A&PII Chapter 19 Part B

hemostasis

• Vascular spasm
• Platelet plug formation
• Coagulation

one of the mechanisms of hemostasis, when smooth muscles that are present in the blood vessel walls constrict (vasospasm)

• one of the mechanisms of hemostasis
• thrombocytes are usually sequestered on the lumens of blood vessels but go through 3 phases when vessels are lacerated.
• 1. Platelet adhesion
• 2. Platelet release reaction
• 3.Platelet aggregation

• Platelet adhesion is the first phase of platelet plug formation
• Thrombocytes accumulate in great numbers at the hemorrhage site and adhere to parts of the damaged vessel

Platelet release reaction is the second phase of platelet plug formation

the platelets undergo changes and release substances that cause the smooth muscles of the vessels to further contract to decrease blood flowhe platelets become extremely sticky and clump with each other at the site of vascular damage.

Platelet aggregation is the 3rd phase of platelet plug formation

thrombocytes are reinforced by fibrin threads and trap other platelets and formed elements to creat a mass called a platelet plug

• One of the 3 mechanisms of hemostasis
• it is the process by which a blood clot is formed
• complex involving a cascade effects which includes coagulation factors (12 main factors identified by Roman numerals)
• Each factor stimulates the formation of the next

There are 12 main coagulation (clotting) factors that are in no particular order

2 pathways lead to the activation of thrombin

Extrinsic pathway - initiated by chemicals outside the blood

Intrinsic pathway - initiated by platelets and plasma coagulation factors inside the blood vessels

Tissue thromboplastin (tissue factor - TF) is released from the tissues surrounding the blood vessels when they are damaged.

TF in the presence of coagulation factor X (Stuart factor) converts to prothrombin. Then calcium (always in blood) causes soluble prothrombin to change to insoluble thrombin.

damaged tissue = tissue thromboplastin +coagulation factor X= prothrombin + calcium = thrombin

the intrinsic pathway is initiated by platelets and plasma coagulation factors inside the blood vessels

the platelets and plasma release prothrombin which in the presence of several factors (all requiring vitamin K) are converted into thrombin

prothrombin + several factors + Vit K = thrombin

The thrombin in the presence of calcium coverts with soluble fibrinogen into a strong meshwork of insoluble fibrin threads. Factor XIII (fibrin stabilizing factor) is essential for this final conversion.

Once formed blood cells become entrapped in the mesh of fibrin threads, threads contract pulling the clot and rupture site together - syneresis. Serum is then squeezed out.

It is dissolved by an enzyme called plasmin in a process called fibrolysis.

Vitamin K is produced by intestinal bacteria and is absorbed when bile is present in the intestinal tract.

It is important in the intrinsic pathway (which leads to the activation of thrombin necessary for coagulation). It is required by several factors which all need it to convert prothrombin into thrombin.

compatible

• agglutination between the red cells
• agglutination results from red cells sticking to each other forming clumps

The antibodies of the plasma (agglutinins) bind with the antigens (agglutinogens) on the surface of the red cells.

antigens - agglutinogens - on the surface of the cells

antibodies - agglutinins - in the plasma

The antigen of the red blood cell.

• Antigen A
• Antibody B

No AB antigens in O blood

A,B antibodies

O is considered universal donor because of the lack of antigens, but they must receive O blood because of the AB antibodies.

Antigens A and B

No antibodies

AB is considered a universal recipient because of the lack of antibodies, but they can only give blood to someone who is AB also.

O - 45%

AB - 4%

No, they will produce them if given Rh positive blood.

• Fetus is Rh+ and mom is Rh-
• fetal blood leaks across the placenta at birth causing mom to produce Rh antibodies
• usually causes problems with later pregnancies, not the first
• the maternal antibodies cross the placenta and cause the fetal RBCs to rupture (hemolyze). Fetus usually dies unless the blood is completely replaced at birth

RhoGAM injection at birth can prevent the formation of anti-Rh antibodies

crossmatching - mixing of blood in vitro (in the glass) prior to in vivo (in the body) transfusion

Done in addition to blood typing and Rh compatibility

Yes, that is why in practice, terms like "universal" are misleading due to other possible incompatible blood systems.

That is why blood is always crossmatched.

Lymph and interstitial fluid are practically identical, lymph originates as interstitial fluid

• They have
• less protein than plasma
• variable # of WBCs
• They
• Do not contain RBC or platelets

lack of intrinsic factor needed for the absorption of vitamin B-12 which is needed for RBC production.

caused by loss of blood

• can be the cause of hemorrhagic anemia
• hidden blood loss often occurring in the gut

• can be cause of hemorrhagic anemia
• gross external blood loss

Fragile RBCs easily rupture

• destruction of bone marrow
• caused by radiation or chemical exposure

caused by abnormally shaped RBCs that are incompetent in transporting gases

• abnormal increase in the number of RBCs
• causes increase in viscosity of blood
• causes rise in BP and contributes to blood clots and hemorrhage

• Epstein-Barr virus
• high percentage of lymphocytes

• malignant disease of blood
• numerous immature and nonfunctional white blood cells

thrombus

embolus

chemical substances injected into the body to help dissolve blood clots

ex. Streptokinase (enzyme)

• they help prevent clot formation by inhibiting coagulation
• they are not blood thinners
• heparin and Coumadin are examples