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Hematology Exam I > Thrombosis > Flashcards

Thrombosis Flashcards

1
Q

Thrombosis

  1. Definition
  2. Virchow’s Triad (Factors predisposing thrombosis)
A
  1. Thrombosis –> Pathological process of blood clotting in uninjured vessel or an exaggerated blood clotting response
  2. Virchow’s Triad (factors predisposing thrombosis)
    - Endothelial injury
    - Blood stasis or turbulence of blood flow
    - Blood hypercoagulability
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2
Q

Where do arterial thrombi grow? Venous thrombi?

A

Arterial –> back to the heart

Venous –> toward the heart

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3
Q

Anti-Thrombic Properties of Endothelium

  1. Anti-platelet effects (2)
  2. Anticoagulant properties (2)
  3. Fibrinolytic properties (1)
A
  1. PGI2 and NO (prevent platelet adhesion)
  2. Heparin-like molecule (activates ATIII) and Thrombomodulin
  3. tPA
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4
Q

Prothrombotic Properties

3 of them

A

vWF

Tissue Factor

Plaminogen Activator Inhibitors (PAI)

-Key regulators of the fibrinolytic system

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5
Q

What does aspirin (ASA) inhibit?

A

Activation and release of contents from platelets

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6
Q

What makes the platlet plug irreversible (secondary hemostatic plug)?

A

Action of Thrombin

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7
Q

Arterial Thrombosis

  1. Key factors
A
  1. Endothelial injury
    - Loss of endothelium will expose ECM and hence activation of platelets and thrombosis

So any factors that damage endothelium will predispose you to thrombosis

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8
Q

How does vWF react to bloodflow?

A

Unfolds under shear stress

***Faster the blood flows, the stickier it gets***

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9
Q

What is the job of Thrombin?

A

Converts Fibrinogen to Fibrin (irreversible plug)

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10
Q

Hypercoagulability

  1. Primary (Genetic) Disorders
A

Factor V Leiden mutation

ATIII deficiency

Protein C deficiency

Protein S deficiency

Prothrombin G20210A gene mutation

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11
Q

Hypercoagulability

  1. Secondary Disorders
A

Anti-phospholipid Syndrome

Lupus anticoagulant

Prolonged immobilization

Cancer

Nephrotic Syndrome

Contraceptive pills

Smoking

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12
Q

Heparin-Induced Thrombocytopenia (HIT Syndrome)

A

***A Hypercoagulable state***

Occurs during heparin therapy

Antibodies bind to platelets and active them continually

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13
Q

Antiphospholipid Syndrome (Lupus Anticoagulant)

A

***A Hypercoagulable state​***

Antibodies to phospholipid (e.g. Cardiolipin)

In vitro –> inhibits coagulation

In-vivo (in life) –> induces coagulation

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14
Q

Disseminated Intravascular Coagulation

  1. What is it?
  2. Occurs in
  3. Leads to
  4. Symptoms
A
  1. Sudden widespread fibrin thrombi in the microcirculation
  2. Occurs in shock, infection, pregnancy, and malignancy (cancer)
  3. Leads to circulatory insufficiency (Brain, lung, heart, kidneys)

Also leads to cosumption of platelets and clotting factors

***So you have clots everywhere and are at increased risk of bleeding all at the time same***

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15
Q

Fate of Thrombus

4 of them

A
  1. Propagation (progression)
  2. Embolization
  3. Lysis
  4. Organization and recanalization (chronic inflammation and fibrosis - Prothrombotic Syndrome)
    - Requires direct lysis (e.g. tPA); Coumadin will just prevent further clot formation, not lyse the clot already there
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16
Q

What is the most common cause of preventable hospital death?

A

PE (Pulmonary Embolism)

17
Q

Pulmonary Thromboembolism

  1. Small
  2. Medium
  3. Large
  4. Massive
A

Small –> Silent or organization with cumulative damage (idiopathic pulmonary hypertension)

Medium –> pulmonary infarct w/ acute cardiorespiratory symptoms

Large –> right heart failure and collapse (>60% pulmonary circulation)

Massive –> sudden DEATH (e.g. saddle embolus)

18
Q
  1. Saddle Embolus
  2. Paradoxical Embolus
A
  1. Occludes main pulmonary artery
  2. Cardiac embolus passing to the right side of the heart through a septal defect
19
Q

What causes 99% of infarction?

