Hemodynamic Disorders (4) - Virchow's Triad Flashcards

1
Q

Blood clot that forms in a vessel

A

Thrombus

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2
Q

Blood clot that dislodges and travels in the blood stream until it reaches a vessel that it is too large to pass through

A

Embolus

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3
Q

What does Virchow’s Triad represent?

A

3 things that can lead to Thrombosis (clot formation)

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4
Q

What 3 things in Virchow’s Triad can lead to Thrombosis?

A
  1. Endothelial Injury
  2. Abnormal blood flow
  3. Hyper-coagulability
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5
Q

Hypercoagulability

A

Increased tendency for blood to clot

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6
Q

What are some stimuli for Endothelial activation (injury)?

A
Smoking
Hypercholesterolemia
Toxins/inflammation
Abnormal blood flow **
Injury
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7
Q

When the Endothelium becomes activated, it turns into a ______ state

A

PROthrombotic

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8
Q

In what 2 ways does Endothelial activation become PROthrombotic?

A
  1. DECREASED Thrombomodulin expression

2. INCREASED secretion of Plasminogen Activator INHIBITORS

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9
Q

Describe the normal pathway and job of the endothelium expressing Thrombomodulin

A

Thrombomodulin binds to Thrombin

  • That complex then activates Protein C (and S)
  • Proteins C and S cleave Factors Va and VIIIa to INACTIVATE them and stop clot formation
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10
Q

Describe what happens when the Endothelium is activated and it DOWNREGULATES Thrombomodulin

A

If Thrombomodulin is downregulated, it will bind less Thrombin
- That complex will then NOT activate Protein C and S
- Protein C and S then can NOT INactivate the coagulation factors Va and VIIIa
= Clot formation CONTINUES

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11
Q

Describe what happens when the Endothelium is activated and it SECRETES Plasminogen Activator Inhibitors

A

Plasminogen Activator Inhibitors INHIBIT t-PA (tissue plasminogen activator)
- If t-PA is inhibited, it cannot activate plasmin
- If plasmin is not activated it will NOT degrade fibrin and the clot
= Clot formation CONTINUES

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12
Q

2 types of blood flow?

A

Laminar (good)

Turbulent (bad)

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13
Q

Stasis

A

Slow blood flow

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14
Q

In what ways does Abnormal Blood Flow contribute to Thrombosis?

A

** Activates Endothelium

Disrupts laminar flow and prevents washout of clotting factors

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15
Q

Abnormal blood flow can occur in many forms. In what type of vessels is it more likely?

A

Dilated vessels

Where vessels bifurcate (split)

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16
Q

Examples of dilated vessels that lead to abnormal blood flow?

A

Aneurysm

Hemorrhoid

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17
Q

Abnormal blood flow can also occur due to obstruction or inadequate heart function. List a few specific examples.

A

Obstruction due to plaque

Atrial fibrillation - inadequate blood pumping

18
Q

What type of disorders are involved with Hypercoagulability?

A

Primary and Secondary

19
Q

Primary disorders that cause Hypercoagulability are caused by?

A

Genetics

20
Q

Secondary disorders that cause Hypercoagulability are caused by?

A

Acquired

21
Q

What is the main Primary disorder of Hypercoagulability?

A

Factor V Leiden Mutation

22
Q

How is Factor V Leiden Mutation inherited?

A

Autosomal Dominant

23
Q

Describe what happens with Factor V Leiden Mutation

A

Factor V is RESISTANT to cleavage and inactivation by Protein C
= Always more likely to clot

24
Q

Primary disorders of Hypercoagulability should be considered if the patient is under what age?

A

40/50

25
Q

What are 3 Secondary disorders that cause Hypercoagulability?

A

Oral Contraceptive use
Heparin-induced Thrombocytopenia
Antiphospholipid Syndrome

26
Q

Oral contraceptive use increases synthesis of?

A

Coagulation factors

27
Q

With Heparin-induced Thrombocytopenia, what must a patient come into contact with?

A

Unfractionated Heparin

28
Q

Platelets contain alpha granules. Upon activation they release them. What is a main product that is released that is important in Heparin-induced Thrombocytopenia?

A

Platelet Factor 4 (PF4)

29
Q

What does Unfractionated Heparin bind?

A

PF4

30
Q

Once Unfractionated Heparin binds PF4 then what occurs?

A

Formation of antibodies to the complex (IgG)

31
Q

Once the IgG antibodies bind to the unfractionated heparin and PF4 complex, then what occurs?

A

The IgG antibodies bind to Fc receptors on more platelet surfaces

32
Q

Once the IgG antibodies - heparin/PF4 complex binds to Fc receptors on platelets, what are the 2 options?

A
  1. Platelet activation and aggregation (clot)

2. Macrophage removal of the platelet (thrombocytopenia)

33
Q

Antibodies against plasma proteins that bind to phospholipids. The patients present with miscarriages, DVT, ect.

A

Antiphospholipid Antibody Syndrome

34
Q

White Thrombus

A

ARTERIAL blood

Contains platelets, RBCs, leukocytes

35
Q

Red Thrombus

A

VENOUS blood

Many RBCs

36
Q

4 fates of a Thrombus?

A

Propagation and continued growth
Recanalization of the vessel
Embolization
Dissolution

37
Q

For Dissolution of a Thrombus, what can be administered to speed the process if given within 6 hours of the onset?

A

t-PA - activates plasmin to degrade clot

38
Q

Disseminated Intravascular Coagulation

A

Systemic activation of thrombin and widespread thrombosis

39
Q

What can Disseminated Intravascular Coagulation lead to?

A

Severe bleeding due to depletion of the platelets being used up in all the clots forming

40
Q

Endothelium dysfunction leads to decreased?

A

NO activity

41
Q

Endothelium dysfunction causes decreased NO activity. What does this cause?

A

Endothelial activation

42
Q

Endothelial activation increases?

A

Adhesion molecules