Disorders of Hemostasis Flashcards

1
Q

Can you name 5 stages of hemostasis?

A

1) Vessel spasm
2) Formation of platelet plug
3) blood coagulation or formation of insoluble fibrin clot
4) clot retraction
5) clot dissolution (break down of clot)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Can you name 5 stages of hemostasis?

A

1) Vessel spasm
2) Formation of platelet plug
3) blood coagulation or formation of insoluble fibrin clot
4) clot retraction
5) clot dissolution (break down of clot)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does a thrombotic disorder do to someone?

A

It causes them to have excessive clotting (like lots and lots of DVT’s. Inappropriate clotting in an intravascular space.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What causes bleeding disorders?

A

Insufficient clotting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are thrombi made out of?

A

Platelets (Arterial thrombi mostly) and Fibrin (venous thrombi mostly)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

An aneurysm a clot from afib are examples of what type of thrombi?

A

Mural. They form on the heart wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

A DVT is an example of what type of thrombi?

A

Venous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Patients with a CVA or CAD have what type of thrombi?

A

Arterial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What’s different about arterial thrombi compared to venous thrombi?

A

Arterial thrombosis obvious occur in the arteries. They occur because of atherosclerotic plaque. They’re made of PLATELETS mostly. Example: limb ischemia, ACS, CVA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What’s Virchow’s triad?

A

Stasis or turbulent blood flow (stasis in venous, turbulent in arterial), endothelial injury, hypercoagulability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What’s Virchow’s triad?

A

Stasis, endothelial injury, hypercoagulability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do we treat arterial thrombi?

A

Think of how we treat a heart attack. ASA, antiplatelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do we treat venous thrombi?

A

Think of a DVT - anticoagulants, warfarin, heparin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does a thrombotic disorder do to someone?

A

It causes them to have excessive clotting (like lots and lots of DVT’s. Inappropriate clotting in an intravascular space.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What causes bleeding disorders?

A

Insufficient clotting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are thrombi made out of?

A

Platelets (Arterial thrombi mostly) and Fibrin (venous thrombi mostly)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

An aneurysm a clot from afib are examples of what type of thrombi?

A

Mural. They form on the heart wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

A DVT is an example of what type of thrombi?

A

Venous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Patients with a CVA or CAD have what type of thrombi?

A

Arterial

20
Q

What are some examples of hypercoagulability states?

A

Any state where you have too many procoagulants and not enough anticoagulants. Example: oral contraceptives, HRT, pregnancy, child birth, cancer, surgery, antiphospholipid, inherited conditions (thrombophilia)

21
Q

How are venous thrombi different from arterial thrombi?

A

Made in veins (duh). They happen because of an issue with the Virchow’s triad (stasis, congestion, clotting cascade). Made of FIBRIN, RBC’s and some platelets. Example: DVT or PE

22
Q

What’s Virchow’s triad?

A

Stasis, endothelial injury, hypercoagulability

23
Q

How do we treat arterial thrombi?

A

Think of how we treat a heart attack. ASA, antiplatelets

24
Q

How do we treat venous thrombi?

A

Think of a DVT - anticoagulants, warfarin, heparin.

25
Q

What are some examples of deep veins? What are deep veins?

A

Deep veins collect blood from the superficial veins and carry it to the heart. Examples: Iliac, femoral, popliteal, tibial (not the saphenous veins)

26
Q

What are the superficial veins? Give an example.

A

The veins that collect blood from beneath the skin surface. Example: Saphenous

27
Q

What sort of pump gets blood from veins to the heart?

A

Skeletal Muscle Pump

28
Q

What prevents the backflow of blood?

A

Venous valves

29
Q

What is so special about Antithrombin III?

A

It’s a circulating glycoprotein made by the liver. It interferes with clotting and PREVENTS FURTHER CLOT GROWTH. When it combines with heparin it’s actions are accelerated and they inactivate thrombin, Factor Xa, and other coagulation factors.

30
Q

How does Factor C/Protein C work and what’s so special about it?

A

Factor C is a plasma protein that acts as an anticoagulant - IT LIMITS FURTHER CLOTTING. It inactivates factors V, & VIII.

1) If there’s too much thrombin it binds to thrombomodulin which is on endothelial surfaces
2) This thrombomodulin/thombin complex activates protein C (aka APC - activated protein C)
3) APC degrades factor VIIIa and Va

31
Q

What are some examples of interventions that cause endothelial injury?

A

Surgery (especially ortho surgery), chemicals (cigarettes and bacterial toxins), IV catheters, Trauma (especially athletic injury)

32
Q

What does a d-dimer really tell us?

A

That there’s increased activity in the fibrinolytic system.. Not DVT specific.

33
Q

When someone has had multple DVT’s or PE’s or miscarriages, what could they have?

A

An inherited thrombophilia condition

34
Q

What’s Factor V Leiden?

A

A mutation that makes factor V resistant to protein C degradation.

35
Q

What’s prothrombin gene mutation?

A

The person makes too much prothrombin. It’s a “gain of function” mutation

36
Q

What’s protein C or AT-III deficiency?

A

A hereditary defect resulting in high circulating levels of homocystein which alters antithrombotic mechanisms. AT-III is important because it inactivates coauglation factors and neutralizes thrombin.

37
Q

What’s the intrinsic pathway?

A

It’s the part of the clotting cascade. It starts in the curculation and gets activated by Factor XII.

38
Q

What’s the extrinsic pathway?

A

Activated by the cellular lipoprotein called “tissue factor” when tissues are injured.

39
Q

What’s similar about both pathways?

A

They both pathways lead to factor X activation, they both lead to prothrombin being converted to thrombin, and make fibrinogen into an fibrin (which holds the clot together).

40
Q

What is so special about Antithrombin III?

A

It’s a circulating glycoprotein make by the liver. It interferes with clotting. When it combines with heparin it’s actions are accelerated and they inactivate thrombin, Factor Xa, and other coagulation factors.

41
Q

How does factor C work and what’s so special about it?

A

Factor C is a plasma protein that acts as an anticoagulant. It inactivates factors V, & VIII.

42
Q

When a thrombus disconnects and heads into circulation what is it called?

A

An embolus

43
Q

What does a d-dimer really tell us?

A

That there’s increased activity in

44
Q

How do thrombolytics work?

A

They activate plasminogen to break down clots

45
Q

What do anticoaculants do?

A

They don’t bust up a clot. They prevent clot growth and new clots from forming.

46
Q

What are 4 ways to treat thombi/emboli

A

1) Anticoagulants
2) Thombolytics
3) Intracaval filter
4) Thombectomy