A

Thrombosis (mostly arterial)

-Venous infarct occurs in organs with single venous outflow (e.g. Testis or Ovary)

20
Q

Factors Influencing Development of Infarct

4 things

A
  1. Vulnerability to Hypoxia

Neuron - 3-4 mins

Heart - 20-30 mins

Fibrous tissue - hours

  1. Oxygen content of the blood (e.g. heart failure pt with low oxygen content)
  2. Nature of Blood Supply (Dual: lung, liver, hands; End-arterial: spleen, kidneys)
  3. Rate of Occlusion (atherosclerosis of coronary arteries is SLOW)
21
Q

Inherited Thrombophilias

  1. Compare Number of Genotypes, Prevalence of Thrombophilia, and RR of thrombosis between AT deficiency, Protein C deficiency, Protein S deficiency, Factor V Leiden, Prothrombin G20120A
A

Antithrombin (AT), Protein C, and Protein S deficiencies all have many genotypes, 5% or less prevalence of thrombophilia, and up to 10 RR of thrombosis

Factor V Leiden –> One Genotype –> 40-50% prevalence of thrombophilia –> 3-7 RR of thrombosis

Prothrombin G20120A –> One Genotype –> 5-10% prevalence of thrombophilia –> 2-3 RR of thrombosis

22
Q

Relative Risk of Venous Thrombosis

  1. Oral Contraceptives
  2. Factor V Leiden (carrier)
  3. Factor V Leidein (carrier) + Oral Contraceptives
A
  1. 7
  2. 9

34.7

23
Q

When in the presence of clot, what will the measurements of Protein C and Protein S be?

A

Low (so does not necessarily indicate a deficiency if clot is present)

24
Q

When to “further evaluate”

A

Young patients

Family history

Thrombosis in absence of known risks

Recurrent miscarriages (Factor V Leidin or Protein C/S deficiency)

Warfarin-induced skin necrosis

Neonatal purpura fulminans

25
Q

Further Evaluation

  1. Lab Tests (7)
A

Factor V Leiden

Prothrombin 20210

Lipoprotein a

Factor VIII and vWF levels

PAI-1

Heparin cofactor 2

Plasminogen

26
Q

What is a commmon inherited thrombophilia that is due to increased production of pro-coagulant?

A

Prothrombin G20120A gene mutation

27
Q

Characteristics of ATIII Deficiency

A

Autosomal dominant inheritance

Quantiative and qualitative defects

Thrombotic phenomena in adolescence or even earlier

Frequently Pulmonary Embolism as first clinical manifestation

***YOUNG CHILDREN***

28
Q

Characteristics of Protein C deficiency

A

Autosomal dominant and recessive inheritance

Quantitative and qualitative defects

Homozygotes is incompatible with life

Thrombotic phenomena in adolescence

***Skin necrosis when WARFARIN THERAPY introduced***

29
Q

Characteristics of Protein S deficiency

A

Autosomal dominant inheritance

Quantitative and qualitative defects

Homozygotes is incompatible with life

Thrombotic phenomena in adolescence

***Skin necrosis when WARFARIN THERAPY introduced***

30
Q

Factor V Leiden

  1. Mutation
  2. Effects
  3. Prevalence
A
  1. Missense muation changes amino acid 506 of factor V from arginine to glycine
  2. Mutation is at preferred protein C cleavage site, slows inactivation of factor Va by protein C

***factor Va procoagulant activity is not affected

  1. VERY COMMON (5% of population is heterozygous and accounts for 50% of inherited thrombophilia)
31
Q

Prothrombin G20210A Mutation

  1. Mutation
  2. Effects
  3. Diagnosis
A
  1. Mutation in 3’ non-coding part of prothrombin gene

***NO EFFECT ON STRUCTURE OR FUNCTION

  1. Heterozygotes have 5-10% higher plasma prothrombin and 2-3 fold risk of venous thrombosis
  2. Diagnosed –> DNA testing
32
Q

Overall Risk

  1. Thrombosis is….
A

MULTI-FACTORIAL

You need at least 2 risk factors if not 3 or 4

(One prothrombotic condition increases the risk of thrombosis by a factor of 5-8)

Hematology Exam I (12 decks)

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