Quiz 5: blood types and clotting (24) Flashcards

1
Q

stages of clotting

A
  • exposed collagen fibers in the walls of blood vessels initiate clotting mechanism through release of Von Willebrand factor from endothelial cells
  • platelets adhere to the free fibers and through use of psuedopods, draw together to form a platelet plug
  • platelets degranulate and release thromboxane A2 which promotes further platelet aggregation and vasoconstriction by the vessel muscularis layer.
  • coagulation of blood. this requires a cascade of events either extrinsic (15 second reaction time) or intrinsic (3-6 minute reaction time).
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2
Q

extrinsic pathway

A
  • initiated by tissue factor 3, released by the surrounding tissues when a blood vessel is ruptured
  • combines with factor 7 to form an enzyme complex, which when with CA+, can activate factor 10 in the blood, initiating common pathway.
  • rate of conversion is proportional to amount of damaged tissue. Abrasion will clot faster than a scalpel cut.

-factor 3 –> factor 7–> +Ca = Factor 10

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3
Q

Intrinsic pathway

A
  • presence of a rough/foreign agent within the blood vessel (eg. atheroma) can initiate an internal clotting mechanism that does not involve the surrounding tissues.
  • since this normally results in the occlusion of the vessel, the body makes it as complex as possible.
  • Platelets release factor 12, beginning the cascade
  • factor 12 activates factor 11, which activates factor 9. when Ca+ is added, this activates factor 8, an enzyme complex (9, 8, Ca) which then activates factor 10 of the common pathway.

factor 12–>factor 11–>factor 9–>factor 8–> + Ca+ =factor 10

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4
Q

common pathway

A
  • the activation of factor 10 sets off series of events that will actually form a clot.
  • factor 10 combines with 3 and 5 in the presence of PF3 and Ca to create Prothrombin Activator
  • the inactive prothrombin in the blood is converted to thrombin, which converts the inactive fibrinogen (also in the blood) to fibrin.
  • factor 13 and Ca produce crosslinks btwn fibrin threads, creating a meshwork (white thrombus). RBCs trapped in it fill up the spaces, producing the red thrombus (clot)
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5
Q

fate of the clot

A
  • clot retraction: fibrin threads adhere to the edges of the wound and after they have attached themselves, they shorten, pulling the edges of the wound together, reducing the size of the opening.
  • normally the clot is fully formed and bleeding stops after about 7 minutes.
  • platelets and endothelium stimulate the adjacent fibroblasts to undergo mitosis, creating granulation tissue under the clot–>initiation of new dermis
  • fibrinolysis–the dissolution fo the clot– begins almost immediatetly, permitting the fibroblasts to infiltrate the wounded area and repair it.
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6
Q

fibrinolysis

A
  • factor 12 and prekallikrein active kallikrein.
  • plasminogen is added and this creates plasmin. This is a positive feedback loop.
  • fibrin polymer is added to plasmin which leaded to clot dissolution and yields fibrin degradation productions.
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7
Q

blood types

A
  • RBCs have surface markers on them that identify the cell as “body own”. If blood is received from a person having different markers, the body will react as if it had a massive infection
  • two major groups and at least another 100 minor groups that mark the RBC surface. They are minor because they rarely cause a reaction when transfused into non-compatible host.
    - ABO and Rh+-
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8
Q

ABO Blood group

A
  • This blood group contains markers A and B. O indicates the absence of any marker
  • If the recipient blood is lacking A or B, then the donor A or B will serve as antigens against the antibodies of the recipient, causing an agglutination (the RBCs will stick together or clump)
  • if the donor has O blood, there are no antigens present on the RBC and no agglutination will occur.
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9
Q

Rh Blood Group

A
  • There are several antigens in this blood group but only Rhd reacts strongly enough with the recipient blood to be of concern. So if Rhd is present, the donor is Rh+. If Rhd is not present, the donor is Rh-
  • antibodies to Rh are not normally present in blood. If the recipient is Rh-, they must first be exposed to Rh before they produce antibodies.
  • Rh- women that give birth to Rh+ babies will have a normal first birth, but the baby’s blood will mingle with the mother’s blood during birth. As a result, she will make antibodies against Rh and subsequent pregnancies will result in erythroblastosis fetalis.
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10
Q

blood group frequencies

A

-occurrence of A, B, and O is not uniformly distributed across the planet.

  • A antigen is more common in europeans and africans
  • B antigen is more common in East Asians
  • O = most common throughout the world and is almost exclusively the blood type of native Americans and Australian aborigines.

Rh is found in 85–99%, making Rh- individuals very rare.

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