hematopoiesis blood cell formation occurs in red bone marrow adult red marrow is found in ribs,...

HEMATOPOIESIS

Blood cell formation

Occurs in red bone marrow

Adult red marrow is found in ribs, vertebrae, sternum, pelvis, proximal humeri, and proximal femurs.

Figure 10.4

HEMATOPOIESIS

All blood cells are derived from a common stem cell (hemocytoblast)

Hemocytoblast differentiationLymphoid stem lymphocytesMyeloid stem cell all other formed elements

FORMATION OF ERYTHROCYTES

Mature RBC are anucleate= NO NUCLEUS. Therefore, Unable to divide, grow, or synthesize proteins Wear out in 100 to 120 days

When worn out, RBCs are eliminated by phagocytes in the spleen or liver

Lost cells are replaced by division of hemocytoblasts in the red bone marrow

CONTROL OF ERYTHROCYTE PRODUCTION

Figure 10.5

Reduced O2

levels in blood

Stimulus: DecreasedRBC count, decreasedavailability of O2 toblood, or increasedtissue demands for O2

IncreasedO2- carryingability of blood

Erythropoietinstimulates

Kidney releaseserythropoietinEnhanced

erythropoiesisRed bonemarrow

MoreRBCs

Normal blood oxygen levels

Imbalance

Imbalance

Rate is controlled by a hormone (erythropoietin)

Kidneys produce most erythropoietin as a response to reduced oxygen levels in the blood

Homeostasis is maintained by negative feedback from blood oxygen levels


Figure 10.5, step 1



Figure 10.5, step 2



Imbalance

Imbalance


Figure 10.5, step 3

Reduced O2

levels in blood



Imbalance

Imbalance


Figure 10.5, step 4

Reduced O2

levels in blood


Kidney releaseserythropoietin


Imbalance

Imbalance


Figure 10.5, step 5

Reduced O2

levels in blood



Kidney releaseserythropoietin

Red bonemarrow


Imbalance

Imbalance


Figure 10.5, step 6

Reduced O2

levels in blood




erythropoiesis

Red bonemarrow

MoreRBCs


Imbalance

Imbalance


Figure 10.5, step 7

Reduced O2

levels in blood





erythropoiesis

Red bonemarrow

MoreRBCs



Figure 10.5, step 8

Reduced O2

levels in blood





erythropoiesis

Red bonemarrow

MoreRBCs


Imbalance

Imbalance

FORMATION OF WHITE BLOOD CELLS

Colony stimulating factors (CSFs) and interleukins prompt bone marrow to generate leukocytes

FORMATION OF PLATELETS

The stem cell (megakaryocyte) undergoes mitosis without cytokinesis many times, forming a large, multinuclear cell, which then fragments into platelets.

HEMOSTASIS

Stoppage of bleeding resulting from a break in a blood vessel

Hemostasis involves three phases1. Vascular spasms2. Platelet plug formation3. Coagulation (blood clotting)

Figure 10.6

HEMOSTASIS

HEMOSTASIS- STEP 1

Figure 10.6, step 1

Step 1: Vascular SpasmsVascular spasms Vasoconstriction causes blood vessel to spasm Spasms narrow the blood vessel, decreasing

blood loss

HEMOSTASIS- STEP 2

Figure 10.6, step 2

Injury to liningof vessel exposescollagen fibers;platelets adhere

Collagenfibers

Step 1: Vascular Spasms

Step 2:Platelet Plug Formation

Platelet plug formation Collagen fibers are exposed by a break in a

blood vessel Platelets become “sticky” and cling to fibers Anchored platelets release chemicals to

attract more platelets Platelets pile up to form a platelet plug

HEMOSTASIS – STEP 3

Figure 10.6, step 4

Injury to liningof vessel exposescollagen fibers;platelets adhere

Plateletplugforms

Platelets release chemicalsthat attract more platelets tothe site and make nearbyplatelets sticky

Collagenfibers Platelets

PF3 fromplatelets Calcium

and otherclottingfactorsin bloodplasma

Tissue factorin damagedtissue

Step 1: Vascular Spasms

Step 2:Platelet Plug Formation

+

Coagulation Injured tissues release tissue factor (TF) PF3 (a phospholipid) interacts with TF,

blood protein clotting factors, and calcium ions to trigger a clotting cascade

Prothrombin activator converts prothrombin to thrombin (an enzyme)

HEMOSTASIS – COAGULATION CONTINUED

Figure 10.6, step 7

Platelets release chemicalsthat attract more platelets tothe site and make nearbyplatelets sticky

PF3 fromplatelets Calcium

and otherclottingfactorsin bloodplasma

Formation ofprothrombinactivator

Prothrombin

Fibrinogen(soluble)

Fibrin(insoluble)

Thrombin

Tissue factorin damagedtissue

Phases ofcoagulation(clottingcascade)

+

Thrombin joins fibrinogen proteins into hair-like molecules of insoluble fibrin

Fibrin forms a meshwork (the basis for a clot)

HEMOSTASIS

Figure 10.7

Blood usually clots within 3 to 6 minutes

The clot remains as endothelium regenerates

The clot is broken down after tissue repair

SUMMARY OF HEMOSTASIS

Hemostasis is initiated by a break in the blood vessel wall (or lining), initiating vascular spasms and causing platelets to cling to the damaged site. Once attached, the platelets release serotonin, which enhances vasoconstriction.

