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Physio Test 2 > Coagulation > Flashcards

Coagulation Flashcards

1
Q

***platelet origin

A
  • myeloid stem cell line in red bone marrow = platelet precursor cell: megakaryocyte - pinched of from these cells = proplatelets –> no nucleus = not their own cells
  • Thrombopeitin (TPO) binds megakaryocytes = cell maturation
  • TPO also expressed on surface of megakar and platelets = the more platelets the more TPO reomved from circulation
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2
Q

***life span of platelets

A

aprox 10 days

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3
Q

*functions of platelets:

A

1) platelet plug - coagulation

2)

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4
Q

***Three major steps of hemostasis:

A
  • Vascular spasm
  • formation of platelet plug
  • Blood coagulation
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5
Q

Vascular spasm – details:

A

1) vasoconstriction is caused by:
a. Local myogenic contraction
b. Local autacoid factors
• From damaged tissue
• From platelets (e.g. thromboxane A2 a vasoconstrictor)
c. Nervous reflexes

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6
Q

Formation of platelet plug details:

A
  • platelet plugs for small holes in a blood vessel (no need for blood clot)
  • blood vessel endothelial cells release blood vessel dialators (NO and prostacyclin) and inh platelet aggregation & damaged endotelium DOES NOT release these factors
  • NO & PROSTACYLCIN RELAX SMOOTH MUSCLE = vasodialation
  • exposed collagen at injury causes platelet adherance
  • von Willebrand factor (vWF) binds to collagen and to a glycoprotein complex on the surface of activated platelets = increases platelet adherence.
  • Von Willebrand factor has another important role in coagulation; coagulation factor VIII circulates in the blood bound to vWF. Coagulation factor VIII is activated when it is separated from von Willebrand factor.]
  • once platelet adhere = “release reaction” -> activation. ==> dense storage granules w/ ADP, Ca++ and serotonin (a vasoconstrictor) and alpha-granules released- contains growth factors and several hemostatic factors – von Willebrand factor, and clotting factors V and fibrinogen and Platelet factor 4
  • Activated platelets use cyclooxygenase to initiate the break down of arachidonic acid to thromboxane A2 . Thromboxane A2 is a vasoconstrictor.
  • ADP and thromboxane A2 then recruit and activate additional platelets from the circulation to the site of vascular injury. Since activated platelets release more ADP and thromboxane A2 this is an example of a positive feedback process.
  • The activated platelets also change their shape and extend many finger-like filopodia.
  • Fibrinogen-induced platelet aggregation
  • Once platelets are activated the platelet glycoprotein IIb/IIIa complex becomes a high affinity receptor for fibrinogen. By binding to receptors on two different platelets, fibrinogen bridges them together. Multiple such bridges cause platelet aggregation.
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7
Q

aspirin effect on platelets:

A
  • aspirin will decrease hemostasis of platelet = they dont work as well –> do not take aspirin before surgery or procedures
  • inh cyclooxygenase and inh thromoxane A2 (vasoconstrictor) production
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8
Q

platelet activators?

A

1) sheer stress
2) thrombin
3) inflammatory cytokines

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9
Q

***what binds two “activated” platelets together?

A

fibrnogen

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10
Q

alpha-granules contents

A

contains growth factors
-several hemostatic factors – von Willebrand factor, and clotting factors V and fibrinogen and Platelet factor 4 (heparin-neutralizing factor- enhances clot formation at site of blood vessel injury

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11
Q

dense granules contents:

A
  • ADP - promotes the adherence and degranulation of nearby platelets. ADP also facilitates fibrinogen –induced aggregation of platelets via its activation of the platelet Glycoprotein GPIIb/IIIa receptor complex.
  • Ca++
  • serotonin (a vasoconstrictor) - Platelets take up serotonin from the blood, they do not synthesize it.
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12
Q

***Thromboxane A2 is a

A
  • cyclooxygenase transforms membrane arachidonic acid into a prostaglandin which in turn is transformed by thromboxane synthase into thromboxane A2
  • vasoconstrictor
  • released by activated platelets to recruit other platelets
  • decreases blood flow which makes clot formation more likely
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13
Q

***glycoprotein IIb/IIIa complex does wjhat?

A
  • a high affinity receptor for fibrinogen.
  • By binding to receptors on two different platelets, fibrinogen bridges them together.
  • Multiple such bridges cause platelet aggregation
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14
Q

thrombocytopenia

A

Patients with thrombocytopenia may develop thousands of small hemorrhagic areas under the skin and in internal tissues.

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15
Q

more extensive damage to a blood vessel then

A
  • blood coagulation is necessary for hemostasis.
  • Platelets are important for the formation of blood clots. e.g. Platelets release some of the clotting factors ( e.g. Factor XIII fibrin-stabilizing factor) and also heparin - neutralizing factor (platelet factor 4) which enhances clot formation by interfering with the anticoagulation action of heparin.
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16
Q

***Blood coagulation - three stages:

A

a. transform blood from liquid to gel by transforming fibrinogen to fibrin
b. origin of fibrin fibers
c. strengthening fibrin meshwork

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17
Q

Fibrinogen-induced platelet aggregation:

A

the platelet glycoprotein IIb/IIIa receptor binds fibrinogen and thus promotes the aggregation of platelets.

