Post on 02-Jan-2016
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
CONTROL OF ERYTHROCYTE PRODUCTION
Figure 10.5, step 2
Stimulus: DecreasedRBC count, decreasedavailability of O2 toblood, or increasedtissue demands for O2
Normal blood oxygen levels
Imbalance
Imbalance
CONTROL OF ERYTHROCYTE PRODUCTION
Figure 10.5, step 3
Reduced O2
levels in blood
Stimulus: DecreasedRBC count, decreasedavailability of O2 toblood, or increasedtissue demands for O2
Normal blood oxygen levels
Imbalance
Imbalance
CONTROL OF ERYTHROCYTE PRODUCTION
Figure 10.5, step 4
Reduced O2
levels in blood
Stimulus: DecreasedRBC count, decreasedavailability of O2 toblood, or increasedtissue demands for O2
Kidney releaseserythropoietin
Normal blood oxygen levels
Imbalance
Imbalance
CONTROL OF ERYTHROCYTE PRODUCTION
Figure 10.5, step 5
Reduced O2
levels in blood
Stimulus: DecreasedRBC count, decreasedavailability of O2 toblood, or increasedtissue demands for O2
Erythropoietinstimulates
Kidney releaseserythropoietin
Red bonemarrow
Normal blood oxygen levels
Imbalance
Imbalance
CONTROL OF ERYTHROCYTE PRODUCTION
Figure 10.5, step 6
Reduced O2
levels in blood
Stimulus: DecreasedRBC count, decreasedavailability of O2 toblood, or increasedtissue demands for O2
Erythropoietinstimulates
Kidney releaseserythropoietinEnhanced
erythropoiesis
Red bonemarrow
MoreRBCs
Normal blood oxygen levels
Imbalance
Imbalance
CONTROL OF ERYTHROCYTE PRODUCTION
Figure 10.5, step 7
Reduced O2
levels in blood
Stimulus: DecreasedRBC count, decreasedavailability of O2 toblood, or increasedtissue demands for O2
IncreasedO2- carryingability of blood
Erythropoietinstimulates
Kidney releaseserythropoietinEnhanced
erythropoiesis
Red bonemarrow
MoreRBCs
Normal blood oxygen levels
CONTROL OF ERYTHROCYTE PRODUCTION
Figure 10.5, step 8
Reduced O2
levels in blood
Stimulus: DecreasedRBC count, decreasedavailability of O2 toblood, or increasedtissue demands for O2
IncreasedO2- carryingability of blood
Erythropoietinstimulates
Kidney releaseserythropoietinEnhanced
erythropoiesis
Red bonemarrow
MoreRBCs
Normal blood oxygen levels
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)
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
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
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?