Injured tissue cells release tissue factor, which interacts with platelet phospholipids (PF3), Ca2+ and plasma clotting factors to form prothrombin activator.

Prothrombin activator converts prothrombin to thrombin. Thrombin, an enzyme, then converts soluble fibrinogen molecules into long fibrin threads, which form the basis of the clot and then traps erythrocytes flowing by in the blood.

UNDESIRABLE CLOTTING

Thrombus A clot in an unbroken blood vessel Can be deadly in areas like the heart

Embolus A thrombus that breaks away and floats freely in the bloodstream Can later clog vessels in critical areas such as the brain

Coagulation can be promoted by: i. Roughened vessel lining, which attracts/activates platelets. ii. Pooling of blood within vessels can result in the activation of clotting factors and the initiation of the coagulation process.

BLEEDING DISORDERSThrombocytopenia Platelet deficiency Even normal movements can cause bleeding from small blood vessels

that require platelets for clotting

The liver is the source of fibrinogen and several other factors that are necessary for clotting. When the liver is damaged and dysfunctional, it becomes unable to synthesize the usual amounts of clotting factors. When this situation happens, abnormal and often severe bleeding episodes can occur

Hemophilia Hereditary bleeding disorder Normal clotting factors are missing

http://www.sciencecases.org/hemo/hemo.asp

THE ROYAL DISEASE

REVIEW QUESTIONS #1

1. What is the name of the stem cell that gives rise to all other formed elements?

2. Name the formed elements that arise from myeloid stem cells. Name those arising from lymphoid stem cells.

3. What property of RBCs dooms them to a limited life span of only 120 days?

4. What WBC type resides primarily in the tissues of the body?

5. How is the production of platelets different from that of all other formed elements?

6. Describe the process of hemostasis. Indicate what starts the process.

7. What factors enhance the risk of thrombus formation in intact blood vessels?

8. How can liver dysfunction cause bleeding disorders?

BLOOD GROUPS AND TRANSFUSIONS

Large losses of blood have serious consequences Loss of 15–30% causes weakness Loss of over 30% causes shock, which can be fatal

Transfusions are the only way to replace blood quickly

Transfused blood must be of the same blood group

HUMAN BLOOD GROUPS

Blood contains genetically determined proteins

Antigens (a substance the body recognizes as foreign) may be attacked by the immune system

Antibodies are the “recognizers”

Blood is “typed” by using antibodies that will cause blood with certain proteins to clump (agglutination)

HUMAN BLOOD GROUPS

There are over 30 common red blood cell antigens

The most vigorous transfusion reactions are caused by ABO and Rh blood group antigens

ABO BLOOD GROUPS

Based on the presence or absence of two antigens Type A Type B

The lack of these antigens is called type O

ABO BLOOD GROUPS

The presence of both antigens A and B is called type AB

The presence of antigen A is called type A

The presence of antigen B is called type B

The lack of both antigens A and B is called type O

ABO BLOOD GROUPS

Blood type AB can receive A, B, AB, and O blood Universal recipient

Blood type B can receive B and O blood

Blood type A can receive A and O blood

Blood type O can receive O blood Universal donor

ABO BLOOD GROUPS

Table 10.3

RH BLOOD GROUPS

Named because of the presence or absence of one of eight Rh antigens (agglutinogen D) that was originally defined in Rhesus monkeys

Most Americans are Rh+ (Rh positive)

Problems can occur in mixing Rh+ blood into a body with Rh– (Rh negative) blood

Percentage of Population with Each Blood Type

Rh+ Rh-

O 38.5% 6.5%

A 34.3% 5.7%

B 8.6% 1.4%

AB 4.3% 0.7%

RH DANGERS DURING PREGNANCY

Danger occurs only when the mother is Rh– and the father is Rh+, and the child inherits the Rh+ factor

RhoGAM shot can prevent buildup of anti-Rh+ antibodies in mother’s blood

RH DANGERS DURING PREGNANCY

The mismatch of an Rh– mother carrying an Rh+ baby can cause problems for the unborn child

The first pregnancy usually proceeds without problems The immune system is sensitized after the first pregnancy In a second pregnancy, the mother’s immune system produces

antibodies to attack the Rh+ blood (hemolytic disease of the newborn)

BLOOD TYPING

Figure 10.8

Blood samples are mixed with anti-A and anti-B serum

Coagulation or no coagulation leads to determining blood type

Typing for ABO and Rh factors is done in the same manner

Cross matching—testing for agglutination of donor RBCs by the recipient’s serum, and vice versa

REVIEW QUESTIONS #2

9. What are the classes of human blood groups based on?

10.What are agglutinins?

11.Name the four ABO blood groups.

12.What is a transfusion reaction? Why does it happen?

10. What is the probable result from infusion of mismatched blood?

11. Cary is bleeding profusely after being hit by a truck as he was pedaling his bike home. At the hospital, the nurse asked him whether he knew his blood type. He told her he “had the same blood as most other people.” What is his ABO blood type?

12.What is the difference between an antigen and an antibody?

13.Explain why a Rh- person does not have a transfusion reaction on the first exposure to Rh+ blood? Why is there a transfusion reaction the second time he or she receives the Rh+ blood?

hematopoiesis blood cell formation occurs in red bone marrow adult red marrow is found in ribs,...

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