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CPR Exam 1 > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

Platelets are derived from

A

GM-CSF thrombo
—> Megakaryocytes*
*hematopoietic linaege

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2
Q

Another name for platlets

A

Thrombocytes

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3
Q

When are platelets formed

A

They are active when they a fragments off the megakaryocytes

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4
Q

Normal levels of platelets

A

150,000-450,000 ul^3

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5
Q

What do platelets contain

A

Actin, myosin, thrombostatin, mitochondria, peroxioomes, COX2, Fribrin
2 granules

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6
Q

2 granules that platelets have

A
  1. a-granules : store Von Willebrand factor, fibrinogen, factor 5 (clotting)
  2. dense-core granules : store ATP, ADP, HT’5, Ca+2
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7
Q

Megakaryocytes and platelets take up what

A

Fibrinogen that they secrete in the liver for Hemostasis

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8
Q

3 steps for platelets

A

Adhesion
Activation
Aggregation

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9
Q

What regulates platelet formation

A

Thrombopoietin (TPO) made in liver and kidney
The C-terminal if it prolongs life of platelet
* increase production and function of hematopoietic stem cells and platelets

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10
Q

How does TPO act

A

It binds to the c-MPL (CD110) receptor on the Megakaryocytes

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11
Q

Low platelet count effect on TPO

A

High free TPOs

C-MPL is not internalized and degraded

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12
Q

High platelet count effect on TPO

A

Low free TPOs and c-MPL receptor is internalized and degraded

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13
Q

4 steps to healing injury

A
  1. Vascular Spasm : severed vessel
  2. Formation of platelet plug : Platelet agglutinate + fibrin appears
  3. Formation of blood clot
  4. Repair of Damage : clot retracts
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14
Q

What is vasospasm

A

Disrupt BF and keep it above the injury = avoid more blood loss

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15
Q

4 things that contribute to vasospasm

A
  1. Myogenic : reflex from damage to SM
  2. Platelet factor : serotonin, thromboxane A2
  3. Release of molecules from endothelial BV cells
  4. Neural reflex from pain or injury
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16
Q

How do platelets bind to the vessels

ADHESION

A

The platelets have glycoproteins

  1. Von Willebrand factor is released from endothelial cells —> GP 1b/a on platelet
  2. Injured endothelial cells expose collagen —> GP 1a/2a on platelet
  3. Laminitis and fibronectin is also exposed —> GP 1c/2a on platelet
17
Q

What regulates adhesion of platelets

A

Negative charges and collagen on the surface

18
Q

What activates the platelet

A

When the GP are bound on its surface

19
Q

3 names for Von Willebrand disease

A

Psudohemophilia
Vascular hemophilia
Angiohemophilia

20
Q

What happens after the GP receptors of the platelet are activated

A
  1. Phospholipase C is activated
  2. CA+2 influx
  3. = causes ATP, ADP, CA+2, HT’5 release from DENSE granules (inside platelet)
    = a-granules release vWF, Factor 5, Fibrinogen, GFs
  4. Finger like filopodia extensions
  5. Arachidonic acid—> Thromboxane A2 (by cyclooxgenase)
21
Q

cyclooxgenase

A

Converts aracidonic acid —> Thromboxane A2

22
Q

How do platelets aggregate

A
  1. ADP is released : —> bind to P2Y12 on other platelets
  2. HT’5 + thromboxane A2 activate other platelets also
  3. Fibrinogen activates another platelet and causes bridges between platelets = PLATELET PLUG
23
Q

Aspirin on platelet aggregation

A

Inhibits cyclooxygenase

—I clotting (low thromboxane A2)

24
Q

Clopidogrel (plavix) on platelet aggregation

A

Inhibits P2Y12 receptors = no further platelet activation and no aggregation

25
Q

What makes one platelet able to bind to fibrinogen

A

Conformational change of the GP 2b/3a receptor of the platelet
= allows fro bridges and forms platelet plug

26
Q

3 steps in making a clot

A
  1. Prothrombin —> thrombin (by pro thrombin activator)
  2. Fibrinogen —> fibrin (by thrombin)
  3. Fibrin polymerizes and makes clot (uses CA+2)
27
Q

How does the vessel wall finally get repaired

A

PDGF (platelet derived GF) secreted by platelet

= allows fibroblasts to grow into the area and differentiate to SM and other cells needed

28
Q

How to remove clots

A

PLASMIN = lysis fibrin + fibrinogen

29
Q

How is plasmin made

A
  1. Protein C —» activated Protein C (by thrombin from endothelial cells)
  2. Activated Protein C —> inactivates t-PA inhibitor (plasminogen activator) = PA can be made now
  3. Plasminogen —> PLASMIN
  4. Lysis of fibrins
30
Q

Protein C inactivated what 3 things

A
  1. T-PA inhibitor
  2. Factor 5a
  3. Factor 8a
31
Q

4 anticoagulants made by body

A
  1. Fibrin : ——I thrombin
  2. Prostacyclin (PG12) : —> vasodilation and X aggregation of P
  3. Antithrombin 3 : binds to thrombin to inhibit coagulation
  4. Heparin : from mast cells to increase anti-thrombin function

CPR Exam 1 (20 decks)

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