Hemodynamic Disorders (4) - Virchow's Triad Flashcards

(42 cards)

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?

20
Q

Secondary disorders that cause Hypercoagulability are caused by?

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?

25
What are 3 Secondary disorders that cause Hypercoagulability?
Oral Contraceptive use Heparin-induced Thrombocytopenia Antiphospholipid Syndrome
26
Oral contraceptive use increases synthesis of?
Coagulation factors
27
With Heparin-induced Thrombocytopenia, what must a patient come into contact with?
Unfractionated Heparin
28
Platelets contain alpha granules. Upon activation they release them. What is a main product that is released that is important in Heparin-induced Thrombocytopenia?
Platelet Factor 4 (PF4)
29
What does Unfractionated Heparin bind?
PF4
30
Once Unfractionated Heparin binds PF4 then what occurs?
Formation of antibodies to the complex (IgG)
31
Once the IgG antibodies bind to the unfractionated heparin and PF4 complex, then what occurs?
The IgG antibodies bind to Fc receptors on more platelet surfaces
32
Once the IgG antibodies - heparin/PF4 complex binds to Fc receptors on platelets, what are the 2 options?
1. Platelet activation and aggregation (clot) | 2. Macrophage removal of the platelet (thrombocytopenia)
33
Antibodies against plasma proteins that bind to phospholipids. The patients present with miscarriages, DVT, ect.
Antiphospholipid Antibody Syndrome
34
White Thrombus
ARTERIAL blood | Contains platelets, RBCs, leukocytes
35
Red Thrombus
VENOUS blood | Many RBCs
36
4 fates of a Thrombus?
Propagation and continued growth Recanalization of the vessel Embolization Dissolution
37
For Dissolution of a Thrombus, what can be administered to speed the process if given within 6 hours of the onset?
t-PA - activates plasmin to degrade clot
38
Disseminated Intravascular Coagulation
Systemic activation of thrombin and widespread thrombosis
39
What can Disseminated Intravascular Coagulation lead to?
Severe bleeding due to depletion of the platelets being used up in all the clots forming
40
Endothelium dysfunction leads to decreased?
NO activity
41
Endothelium dysfunction causes decreased NO activity. What does this cause?
Endothelial activation
42
Endothelial activation increases?
Adhesion molecules