packet 9 Flashcards
surfaces are marked by genetically determined glycoproteins & glycolipids
agglutinogens or isoantigens
RBC
display only antigen A
type A
display only antigen B
type B
display both antigens A & B
type AB
display neither antigen
type O
contains isoantibodies or agglutinins to the A or B antigens not found in your blood
plasma
anti-A antibody reacts with
antigen A
anti-B antibody reacts with
antigen B
People with Rh agglutinogens on RBC surface are
Rh+
Antibodies develop only in Rh- blood type & only with exposure to the antigen through
transfusion of positive blood
during a pregnancy with a positive blood type fetus
Transfusion reaction upon 2nd exposure to the antigen results in __ of the RBCs in the donated blood
hemolysis
People with type __blood called “universal recipients” since have no antibodies in plasma
*only true if cross match the blood for other antigens
AB
People with type _ blood cell called “universal donors” since have no antigens on their cells
*theoretically can be given to anyone
O
Stoppage of bleeding in a quick & localized fashion when blood vessels are damaged Prevents hemorrhage (loss of a large amount of blood)
hemostasis
methods used for hemostasis
vascular spasm
platelet plug formation
blood clotting (coagulation = formation of fibrin threads)
Platelets store a lot of chemicals in granules needed for
platelet plug formation
Steps in the process
of platelet plug formation
(1) platelet adhesion (2) platelet release reaction (3) platelet aggregation
Platelets stick to exposed collagen underlying damaged endothelial cells in vessel wall
platelet adhesion
Platelets activated by adhesion
Extend projections to make contact with each other
Release thromboxane & activate other platelets
Thromboxane is also a vasoconstrictor decreasing blood flow through the injured vessel
platelet release reaction
Activated platelets stick together and activate new platelets to form a mass called a platelet plug
Plug reinforced by fibrin threads formed during clotting process
platelet aggregation
three pathways of clotting
- extrinsic pathway
- intrinsic pathway
- final common pathway
Damaged tissues leak tissue factor (thromboplastin) into bloodstream
Prothrombinase forms in seconds
In the presence of Ca+2, clotting factor X combines with V to form prothrombinase
extrinsic pathway
Activation occurs
endothelium is damaged & platelets come in contact with collagen of blood vessel wall
platelets damaged & release phospholipids
Requires several minutes for reaction to occur
Substances involved: Ca+2 and clotting factors XII, X and V
intrinsic pathway
Prothrombinase and Ca+2
thrombin
final common pathway
catalyze the conversion of prothrombin to thrombin
Prothrombinase and Ca+2
in the presence of Ca+2 converts soluble fibrinogen to insoluble fibrin threads
activates fibrin stabilizing factor XIII
positive feedback effects of thrombin
accelerates formation of prothrombinase
activates platelets to release phospholipids
thrombin
fat soluble vitamin absorbed if lipids are present
absorption slowed if bile release is insufficient
Required for synthesis of 4 clotting factors by hepatocytes
factors II (prothrombin), VII, IX and X
Produced by bacteria in large intestine
vitamin K for clotting
clot (thrombus) forming in an unbroken blood vessel
forms on rough inner lining of BV
if blood flows too slowly (stasis) allowing clotting factors to build up locally & cause coagulation
may dissolve spontaneously or dislodge & travel
thrombosis
clot, air bubble or fat from broken bone in the blood
pulmonary embolus is found in lungs
embolus
types of intravascular clotting
thrombosis
embolus
Inherited deficiency of clotting factors
bleeding spontaneously or after minor trauma
subcutaneous & intramuscular hemorrhaging
nosebleeds, blood in urine, articular bleeding & pain
hemophilia
Hemophilia A lacks factor (males only)
factor VIII
Hemophilia B lacks factor (males only))
factor IX
less severe because alternate clotting activator exists
males and females
hemophilia C
treatment for hemphilia
transfusions of fresh plasma or concentrates of the missing clotting factor
