Download Blood+&+Clot+Formation+Blood+Groups

HEMATOPOIESIS
Blood cell formation
Occurs in red bone marrow
Adult red marrow is found in ribs, vertebrae, sternum, pelvis, proximal humeri, and
proximal femurs.
HEMATOPOIESIS
All blood cells are derived from a
common stem cell (hemocytoblast)
Hemocytoblast differentiation
Lymphoid stem lymphocytes
Myeloid stem cell all other formed
elements
Figure 10.4
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
Stimulus: Decreased
RBC count, decreased
availability of O2 to
blood, or increased
Normal blood oxygen levels tissue demands for O
2
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
Increased
O2- carrying
ability of blood
Reduced O2
levels in blood
More
RBCs
Enhanced
Erythropoietin
erythropoiesis
Red bone stimulates
marrow
Kidney releases
erythropoietin
Figure 10.5
CONTROL OF ERYTHROCYTE PRODUCTION
Normal blood oxygen levels
Figure 10.5, step 1
CONTROL OF ERYTHROCYTE PRODUCTION
Normal blood oxygen levels
Stimulus: Decreased
RBC count, decreased
availability of O2 to
blood, or increased
tissue demands for O2
Figure 10.5, step 2
CONTROL OF ERYTHROCYTE PRODUCTION
Normal blood oxygen levels
Stimulus: Decreased
RBC count, decreased
availability of O2 to
blood, or increased
tissue demands for O2
Reduced O2
levels in blood
Figure 10.5, step 3
CONTROL OF ERYTHROCYTE PRODUCTION
Normal blood oxygen levels
Stimulus: Decreased
RBC count, decreased
availability of O2 to
blood, or increased
tissue demands for O2
Reduced O2
levels in blood
Kidney releases
erythropoietin
Figure 10.5, step 4
CONTROL OF ERYTHROCYTE PRODUCTION
Normal blood oxygen levels
Stimulus: Decreased
RBC count, decreased
availability of O2 to
blood, or increased
tissue demands for O2
Reduced O2
levels in blood
Kidney releases
erythropoietin
Erythropoietin
stimulates
Red bone
marrow
Figure 10.5, step 5
CONTROL OF ERYTHROCYTE PRODUCTION
Normal blood oxygen levels
Stimulus: Decreased
RBC count, decreased
availability of O2 to
blood, or increased
tissue demands for O2
Reduced O2
levels in blood
More
RBCs
Kidney releases
erythropoietin
Enhanced
erythropoiesis
Erythropoietin
stimulates
Red bone
marrow
Figure 10.5, step 6
CONTROL OF ERYTHROCYTE PRODUCTION
Normal blood oxygen levels
Stimulus: Decreased
RBC count, decreased
availability of O2 to
blood, or increased
tissue demands for O2
Increased
O2- carrying
ability of blood
Reduced O2
levels in blood
More
RBCs
Kidney releases
erythropoietin
Enhanced
erythropoiesis
Erythropoietin
stimulates
Red bone
marrow
Figure 10.5, step 7
CONTROL OF ERYTHROCYTE PRODUCTION
Normal blood oxygen levels
Stimulus: Decreased
RBC count, decreased
availability of O2 to
blood, or increased
tissue demands for O2
Increased
O2- carrying
ability of blood
Reduced O2
levels in blood
More
RBCs
Kidney releases
erythropoietin
Enhanced
erythropoiesis
Erythropoietin
stimulates
Red bone
marrow
Figure 10.5, step 8
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 phases
1. Vascular spasms
2. Platelet plug formation
3. Coagulation (blood clotting)
HEMOSTASIS
Figure 10.6
HEMOSTASIS- STEP 1
Vascular spasms
 Vasoconstriction causes blood vessel to spasm
 Spasms narrow the blood vessel, decreasing blood
loss
Step 1: Vascular Spasms
Figure 10.6, step 1
HEMOSTASIS- STEP 2
Step 1: Vascular Spasms
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
Step 2:
Platelet Plug Formation
Injury to lining
of vessel exposes
collagen fibers;
platelets adhere
Collagen
fibers
Figure 10.6, step 2
HEMOSTASIS – STEP 3
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)
Step 1: Vascular Spasms
Step 2:
Platelet Plug Formation
Injury to lining
Platelet
of vessel exposes plug
collagen fibers;
forms
platelets adhere
Collagen
Platelets
fibers
Platelets release chemicals
that attract more platelets to
the site and make nearby
platelets sticky
PF3 from
platelets
+
Calcium
and other
clotting
factors
in blood
plasma
Tissue factor
in damaged
tissue
Figure
10.6, step 4
HEMOSTASIS – COAGULATION CONTINUED
 Thrombin joins fibrinogen proteins
into hair-like molecules of
insoluble fibrin
 Fibrin forms a meshwork (the
basis for a clot)
Platelets release chemicals
that attract more platelets to
the site and make nearby
platelets sticky
PF3 from
platelets
+
Tissue factor
in damaged
tissue
Phases of
coagulation
(clotting
cascade)
Prothrombin
Fibrinogen
(soluble)
Calcium
and other
clotting
factors
in blood
plasma
Formation of
prothrombin
activator
Thrombin
Fibrin
Figure 10.6, step 7
(insoluble)
HEMOSTASIS
Blood usually clots within 3 to 6
minutes
The clot remains as endothelium
regenerates
The clot is broken down after tissue
repair
Figure 10.7
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 DISORDERS
Thrombocytopenia
 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
Blood samples are mixed with antiA 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
Figure 10.8
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?