Blood production and Clotting

Question 1

ERYTHROPOIESIS
What is erythropoiesis?
What stimulates the process?
What is the hormone and where is it secreted that creates this process?

Answer 1

The creation of red blood cells.
Tissue hypoxia (O2 level is below normal in tissue).
Erythropoietin is secreted by the kidney.

Question 2

RBC Antigens and Antibodies.

Name the two blood systems

Answer 2

ABO System

RH Factor

Question 3

Explain the ABO system.

Answer 3

Red blood cells contain antigens on their cellular membrane. These identify blood type. A, B, O, and AB. Blood develops antibodies to other antigens besides the one you have. Generally A or B

Antigen A — Anti-B
Antigen B — Anti-A
Antigen O — Anti-A and Anti-B
Antigen AB –Neither Anti-A nor Anti-B

Question 4

EMERGENCY TRANSFUSIONS

Explain Universal Donor and Universal Recipient.

Answer 4

Universal Donor is Type O–Since type O has no antigens, the antibodies of the recipient will not attack it regardless of blood type of recipient.

Universal Recipient is Type AB–Since type AB has neither A nor B antibodies, it will not attack donor RBCs regardless of antigen type.

Question 5

What determines Rh Factor?

What is the Rh factor?

Why is it important?

Answer 5

Determined by the presence or absence of an antigen (termed D) on RBC surface.

Rh + … D is present.
Rh - … D is absent.

Rh is important in hemolytic anemia.

Question 6

Hemolytic anemia. explain the four steps.

Answer 6

1st pregnancy, Mother is Rh-, fetus is Rh+.

Childbirth, during childbirth, blood from mother and fetus mix exposing mother to the D antigen.

Mother develops antibodies to D.

2nd childbirth, when blood from mother containing Anti-D mixes with fetus (Rh+) it causes RBCs of child to hemolyze. Child could become anemic and die.

Question 7

Hemostasis

what is it?
What are the three steps to fix it?

Answer 7

Damage of a blood vessel.

All 3 are initiated simultaneously. Some are faster than others.
Vascular spasm.
Formation of a platelet plug.
Formation of a clot.

Question 8

VASCULAR SPASM

Describe the 3 parts to the process

Answer 8

Immediate response (vascular constriction)–purpose is to reduce blood flow to area keeping blood loss to a minimum as clot is formed.

Intrinsic mechanism (poorly understood), initiated at site of damage.

Sympathetic nervous system activation causes further vasoconstriction. (a1–excitatory stimulus constricts blood vessel.

Question 9

PLATELETS

What are they?

***What special components do they add to plasma? 5

Answer 9

Non-nucleated fragments of megakaryocytes.

Possess granules containing a variety of substances that can be secreted into plasma to create a blood clot.
ADP
Serotonin
Epinephrine
Thromboxane A2
vonWillebrand factor (vWf)

Question 10

Under normal circumstances, blood vessel endothelium secretes two substances to inhibit platelet aggregation (make platelets repel each other). What are they?

Answer 10

Prostacyclin and Nitric Oxide.

Question 11

von WILLEBRAND FACTOR

Where is it synthesized?

How much of it and where is it found?

***What is its key function?

Answer 11

Synthesized in the liver. Dumped in plasma.

Protein found in plasma in relatively small quantities under normal conditions.

Also secreted by platelets and blood vessel endothelial cells.

Key protein in the initiation of the formation of a platelet plug.

Question 12

FORMATION OF A PLATELET PLUG

What is the 3 step process?

Answer 12

When blood contacts NEGATIVELY charged high concentration of collagen fibers in subendothelial tissue, vWf binds to collagen and attracts platelets.

Platelets then bind to vWf anchoring them in place.

When platelets bind to vWf they undergo a “platelet release reaction”. (dump granular components into region. )

Question 13

PLATELET RELEASE

What type of feedback system is this?
What causes vasoconstriction?
What does ADP do?
What happens once platelets are aggregated?
What is the second function of ADP and its three outcomes?

Answer 13

Major positive feedback system.

Serotonin and epinephrine cause vasoconstriction.

ADP (makes platelets sticky) stimulates morphological change in platelets, causing them to adhere to one another and aggregate.

Aggregated platelets release more ADP causing more aggregation (positive feedback).

ADP also stimulates the release of Thrmboxane A2, which has 3 hemostatic functions…
Vasoconstriction
Stimulation of platelet aggregation
Promote ADP release from platelets.

Question 14

FORMATION OF A CLOT

What protein helps make the clot?
What other molecules are utilized to form a clot?
What motion solidifies the clot?

Answer 14

Formation of a FIBRIN web around platelet plug and RBCs.

Utilizes phospholipids on surface of activated platelets and secretory products of aggregated platelets.

Squeezes and contracts to make a clot.

Question 15

CLOTTING FACTORS
What are always present?
What activates them?

Answer 15

Plasma proteins are ALWAYS present in inactive form.

Activation results from proteolytic (enzymatic) hydrolysis of certain peptide bonds.

Question 16

What is the key to clot formation? (enzyme)

Describe how this key turns fibrinogen into fibrin. 6 steps

Answer 16

Thrombin

Convert fibrinogen to insoluble fibrin in order to contract and bind the clot to make it stable.
Needs thrombin to catalyze fibrinogen.
Thrombin is originally inactive as Prothrombin.
Clotting factor 10 (Xa) is activated.
Xa, V, Ca++, and PF3 (platelet factor 3) form a prothrombin activation complex to convert prothrombin to thrombin. Thrombin then converts fibrinogen to fibrin.

Question 17

In addition to converting fibrinogen to fibrin, thrombin has additional roles. name them.

Answer 17

Activates Factor XIII (fibrin-stabilizing factor), form covalent links between strands of fibrin to tighten the meshwork.

Provides positive feedback for its own activation.

Question 18

What initiates the Intrinsic pathway to clot formation? What are the five chain steps till inactive X?

Answer 18

Inactive XII contacts the negative collagen surface and activates. This initiates the chain.

1. Inactive XII contacts collagen–activates to XIIa.
2. XIIa activates inactive XI–XIa.
3. XIa forma a complex with Ca++ and activates inactive IX–IXa.
4. IXa combines with VIII, Ca++, and PF3 to activate inactive X–Xa
5. Xa, V, Ca++, and PF3 (platelet factor 3) form a prothrombin(II) activation complex to convert prothrombin to thrombin(IIa).
6. Thrombin then converts fibrinogen to fibrin (loose), and activates inactive XIII–XIIIa
7. XIIIa tightens fibrin (loose) to fibrin (stabilized meshwork).

Question 19

What initiates the Extrinsic pathway to clot formation? What is its step to shortcut to pathway formation?

Answer 19

1. Tissue damage allows Inactive tissue factor (III) and Inactive VII and Ca++ make a complex–Tissue factor/VIIa complex.
2. Tissue factor/VIIa complex activates inactive X–Xa
3. Xa, V, Ca++, and PF3 (platelet factor 3) form a prothrombin(II) activation complex to convert prothrombin to thrombin(IIa).
4. Thrombin then converts fibrinogen to fibrin (loose), and activates inactive XIII–XIIIa
5. XIIIa tightens fibrin (loose) to fibrin (stabilized meshwork).

Question 20

DISSOLVING CLOTS
What dissolves clots?
What biomolecule is this enzyme derived from and what is it’s name?

Answer 20

Clots are dissolved by PLASMIN, an ENZYME.

Plasmin is derived from PLASMINOGEN, and plasma PROTEIN.