulant (LA) and anticardiolipin Ab (aCL) and several subgroups which recognize phopholipids and phospholipid binding protein
  2. Heparin-induced Thrombocytopenia (Type 2)
    - Usually with unfractionated heparin
  3. Thrombotic microangiopathies (TMA)
    - Clinical disease featured by presence of microangiopathic hemolytic anemia (MAHA)
    - Presence of schistocytes > 1%
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11
Q

What is the mechanism of thrombosis in APLS?

A

APLS
Anticoagulants inhibition:
- Interference with PC activation
- Inhibition of heparan sulfate interaction with antithrombin
- Decreased TFPI
- Inhibition of prostacyclin
- Blocking tPA and plasminogen, increases PAI-1

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12
Q

What is the laboratory investigation for APLS?

A
  1. Diagnosis required demonstration of LA or relevant protein cofactor
  2. Positive result should be persistent
  3. Test for protein cofactors - ELISA
  4. Evaluation of LA - clot based factors
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13
Q

What is the mechanism of heparin-induced thrombocytopenia (type 2)?

A
  1. Platelet factor 4 (PF4) is released during platelet activation and binds to heparin
  2. Heparin/PF4 complex attaches to platelet surface
  3. Body view complex as foreign and Ab is formed against complex
  4. Ab binds to complex and platelets are destroyed
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14
Q

What are the laboratory investigations for heparin-induced thrombocytopenia?

A
  1. Functional platelet activation assay
  2. Immunoassay - ELISA for detecting anti PF4/heparin Ab
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15
Q

What are some examples of thrombotic microangiopathies (TMA)? What are they caused by?

A
  1. Disseminated intravascular coagulation
    - Cancer, sepsis, shock, significant emboli
  2. Thrombotic thrombocytopenic purpura (TTP)
    - Cleaving factor missing: ADAMTS-13
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16
Q

What are the lab signs of disseminated intravascular coagulation (DIC)? [EXAM]

A

Increased INR
Prolonged PTT
Decreased fibrinogen
Low platelets

17
Q

What are the types of heparin and what is their function?

A

Unfractionated heparin enhances the activity of antithrombin and inhibits factor Xa.

Low molecular weight heparin (LMWH) inhibits factor Xa only, which inhibits coagulation. LMWH is only given at hospitals.

18
Q

What are the monitoring methods used for heparin?

A

For unfractionated heparin:
- aPTT and Anti-Xa activity

For LMWH:
- Anti-Xa activity

19
Q

What are the possible complications of using heparin? What can we do to treat them?

A

Bleeding
- Reversible if stopped
- If critical, use protamine sulphate

Heparin induced Thrombocytopenia (HIT)
- Stop use immediately

20
Q

What is the mechanism of Vitamin K antagonists? Give an example.

A

Warfarin is an example of a VKA.
- Prevents Vit K from participating in hepatic carboxylation

21
Q

How to monitor the use of VKA? What are the adverse events that could happen and what can we do to treat it?

A

Monitor using prothrombin time (PT) however each lab is different, not standardized.

Adverse effects include:
1. Bleeding
2. Lack of efficacy due to a mutation in gene which makes a person resistant to Vit K antagonist

In case of bleeding, give patient prothrombin complex as an antidote.

22
Q

What are the advantages of DOACs over warfarin?

A
  1. No monitoring
  2. No food and less drug interactions
  3. Fixed dosing
23
Q

What are the disadvantages of DOACs compared to warfarin?

A
  1. Renal function effects
  2. Not in liver dysfunction
  3. No reversal agents
24
Q

What are examples of anticoagulant medications? What does each drug inhibit?

A

Dabigatran
- Inhibits free and clot-bound thrombin

Rivaroxaban
- Inhibits Factor Xa

25
Q

What coagulation reactions will be blocked when using dabigatran? (EXAM)

A

Thrombin conversion of fibrinogen to fibrin which will block coagulation

26
Q

What are the coagulation tests that are affected by Dabigatran and Rivaroxaban? (EXAM)

A

Dabigatran - Prothrombin time

Rivaroxaban - Prothrombin time (main) and PTT

PATH 402 (7 decks)

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