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18
Q

Blood Coagulation - Clotting

A
  • Need to convert blood from liquid to gel
  • Blood clot is made up of a meshwork of fibrin fibers.
  • Fibrin fibers entrap platelets, blood cells and plasma.
  • Fibrin fibers also adhere to damaged portion of blood vessel.
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19
Q

Origin of Fibrin Fibers

A
  • Fibrinogen is made in the liver.
  • Fibrinogen then circulates in the blood plasma. (100 to 700 mg/dl)
  • Thrombin is an enzyme which acts on fibrinogen to form fibrin monomer.
  • Fibrin monomer molecules polymerize into long fibrin fibers.
20
Q

***Stages of coagulation

A

Stage I - development of prothrombin activator complex
Stage II - conversion of prothrombin to thrombin
Stage III - conversion of fibrinogen to fibrin, clot formation and retraction

21
Q

***Stage I - development of prothrombin activator complex

A

NEED SOMETHING TO ACTIVATE FACTOR X (AND USE THAT TO ACTIVATE PROTHROMBIN LATER STAGES)
i. Contact Activation pathway (older name Intrinsic pathway – since all factors needed for clotting are present in the blood)
**• In classical description starts with activation of Hageman factor (XII)
**• Hageman factor can be activated by contact with collagen in injured vessel or foreign substance such as glass walls of test tube
ii. Tissue Factor pathway (older name Extrinsic pathway)
• Starts with tissue damage that causes release of tissue thromboplastin (tissue factor)
iii. Both pathways cause factor X to be activated

22
Q

***which caogulation pathway has more steps?

A

intrinsic

23
Q

***whcih coagulation pathway includes factos IX and VIII?

A

intrinsic path

24
Q

high/low levels of Factor XI gives what risk?

A

risk factor for venous thrombosis if high and hemophelia C if low

25
Q

***Stage II of Coagulation

A

-conversion of prothrombin to thrombin
-Prothrombin Activator: a complex of Xa,
Va, and Platelet phospholipids
-needs Ca

26
Q

***Stage III of coagulation -

A

-conversion of fibrinogen to fibrin, clot formation and retraction

27
Q

Strengthening Fibrin Meshwork

A
  • At first blood clot is weak.
  • Thrombin activates fibrin-stabilizing factor ( Coagulation Factor XIII ).
  • This factor then acts as an enzyme to cause covalent bonds between the fibrin monomers (instead of the weaker hydrogen bonds that formed earlier)
  • Factor XIIIa also causes formation of multiple cross linkages between adjacent fibrin fibers.
28
Q

whcih factor stabilizes the bond between fibrin monomers to strengthen the fibrin meshwork?

A
  • fibrin stabilizing factor (COAG FACTOR XIII)

- replaces h-bonds with covalent bonds

29
Q

***alternative way to start intrinsic pathway?

A

-Factor IX of the intrinsic pathway can also be activated by Factor VIIa from the extrinsic pathway. This is an alternate way to start the intrinsic pathway

30
Q

***factor II is what?

A

prothrombin

31
Q

***factor VIII is what?

A
  • Antihemophilic factor (AHF) or antihemophilic globulin (AHG) or antihemophilic factor A
  • Factor VIII circulates in the blood stream bound to von Willebrand factor
  • lacking this factor = haemophilia
32
Q

***factor XII is what?

A

hageman factor

  • binds collagen and platelet
  • helps keep factor VIII around longer since it binds it
33
Q

HEMOSTASIS definition

A

Arrest of Bleeding or prevention of blood loss after a blood vessel is injured

34
Q

von wildebrand factor

A
  • von Willebrand factor (vWF) binds to collagen and to a glycoprotein complex on the surface of activated platelets = increases platelet adherence.
  • Von Willebrand factor has another important role in coagulation; coagulation factor VIII circulates in the blood bound to vWF. Coagulation factor VIII is activated when it is separated from von Willebrand factor.]
35
Q

***hemophilia B

A

lacking Factor IX - X linked

36
Q

***hemophilia A

A

lacking Factor VIII - X linked

37
Q

***hemophilia is classically caused by:

A

lack of a factor in the contact activation/intrinsic pathway

38
Q

***Thrombomodulin

A

-

39
Q

***Tissue factor (tissue thromboplastin)

A
  • activates extrinsic pathway when plasma comes in contact with tissue factor
  • binds factor VIIa
40
Q

***Protein S

A

-

41
Q

***Protein C

A

-

42
Q

***Antithrombin III (also called antithrombin)

A

-

43
Q

***Factor XIII (fibrin-stabilizing factor)

A

-cross liinks shit

44
Q

***Prostacyclin (prostaglandin I2)

A

-

45
Q

***Heparin

A

-

46
Q

***Tissue plasminogen activators

A

-

Physio Test 2 (10 decks)

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