Blood (p2) Flashcards

1
Q

What is fibrinolysis?

A

Removal of clot when its no longer needed

  • key enzyme = plasmin (precursor is plasminogen, a plasma protein that gets incorporated into the clot)
  • plasminogen is ctivated by tPA (tissue plasminogen activator) released by endothelial cells
  • begins within 2 days at outer edges and continues until clot is fully dissolved
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2
Q

What are the 2 homeostatic mechanisms to control the size of a clot?

A

1) swift removal of coagulation factors - procoagulation factions; ensures clotting doesnt occur where its not needed

2) inhibition of activated clotting factors - so clotting does not expand too far from the initial clot

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3
Q

What are the different concentrations that clot formation requires?

A

[procoagulation factors] > [anticoagulation factors]

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4
Q

What are some factors that limit clot growth/formation?

A
  • normally flowing blood washes away procoagulants (importance of vascular spasms in response to injury - slowing down blood flow)
  • as thrombin forms, it is adsorbed onto fibrin threads, to keep it in the vicinity of injury
  • antithrombin III inactivates any escaping thrombin
  • antithrombin III and protein C inaactivate many intrinsic pathway (slower) procoagulants (prevents clot from getting too large)
  • heparin (basophils and mast cells) enhance activity of antithrombin III and inhibits intrinsic pathway
  • smooth endothelial lining of undamaged blood vessels prevents undesirable clotting (no access to collagen)
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5
Q

what is a thrombus?

A

clot that develops and pesists in an unbroken blood vessel - can block critical blood circulation to those tissues

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6
Q

What might promote thrombus formation in an unbroken blood vessel?

A

Could be veins in someone on a plane who isnt moving around very much

Could be someone with atherosclerosis (slight damage to the inside in some areas of blood vessel walls - endothelial cells are more prone to peeling off)

Could have hypertension (increased blood pressure) which might increase peeling

Exposure to inner vessel to collagen triggering blood clotting

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7
Q

What is an embolus ?

A

A thrombus which has broken free, can get stuck in a vessel of small diameter

  • Completely blocks blood flow in smaller diameter veseels (pulmonary or cererbral emboli)
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8
Q

Why is a low dose aspirin a good preventative therapy in heart attack risk patients?

A

Low does aspirin = blood thinner

  • can interfere with production of prostaglandins that are prcoagulants
  • prevents too much blood clotting in people who are at risk of excessive clotting without completely interfering with blodd clot formation inside and outside
  • inside clotting = bruises
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9
Q

What are some examples of bleeding disorders that interfere with normal clotting?

A

1) Thrombocytopenia = any condition harmful to bone marrow -> easy bruising due to internal hemorrhage

  • ex. petechiae
  • platelet count is below the normal range but there are still some
  • whole blood transfusions are temporary -> bc lifespan of a platelet is only 10 days (short-lived)

2) Impaired liver function = liver disease also associated with reudced bile production - bile needed to adsorb vitamin K

  • vitamin K = important in some factors involving the intrinsic pathways; fat soluble vitamin deficient in some procoagulants as a result

3) Hemophilias = hereditary bleeding disorders due to deficiencies in intrinsic pathway factors; sex-linked and require regular transfusions

  • hemophilia A = lacking factor VIII
  • hemophilia B = lacking factor IX
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10
Q

What is donor blood mixed with?

A

Anticoagulant - citrate dextrose, a calcium chelator

  • Ca+2 is a very important cofactor in the process of blood clotting, soaking it up will keep blood from coagulating, keeping it nice and fluid
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11
Q

Why is type O the universal donor? Why is type AB the universal recipient?

A

Type O = RBCs have neither antigen ∴ will not induce antibodies

Type AB = Dont produce eihter antibodies

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12
Q

Which blood type is the most common? the least common?

A

Most = O or A
Least = AB

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13
Q

What do RBC antigens do?

A

Promote agglutination - antibodies that bind to antigens

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14
Q

How are Rh antibodies formed?

A

Not spontaneously formed in blood of Rh- indivs

  • indivs become sensitized upon first exposure to Rh antigens (tranfusions, carrying an Rh+ fetus)
  • antibodies will attack donor RBCs in response to second and subsequent exposures
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15
Q

What are Rh- mothers treated with if they are carrying an Rh+ fetus?

A

RhoGAM = an anti-Rh serum

  • prevents erythroblastosis fetalis
  • keeps her nbody from reacting to the Rh+ factor in fetus
  • keeps her immune system from creating antibodies that attack the fetus
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16
Q

In a transfusion reaction, why is the problem the recipients agglutinis (antibodies), not the donors?

A

If someone is given a mismatched transfusion there is a finite amount of antibodies (if any), it will get diluted in the recipients circulatory system

  • then antibodies wont remain for long but may still cause agglutination

1) agglutination = clogs small blood vessels
2) clumped RBC s rupture/destroyed by phagocytes and Hb released

17
Q

What is an autolgous transfusion?

A

Someone can donate their own blood prior to a surgery that may need it and have that blood e stored and used when and if needed for them

  • this is the best way to prevent agglutination/immune responses from blood of someone else
18
Q

What is blood typing?

A

Uses serum containing anti-A or anti-B agglutinins

  • reacting with the anti-serums indicates that blood type is present
  • Anti-B serum responds to type B blood and vice versa with Anti-A serum

A and B react = type AB
Only A reacts = type A
Only B reacts = type B
Neither A or B reacts = type O