Chapter 11 - Blood

I. erythrocytes (RBCs) carry oxygen and CO2

A. structure reflects function:

1. biconcave disk

a. large surface area for diffusion

b. short diffusion distance

c. flexible

2. no nucleus or organelles

B. hemoglobin (Hb)

1. structure: each molecule consists of 4 units, each containing

a. a peptide chain (normal adult Hb has 2 alpha and 2 beta peptide chains)

the peptide part of the molecule carries CO2 and buffers H+

b. a heme group (Fe:O2)

2. normal adult levels:

a. female - 14 g/dL

b. male - 16 g/dL

C. erythropoiesis

1. occurs in myeloid tissue (red bone marrow)

stem cells = hemocytoblasts divide by mitosis

one daughter cell becomes the new hemocytoblast

the other daughter cell differentiates into an erythrocyte

synthesis of Hb, loss of nucleus and organelles

2. control

a. hypoxia causes kidneys to secrete erythropoietin (EPO)

b. erythropoietin acts on partly differentiated cells in RBC lineage to increase rate of maturation

c. negative feedback controls erythropoietin secretion

 

D. disorders

1. anemia = decreased ability of blood to carry O2

2. polycythemia = excess RBCs (primary or secondary)

a. causes

primary - tumor in bone marrow

secondary:

b. effects: increased blood viscosity, increased PR, increased MAP

 

II. leukocytes (WBC's)

A. functions

1. general:

a. defend body against pathogens

b. destroy cancer cells

c. remove dead and injured cells

2. specific:

a. neutrophils - phagocytes; engulf and destroy bacteria and debris

b. eosinophils - attack antibody-coated objects; release toxic chemicals

c. basophils - release histamine

d. lymphocytes - secrete antibodies

e. monocytes - become tissue macrophages

B. leukopoiesis

all WBCs originate in bone marrow

lymphocytes migrate to lymphoid tissue and are later cloned there

stem cell = hemocytoblast

rate controlled by colony-stimulating factors released by damaged tissue or leukocytes

III. platelets/thrombocytes

cell fragments - plasma membrane + granules of chemicals + actin and myosin

produced by bone marrow cells called megakaryocytes (derived from hemocytoblasts)

many stored in the spleen

involved in hemostasis and tissue repair

number controlled by thrombopoietin secreted by liver and kidney

IV. hemostasis = vascular spasm + platelet aggregation + coagulation

A. vascular spasm in muscular arteries and arterioles

1. intrinsic stimulus = chemicals from damaged cells

2. extrinsic stimulus = sympathetic stimulation and platelets

B. platelets attach to exposed collagen in blood vessel wall and then to each other (aggregation) and release chemicals (degranulation)

1. function of aggregation - to seal small breaks in vessel walls

2. aggregation is controlled by chemicals

a. ADP released by aggregated platelets causes free platelets to stick (positive feedback)

b. serotonin, epinephrine and thromboxane A2 from aggregated platelets reinforce vascular spasm

c. prostacyclin and NO released by undamaged endothelium inhibit platelet aggregation

d. platelet factor 3 participates in coagulation

C. coagulation

1. general mechanism (amplification)

a. formation of activated factor X (either pathway)

 

b. conversion of prothrombin into thrombin

 

c. conversion of fibrinogen into fibrin

 

d. clot retraction - activated fibrin forms a mesh that traps formed elements and plasma

platelets trapped in the clot contract

fibrin mesh shrinks (factor XIII)

2. alternate pathways for factor X activation

a. intrinsic pathway (slower)

exposed collagen or foreign surface

factor XII begins cascade

b. extrinsic pathway (faster)

damaged cells release tissue thromboplastin

requires Ca and factor VII

3. clot removal and prevention

a. removal of existing clots by plasmin (fibrinolysin)

plasminogen (made in liver, circulates in plasma) is activated by clotting factors

plasmin is a fibrinolytic enzyme that is activated and trapped in the clot as it forms

at first, clot formation exceeds clot removal; later removal exceeds formation until the clot is gone

b. prevention of unwanted clots

lungs secrete tPA, which activates plasminogen

heparin may prevent clots by inhibiting clotting factors

 

V. blood typing

A. blood groups are genetically determined by the presence of glycoprotein antigens (Ag) on the RBC membranes

B. plasma contains antibodies (Ab) that react against blood group antigens that are foreign

ABO: antibodies are formed by exposure to similar intestinal bacterial antigens after 6 mo of age

Rh: antibodies do not appear unless a person born without the Rh factor (Rh-) is later exposed to Rh antigens (from Rh+ blood)

   ABO  Rh
 Ag  A and B  8 altogether; D (RhD) is the one tested for
 Ab  anti-A and anti-B (preformed)  anti-Rh (anti-D)


 blood type  Ag  preformed Ab  Ab formed after exposure
 A neg      
 B neg      
 AB neg      
 O neg      
 A pos      
 B pos      
 AB pos      
 O pos      

C. transfusion reactions

 

   donor blood  recipient blood
 Ag    
 Ab    

1. reaction depends on volume:

a. small volume - recipient Abs attack donor Ags

b. large volume - donor Abs attack recipient Ags

2. effects:

a. agglutination - plasma Abs attach to RBC Ags and cause RBCs to stick together; clumps of agglutinated RBCs clog blood vessels

b. hemolysis - Hb blocks kidney tubules; causes renal failure

3. Rh - anti-Rh Abs are not developed until after an Rh- person has been exposed to Rh Ags by transfusion or through pregnancy

4. Rh factors and pregnancy:

   mother Rh+  mother Rh-
 fetus Rh+    
 fetus Rh-    

a. first pregnancy - usually no problem

mother is not exposed to fetal Rh Ags until delivery

she has no anti-Rh Abs in her blood during the pregnancy

b. subsequent pregnancy:

mother not treated:

anti-Rh Abs in her plasma cross placenta and attack fetal RBCs

mother treated:

after first pregnancy, mother given anti-Rh to block her immune response

no anti-Rh Abs are formed